Input: Intracavitary chemotherapy (paclitaxel / carboplatin liquid crystalline cubic phases) for recurrent glioblastoma - - clinical observations. Human malignant brain tumors have a poor prognosis in spite of surgery and radiation therapy. Cubic phases consist of curved biocontinuous lipid bilayers, separating two congruent networks of water channels. Used as a host for cytotoxic drugs, the gel - like matrix can easily be applied to the walls of a surgical resection cavity. For human glioblastoma recurrences, the feasibility, safety, and short - term effects of a surgical intracavitary application of paclitaxel and carboplatin encapsulated by liquid crystalline cubic phases are examined in a pilot study. A total of 12 patients with a recurrence of a glioblastoma multiforme underwent re - resection and received an intracavitary application of paclitaxel and carboplatin cubic phases in different dosages. Six of the patients received more than 15 mg paclitaxel and suffered from moderate to severe brain edema, while the remaining patients received only a total of 15 mg paclitaxel. In the latter group, brain edema was markedly reduced and dealt medically. Intracavitary chemotherapy in recurrent glioblastoma using cubic phases is feasible and safe, yet the clinical benefit remains to be examined in a clinical phase II study.

paclitaxel

carboplatin

paclitaxel

carboplatin

paclitaxel

carboplatin

paclitaxel

paclitaxel

glioblastoma

brain tumors

glioblastoma

glioblastoma

brain edema

brain edema

glioblastoma

paclitaxel

brain edema

paclitaxel

brain edema

paclitaxel

brain edema

paclitaxel

brain edema

paclitaxel

brain edema

paclitaxel

brain edema

paclitaxel

brain edema

paclitaxel

brain edema

paclitaxel

brain edema

paclitaxel

brain edema


Input: Methylphenidate - induced obsessive - compulsive symptoms in an elderly man. An 82 - year - old man with treatment - resistant depression and early Alzheimer' s disease was started on methylphenidate. Significant obsessive - compulsive behavior ensued but diminished over several weeks when methylphenidate was replaced by fluvoxamine. The patient had no prior psychiatric history, but he had a sister with obsessive - compulsive disorder. It appears that methylphenidate precipitated the patient' s pathological behavior.

Methylphenidate

methylphenidate

methylphenidate

fluvoxamine

methylphenidate

obsessive - compulsive symptoms

treatment - resistant depression

Alzheimer' s disease

obsessive - compulsive behavior

psychiatric

obsessive - compulsive disorder

Methylphenidate

obsessive - compulsive symptoms

Methylphenidate

obsessive - compulsive behavior

Methylphenidate

obsessive - compulsive disorder

methylphenidate

obsessive - compulsive symptoms

methylphenidate

obsessive - compulsive behavior

methylphenidate

obsessive - compulsive disorder

methylphenidate

obsessive - compulsive symptoms

methylphenidate

obsessive - compulsive behavior

methylphenidate

obsessive - compulsive disorder

methylphenidate

obsessive - compulsive symptoms

methylphenidate

obsessive - compulsive behavior

methylphenidate

obsessive - compulsive disorder


Input: Cardiac arrest after intravenous metoclopramide - a case of five repeated injections of metoclopramide causing five episodes of cardiac arrest. We describe a patient where intravenous injection of metoclopramide was immediately followed by asystole repeatedly. The patient received metoclopramide 10 mg i. v. five times during 48 h. After interviewing the attending nurses and reviewing the written documentation, it is clear that every administration of metoclopramide was immediately (within s) followed by asystole. The asystole lasted 15 - 30 s on four occasions, on one occasion it lasted 2 min. The patient received atropine 0. 5 - 1 mg and chest compressions, before sinus rhythm again took over. We interpret this as episodes of cardiac arrest caused by metoclopramide. The rapid injection via the central venous route and the concomitant tapering of dopamine infusion might have contributed in precipitating the adverse drug reaction.

Cardiac arrest

cardiac arrest

asystole

asystole

asystole

cardiac arrest

metoclopramide

metoclopramide

metoclopramide

metoclopramide

metoclopramide

atropine

metoclopramide

dopamine

metoclopramide

Cardiac arrest

metoclopramide

cardiac arrest

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

cardiac arrest

metoclopramide

Cardiac arrest

metoclopramide

cardiac arrest

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

cardiac arrest

metoclopramide

Cardiac arrest

metoclopramide

cardiac arrest

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

cardiac arrest

metoclopramide

Cardiac arrest

metoclopramide

cardiac arrest

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

cardiac arrest

metoclopramide

Cardiac arrest

metoclopramide

cardiac arrest

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

cardiac arrest

metoclopramide

Cardiac arrest

metoclopramide

cardiac arrest

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

asystole

metoclopramide

cardiac arrest


Input: Severe immune hemolytic anemia associated with prophylactic use of cefotetan in obstetric and gynecologic procedures. Second - and third - generation cephalosporins, especially cefotetan, are increasingly associated with severe, sometimes fatal immune hemolytic anemia. We noticed that 10 of our 35 cases of cefotetan - induced hemolytic anemias were in patients who had received cefotetan prophylactically for obstetric and gynecologic procedures. Eight of these cases of severe immune hemolytic anemia are described.

hemolytic anemia

hemolytic anemia

hemolytic anemias

hemolytic anemia

cefotetan

cephalosporins

cefotetan

cefotetan

cefotetan

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemias

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemias

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemias

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemias

cefotetan

hemolytic anemia


Input: Cauda equina syndrome after spinal anaesthesia with hyperbaric 5% lignocaine: a review of six cases of cauda equina syndrome reported to the Swedish Pharmaceutical Insurance 1993 - 1997. Six cases of cauda equina syndrome with varying severity were reported to the Swedish Pharmaceutical Insurance during the period 1993 - 1997. All were associated with spinal anaesthesia using hyperbaric 5% lignocaine. Five cases had single - shot spinal anaesthesia and one had a repeat spinal anaesthetic due to inadequate block. The dose of hyperbaric 5% lignocaine administered ranged from 60 to 120 mg. Three of the cases were most likely caused by direct neurotoxicity of hyperbaric 5% lignocaine. In the other 3 cases, direct neurotoxicity was also probable, but unfortunately radiological investigations were not done to definitely exclude a compressive aetiology. All cases sustained permanent neurological deficits. We recommend that hyperbaric lignocaine should be administered in concentrations not greater than 2% and at a total dose preferably not exceeding 60 mg.

Cauda equina syndrome

cauda equina syndrome

cauda equina syndrome

neurotoxicity

neurotoxicity

neurological deficits

lignocaine

lignocaine

lignocaine

lignocaine

lignocaine

lignocaine

Cauda equina syndrome

lignocaine

cauda equina syndrome

lignocaine

cauda equina syndrome

lignocaine

Cauda equina syndrome

lignocaine

cauda equina syndrome

lignocaine

cauda equina syndrome

lignocaine

Cauda equina syndrome

lignocaine

cauda equina syndrome

lignocaine

cauda equina syndrome

lignocaine

Cauda equina syndrome

lignocaine

cauda equina syndrome

lignocaine

cauda equina syndrome

lignocaine

Cauda equina syndrome

lignocaine

cauda equina syndrome

lignocaine

cauda equina syndrome


Input: Cortical motor overactivation in parkinsonian patients with L - dopa - induced peak - dose dyskinesia. We have studied the regional cerebral blood flow (rCBF) changes induced by the execution of a finger - to - thumb opposition motor task in the supplementary and primary motor cortex of two groups of parkinsonian patients on L - dopa medication, the first one without L - dopa induced dyskinesia (n = 23) and the other with moderate peak - dose dyskinesia (n = 15), and of a group of 14 normal subjects. Single photon emission tomography with i. v. 133Xe was used to measure the rCBF changes. The dyskinetic parkinsonian patients exhibited a pattern of response which was markedly different from those of the normal subjects and non - dyskinetic parkinsonian patients, with a significant overactivation in the supplementary motor area and the ipsi - and contralateral primary motor areas. These results are compatible with the hypothesis that an hyperkinetic abnormal involuntary movement, like L - dopa - induced peak dose dyskinesia, is due to a disinhibition of the primary and associated motor cortex secondary to an excessive outflow of the pallidothalamocortical motor loop.

parkinsonian

dyskinesia

parkinsonian

dyskinesia

dyskinesia

dyskinetic

parkinsonian

dyskinetic

parkinsonian

hyperkinetic

abnormal involuntary movement

dyskinesia

L - dopa

L - dopa

L - dopa

L - dopa

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinetic

L - dopa

dyskinetic

L - dopa

abnormal involuntary movement

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinetic

L - dopa

dyskinetic

L - dopa

abnormal involuntary movement

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinetic

L - dopa

dyskinetic

L - dopa

abnormal involuntary movement

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinesia

L - dopa

dyskinetic

L - dopa

dyskinetic

L - dopa

abnormal involuntary movement

L - dopa

dyskinesia


Input: Dexamethasone - induced ocular hypertension in perfusion - cultured human eyes. PURPOSE: Glucocorticoid administration can lead to the development of ocular hypertension and corticosteroid glaucoma in a subset of the population through a decrease in the aqueous humor outflow facility. The purpose of this study was to determine whether glucocorticoid treatment can directly affect the outflow facility of isolated, perfusion - cultured human eyes. METHODS: The anterior segments of human donor eyes from regional eye banks were placed in a constant flow, variable pressure perfusion culture system. Paired eyes were perfused in serum - free media with or without 10 (- 7) M dexamethasone for 12 days. Intraocular pressure was monitored daily. After incubation, the eyes were morphologically characterized by light microscopy, transmission and scanning electron microscopy, and scanning laser confocal microscopy. RESULTS: A significant increase in intraocular pressure developed in 13 of the 44 pairs of eyes perfused with dexamethasone with an average pressure rise of 17. 5 + / - 3. 8 mm Hg after 12 days of dexamethasone exposure. The contralateral control eyes, which did not receive dexamethasone, maintained a stable intraocular pressure during the same period. The outflow pathway of the untreated eyes appeared morphologically normal. In contrast, the dexamethasone - treated hypertensive eyes had thickened trabecular beams, decreased intertrabecular spaces, thickened juxtacanalicular tissue, activated trabecular meshwork cells, and increased amounts of amorphogranular extracellular material, especially in the juxtacanalicular tissue and beneath the endothelial lining of the canal of Schlemm. The dexamethasone - treated nonresponder eyes appeared to be morphologically similar to the untreated eyes, although several subtle dexamethasone - induced morphologic changes were evident. CONCLUSION: Dexamethasone treatment of isolated, perfusion - cultured human eyes led to the generation of ocular hypertension in approximately 30% of the dexamethasone - treated eyes. Steroid treatment resulted in morphologic changes in the trabecular meshwork similar to those reported for corticosteroid glaucoma and open angle glaucoma. This system may provide an acute model in which to study the pathogenic mechanisms involved in steroid glaucoma and primary open angle glaucoma.

Dexamethasone

dexamethasone

dexamethasone

dexamethasone

dexamethasone

dexamethasone

dexamethasone

dexamethasone

Dexamethasone

dexamethasone

Steroid

ocular hypertension

ocular hypertension

corticosteroid glaucoma

hypertensive eyes

ocular hypertension

corticosteroid glaucoma

open angle glaucoma

steroid glaucoma

primary open angle glaucoma

Dexamethasone

ocular hypertension

Dexamethasone

ocular hypertension

Dexamethasone

hypertensive eyes

Dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

hypertensive eyes

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

hypertensive eyes

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

hypertensive eyes

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

hypertensive eyes

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

hypertensive eyes

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

hypertensive eyes

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

hypertensive eyes

dexamethasone

ocular hypertension

Dexamethasone

ocular hypertension

Dexamethasone

ocular hypertension

Dexamethasone

hypertensive eyes

Dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

ocular hypertension

dexamethasone

hypertensive eyes

dexamethasone

ocular hypertension


Input: Cognitive deterioration from long - term abuse of dextromethorphan: a case report. Dextromethorphan (DM), the dextrorotatory isomer of 3 - hydroxy - N - methylmorphinan, is the main ingredient in a number of widely available, over - the - counter antitussives. Initial studies (Bornstein 1968) showed that it possessed no respiratory suppressant effects and no addiction liability. Subsequently, however, several articles reporting abuse of this drug have appeared in the literature. The drug is known to cause a variety of acute toxic effects, ranging from nausea, restlessness, insomnia, ataxia, slurred speech and nystagmus to mood changes, perceptual alterations, inattention, disorientation and aggressive behavior (Rammer et al 1988; Katona and Watson 1986; Isbell and Fraser 1953; Devlin et al 1985; McCarthy 1971; Dodds and Revai 1967; Degkwitz 1964; Hildebrand et al 1989). There have also been two reported fatalities from DM overdoses (Fleming 1986). However, there are no reports describing the effects of chronic abuse. This report describes a case of cognitive deterioration resulting from prolonged use of DM.

Cognitive deterioration

nausea

restlessness

insomnia

ataxia

nystagmus

aggressive behavior

cognitive deterioration

dextromethorphan

Dextromethorphan

DM

3 - hydroxy - N - methylmorphinan

DM

DM

dextromethorphan

Cognitive deterioration

dextromethorphan

cognitive deterioration

Dextromethorphan

Cognitive deterioration

Dextromethorphan

cognitive deterioration

DM

Cognitive deterioration

DM

cognitive deterioration

DM

Cognitive deterioration

DM

cognitive deterioration

DM

Cognitive deterioration

DM

cognitive deterioration


Input: Long - term lithium treatment and the kidney. Interim report on fifty patients. This is a report on the first part of our study of the effects of long - term lithium treatment on the kidney. Creatinine clearance, maximum urinary osmolality and 24 hour urine volume have been tested in 50 affectively ill patients who have been on long - term lithium for more than one year. These findings have been compared with norms and with values of the same tests from screening prior to lithium, available for most of our patients. No evidence was found for any reduction of glomerular filtration during lithium treatment. Low clearance values found in several patients could be accounted for by their age and their pre - lithium values. Urinary concentration defect appeared frequent but the extent of the impairment is difficult to assess because of the uncertainty about the norms applicable to this group of patients. The concentration defect appeared reversible, at least in part. Polyuria above 3 litres / 24 hours was found in 10% of patients. An attempt is made to draw practical conclusions from the preliminary findings.

lithium

lithium

Creatinine

lithium

lithium

lithium

lithium

Polyuria

lithium

Polyuria

lithium

Polyuria

lithium

Polyuria

lithium

Polyuria

lithium

Polyuria

lithium

Polyuria


Input: Complete heart block following a single dose of trazodone. Forty minutes after receiving a single starting dose of trazodone, a patient developed complete heart block. The case illustrates that, despite the results of earlier studies, trazodone' s effect on cardiac conduction may be severe in individuals at risk for conduction delay.

heart block

heart block

trazodone

trazodone

trazodone

trazodone

heart block

trazodone

heart block

trazodone

heart block

trazodone

heart block

trazodone

heart block

trazodone

heart block


Input: Quinidine phenylethylbarbiturate - induced fulminant hepatitis in a pregnant woman. A case report. We report the case of a 19 - year - old Laotian patient affected by fulminant hepatitis during the third trimester of her pregnancy after a 1 - month administration of quinidine phenylethylbarbiturate. After delivery, the patient underwent orthotopic liver transplantation. The patient was in good condition 16 months after liver transplantation. Quinidine itself or phenylethylbarbiturate may be responsible for fulminant hepatitis in this patient.

Quinidine phenylethylbarbiturate

quinidine phenylethylbarbiturate

Quinidine

phenylethylbarbiturate

hepatitis

hepatitis

hepatitis

Quinidine phenylethylbarbiturate

hepatitis

Quinidine phenylethylbarbiturate

hepatitis

Quinidine phenylethylbarbiturate

hepatitis

quinidine phenylethylbarbiturate

hepatitis

quinidine phenylethylbarbiturate

hepatitis

quinidine phenylethylbarbiturate

hepatitis

phenylethylbarbiturate

hepatitis

phenylethylbarbiturate

hepatitis

phenylethylbarbiturate

hepatitis


Input: The epidemiology of the acute flank pain syndrome from suprofen. Suprofen, a new nonsteroidal anti - inflammatory drug, was marketed in early 1986 as an analgesic agent. Until physicians began reporting an unusual acute flank pain syndrome to the spontaneous reporting system, 700, 000 persons used the drug in the United States. Through August 1986, a total of 163 cases of this syndrome were reported. To elucidate the epidemiology of the syndrome, a case - control study was performed, comparing 62 of the case patients who had been reported to the spontaneous reporting system to 185 suprofen - exposed control subjects who did not have the syndrome. Case patients were more likely to be men (odds ratio, 3. 8; 95% confidence interval, 1. 2 - 12. 1), suffer from hay fever and asthma (odds ratio, 3. 4; 95% confidence interval, 1. 0 - 11. 9); to participate in regular exercise (odds ratio, 5. 9; 95% confidence interval, 1. 1 - 30. 7), especially in the use of Nautilus equipment (p = 0. 02); and to use alcohol (odds ratio, 4. 4; 95% confidence interval, 1. 1 - 17. 5). Possible risk factors included young age, concurrent use of other analgesic agents (especially ibuprofen), preexisting renal disease, a history of kidney stones, a history of gout, a recent increase in activity, a recent increase in sun exposure, and residence in the Sunbelt. These were findings that were suggestive but did not reach conventional statistical significance. These findings are consistent with the postulated mechanism for this unusual syndrome: acute diffuse crystallization of uric acid in renal tubules.

flank pain

flank pain

hay fever

asthma

renal disease

kidney stones

gout

suprofen

Suprofen

suprofen

alcohol

ibuprofen

uric acid

suprofen

flank pain

suprofen

flank pain

Suprofen

flank pain

Suprofen

flank pain

suprofen

flank pain

suprofen

flank pain


Input: Hemolytic - uremic syndrome associated with ingestion of quinine. Hemolytic - uremic syndrome following quinine ingestion is a newly described phenomenon, with just two previous descriptions of 4 cases in the literature. We describe a 5th case. The reaction may be mediated by the presence of antibodies reactive against platelets in the presence of quinine. Treatment has included use of plasma exchange, prednisone, aspirin, and dipyridamole. The patients have all regained some degree of renal function. However, it is unclear whether pharmacological treatment or spontaneous resolution is responsible for the improvement. Quinine - associated hemolytic - uremic syndrome probably occurs more often than is recognized. It is important to recognize this reaction when it occurs and to avoid further quinine exposure, since the reaction seems to be recurrent.

Hemolytic - uremic syndrome

Hemolytic - uremic syndrome

hemolytic - uremic syndrome

quinine

quinine

quinine

prednisone

aspirin

dipyridamole

Quinine

quinine

quinine

Hemolytic - uremic syndrome

quinine

Hemolytic - uremic syndrome

quinine

hemolytic - uremic syndrome

quinine

Hemolytic - uremic syndrome

quinine

Hemolytic - uremic syndrome

quinine

hemolytic - uremic syndrome

quinine

Hemolytic - uremic syndrome

quinine

Hemolytic - uremic syndrome

quinine

hemolytic - uremic syndrome

Quinine

Hemolytic - uremic syndrome

Quinine

Hemolytic - uremic syndrome

Quinine

hemolytic - uremic syndrome

quinine

Hemolytic - uremic syndrome

quinine

Hemolytic - uremic syndrome

quinine

hemolytic - uremic syndrome


Input: Pyeloureteral filling defects associated with systemic anticoagulation: a case report. The etiology of pyeloureteritis cystica has long been attributed to chronic infection and inflammation. A case is presented that is unique in that the acute onset and the rapid resolution of pyeloureteral filling defects in this patient were documented by radiography. There is no evidence of antecedent or concurrent infection in this patient. The disease occurred subsequent to the initiation of heparin therapy for suspected pelvic thrombophlebitis and cleared rapidly subsequent to its discontinuation. The rate of resolution of the radiographic findings may be helpful in distinguishing between true pyeloureteritis cystica and submucosal hemorrhage.

pyeloureteritis cystica

infection

inflammation

infection

thrombophlebitis

pyeloureteritis cystica

submucosal hemorrhage

heparin

heparin

pyeloureteritis cystica

heparin

pyeloureteritis cystica


Input: Changes in peroxisomes in preneoplastic liver and hepatoma of mice induced by alpha - benzene hexachloride. Peroxisomes in hepatomas and hyperplastic preneoplastic liver lesions induced in mice by 500 ppm alpha - benzene hexachloride were examined histochemically and electron microscopically. Although most of the hepatomas were well - differentiated tumors and contained a considerable number of peroxisomes, the tumor cells did not respond to ethyl - alpha - p - chlorophenoxyisobutyrate with proliferation of peroxisomes. At the 16th week of carcinogen feeding, hyperplastic nodules appeared and advanced to further stages. A majority of the nodules showed a considerable number of peroxisomes and the inductive proliferation of peroxisomes. Within the nodules, foci of proliferation of the cells that showed no inducibility of proliferation of peroxisomes appeared. These cells proliferated further, replacing the most part of the nodules, and with this process hepatomas appeared to have been formed. No abnormal matrical inclusions of peroxisomes were formed in the cells of hyperplastic nodules by ethyl - alpha - p - chlorophenoxyisobutyrate unlike in the case of rats.

hepatoma

hepatomas

liver lesions

hepatomas

tumors

tumor

hepatomas

alpha - benzene hexachloride

alpha - benzene hexachloride

ethyl - alpha - p - chlorophenoxyisobutyrate

ethyl - alpha - p - chlorophenoxyisobutyrate

alpha - benzene hexachloride

hepatoma

alpha - benzene hexachloride

hepatomas

alpha - benzene hexachloride

hepatomas

alpha - benzene hexachloride

hepatomas

alpha - benzene hexachloride

hepatoma

alpha - benzene hexachloride

hepatomas

alpha - benzene hexachloride

hepatomas

alpha - benzene hexachloride

hepatomas


Input: Quinidine hepatitis. Long - term administration of quinidine was associated with persistent elevation of serum concentrations of SGOT, lactic acid dehydrogenase, and alkaline phosphatase. Liver biopsy showed active hepatitis. Discontinuance of quinidine therapy led to normalization of liver function tests. A challenge dose of quinidine caused clinical symptoms and abrupt elevation of SGOT, alkaline phosphatase, and lactic acid dehydrogenase values. We concluded that this patient had quinidine hepatotoxicity and believe that this is the first case reported with liver biopsy documentation. This report also suggests that, even after long - term administration, the hepatic toxicity is reversible.

Quinidine

quinidine

lactic acid

quinidine

quinidine

lactic acid

quinidine

hepatitis

hepatitis

hepatotoxicity

hepatic toxicity

Quinidine

hepatitis

Quinidine

hepatitis

Quinidine

hepatotoxicity

Quinidine

hepatic toxicity

quinidine

hepatitis

quinidine

hepatitis

quinidine

hepatotoxicity

quinidine

hepatic toxicity

quinidine

hepatitis

quinidine

hepatitis

quinidine

hepatotoxicity

quinidine

hepatic toxicity

quinidine

hepatitis

quinidine

hepatitis

quinidine

hepatotoxicity

quinidine

hepatic toxicity

quinidine

hepatitis

quinidine

hepatitis

quinidine

hepatotoxicity

quinidine

hepatic toxicity


Input: Cholesteryl hemisuccinate treatment protects rodents from the toxic effects of acetaminophen, adriamycin, carbon tetrachloride, chloroform and galactosamine. In addition to its use as a stabilizer / rigidifier of membranes, cholesteryl hemisuccinate, tris salt (CS) administration has also been shown to protect rats from the hepatotoxic effects of carbon tetrachloride (CCl4). To further our understanding of the mechanism of CS cytoprotection, we examined in rats and mice the protective abilities of CS and the non - hydrolyzable ether form of CS, gamma - cholesteryloxybutyric acid, tris salt (CSE) against acetaminophen -, adriamycin -, carbon tetrachloride -, chloroform - and galactosamine - induced toxicity. The results of these studies demonstrated that CS - mediated protection is not selective for a particular species, organ system or toxic chemical. A 24 - h pretreatment of both rats and mice with a single dose of CS (100mg / kg, i. p.), resulted in significant protection against the hepatotoxic effects of CCl4, CHCl3, acetaminophen and galactosamine and against the lethal (and presumably cardiotoxic) effect of adriamycin administration. Maximal CS - mediated protection was observed in experimental animals pretreated 24 h prior to the toxic insult. These data suggest that CS intervenes in a critical cellular event that is an important common pathway to toxic cell death. The mechanism of CS protection does not appear to be dependent on the inhibition of chemical bioactivation to a toxic reactive intermediate (in light of the protection observed against galactosamine hepatotoxicity). However, based on the data presented, we can not exclude the possibility that CS administration inhibits chemical bioactivation. Our findings do suggest that CS - mediated protection is dependent on the action of the intact anionic CS molecule (non - hydrolyzable CSE was as protective as CS), whose mechanism has yet to be defined.

Cholesteryl hemisuccinate

acetaminophen

adriamycin

carbon tetrachloride

chloroform

galactosamine

cholesteryl hemisuccinate

tris salt

CS

carbon tetrachloride

CS

CS

CS

gamma - cholesteryloxybutyric acid

tris salt

CSE

acetaminophen

adriamycin

carbon tetrachloride

chloroform

galactosamine

CS

CS

acetaminophen

galactosamine

adriamycin

CS

CS

CS

galactosamine

CS

CS

CS

CSE

CS

hepatotoxic

toxicity

hepatotoxic

cardiotoxic

hepatotoxicity

carbon tetrachloride

hepatotoxic

carbon tetrachloride

hepatotoxic

carbon tetrachloride

hepatotoxicity

carbon tetrachloride

hepatotoxic

carbon tetrachloride

hepatotoxic

carbon tetrachloride

hepatotoxicity

hepatotoxic

hepatotoxic

hepatotoxicity

carbon tetrachloride

hepatotoxic

carbon tetrachloride

hepatotoxic

carbon tetrachloride

hepatotoxicity

hepatotoxic

hepatotoxic

hepatotoxicity

chloroform

hepatotoxic

chloroform

hepatotoxic

chloroform

hepatotoxicity

chloroform

hepatotoxic

chloroform

hepatotoxic

chloroform

hepatotoxicity

hepatotoxic

hepatotoxic

hepatotoxicity

acetaminophen

hepatotoxic

acetaminophen

hepatotoxic

acetaminophen

hepatotoxicity

acetaminophen

hepatotoxic

acetaminophen

hepatotoxic

acetaminophen

hepatotoxicity

acetaminophen

hepatotoxic

acetaminophen

hepatotoxic

acetaminophen

hepatotoxicity

galactosamine

hepatotoxic

galactosamine

hepatotoxic

galactosamine

hepatotoxicity

galactosamine

hepatotoxic

galactosamine

hepatotoxic

galactosamine

hepatotoxicity

galactosamine

hepatotoxic

galactosamine

hepatotoxic

galactosamine

hepatotoxicity

galactosamine

hepatotoxic

galactosamine

hepatotoxic

galactosamine

hepatotoxicity

adriamycin

cardiotoxic

adriamycin

cardiotoxic

adriamycin

cardiotoxic


Input: DSMM XI study: dose definition for intravenous cyclophosphamide in combination with bortezomib / dexamethasone for remission induction in patients with newly diagnosed myeloma. A clinical trial was initiated to evaluate the recommended dose of cyclophosphamide in combination with bortezomib and dexamethasone as induction treatment before stem cell transplantation for younger patients with newly diagnosed multiple myeloma (MM). Thirty patients were treated with three 21 - day cycles of bortezomib 1. 3 mg / m (2) on days 1, 4, 8, and 11 plus dexamethasone 40 mg on the day of bortezomib injection and the day after plus cyclophosphamide at 900, 1, 200, or 1, 500 mg / m (2) on day 1. The maximum tolerated dose of cyclophosphamide was defined as 900 mg / m (2). At this dose level, 92% of patients achieved at least a partial response. The overall response rate [complete response (CR) plus partial response (PR)] across all dose levels was 77%, with a 10% CR rate. No patient experienced progressive disease. The most frequent adverse events were hematological and gastrointestinal toxicities as well as neuropathy. The results suggest that bortezomib in combination with cyclophosphamide at 900 mg / m (2) and dexamethasone is an effective induction treatment for patients with newly diagnosed MM that warrants further investigation.

cyclophosphamide

bortezomib

dexamethasone

cyclophosphamide

bortezomib

dexamethasone

bortezomib

dexamethasone

bortezomib

cyclophosphamide

cyclophosphamide

bortezomib

cyclophosphamide

dexamethasone

myeloma

multiple myeloma

MM

hematological and gastrointestinal toxicities

hematological and gastrointestinal toxicities

gastrointestinal toxicities

neuropathy

MM

dexamethasone

hematological and gastrointestinal toxicities

dexamethasone

hematological and gastrointestinal toxicities

dexamethasone

hematological and gastrointestinal toxicities

dexamethasone

hematological and gastrointestinal toxicities

dexamethasone

hematological and gastrointestinal toxicities

dexamethasone

hematological and gastrointestinal toxicities

dexamethasone

hematological and gastrointestinal toxicities

dexamethasone

hematological and gastrointestinal toxicities

bortezomib

hematological and gastrointestinal toxicities

bortezomib

gastrointestinal toxicities

bortezomib

hematological and gastrointestinal toxicities

bortezomib

gastrointestinal toxicities

bortezomib

hematological and gastrointestinal toxicities

bortezomib

gastrointestinal toxicities

bortezomib

hematological and gastrointestinal toxicities

bortezomib

gastrointestinal toxicities

bortezomib

hematological and gastrointestinal toxicities

bortezomib

gastrointestinal toxicities

cyclophosphamide

hematological and gastrointestinal toxicities

cyclophosphamide

hematological and gastrointestinal toxicities

cyclophosphamide

hematological and gastrointestinal toxicities

cyclophosphamide

hematological and gastrointestinal toxicities

cyclophosphamide

hematological and gastrointestinal toxicities

cyclophosphamide

hematological and gastrointestinal toxicities

cyclophosphamide

hematological and gastrointestinal toxicities

cyclophosphamide

hematological and gastrointestinal toxicities

cyclophosphamide

hematological and gastrointestinal toxicities

cyclophosphamide

hematological and gastrointestinal toxicities

dexamethasone

gastrointestinal toxicities

dexamethasone

gastrointestinal toxicities

dexamethasone

gastrointestinal toxicities

dexamethasone

gastrointestinal toxicities

bortezomib

neuropathy

bortezomib

neuropathy

bortezomib

neuropathy

bortezomib

neuropathy

bortezomib

neuropathy

cyclophosphamide

gastrointestinal toxicities

cyclophosphamide

gastrointestinal toxicities

cyclophosphamide

gastrointestinal toxicities

cyclophosphamide

gastrointestinal toxicities

cyclophosphamide

gastrointestinal toxicities

bortezomib

hematological and gastrointestinal toxicities

bortezomib

hematological and gastrointestinal toxicities

bortezomib

hematological and gastrointestinal toxicities

bortezomib

hematological and gastrointestinal toxicities

bortezomib

hematological and gastrointestinal toxicities

dexamethasone

neuropathy

dexamethasone

neuropathy

dexamethasone

neuropathy

dexamethasone

neuropathy

cyclophosphamide

neuropathy

cyclophosphamide

neuropathy

cyclophosphamide

neuropathy

cyclophosphamide

neuropathy

cyclophosphamide

neuropathy


Input: Results of a comparative, phase III, 12 - week, multicenter, prospective, randomized, double - blind assessment of the efficacy and tolerability of a fixed - dose combination of telmisartan and amlodipine versus amlodipine monotherapy in Indian adults with stage II hypertension. OBJECTIVE: The aim of this study was to evaluate the efficacy and tolerability of a new fixed - dose combination (FDC) of telmisartan 40 mg + amlodipine 5 mg (T + A) compared with amlodipine 5 - mg monotherapy (A) in adult Indian patients with stage II hypertension. METHODS: This comparative, Phase III, 12 - week, multicenter, prospective, randomized, double - blind study was conducted in Indian patients aged 18 to 65 years with established stage II hypertension. Patients were treated with oral FDC of T + A or A QD before breakfast for 12 weeks; blood pressure (BP) and heart rate were measured in the sitting position. Primary efficacy end points were reduction in clinical systolic BP (SBP) / diastolic BP (DBP) from baseline to study end and number of responders (ie, patients who achieved target SBP / DBP < 130 / < 80 mm Hg) at end of study. Tolerability was assessed by treatment - emergent adverse events, identified using physical examination, laboratory analysis, and electrocardiography. RESULTS: A total of 210 patients were enrolled in the study; 203 patients (143 men, 60 women) completed the study while 7 were lost to follow - up (4 patients in the T + A group and 3 in the A group) and considered with - drawn. At study end, statistically significant percentage reductions from baseline within groups and between groups were observed in SBP (T + A [- 27. 4%]; A [- 16. 6%]) and DBP (T + A [- 20. 1%]; A [- 13. 3%]) (all, P < 0. 05). Response rates were 87. 3% (89 / 102) in the T + A group and 69. 3% (70 / 101) in the A group (P < 0. 05). The prevalences of adverse events were not significantly different between the 2 treatment groups (T + A, 16. 0% [17 / 106]; A, 15. 4% [16 / 104]). Peripheral edema was reported in 8. 5% patients (9 / 106) in the T + A group compared with 13. 5% (14 / 104) in the A group, and cough was reported in 3. 8% patients (4 / 106) in the T + A group and 1. 0% (1 / 104) patients in the A group; these differences did not reach statistical significance. The incidences of headache, dizziness, and diarrhea were similar between the 2 groups. CONCLUSIONS: Among these Indian patients with stage II hypertension, the FDC of T + A was found to be significantly more effective, with regard to BP reductions, than A, and both treatments were well tolerated.

telmisartan

amlodipine

amlodipine

telmisartan

amlodipine

amlodipine

hypertension

hypertension

hypertension

edema

cough

headache

dizziness

diarrhea

hypertension

amlodipine

headache

amlodipine

headache

amlodipine

headache

amlodipine

headache

telmisartan

dizziness

telmisartan

dizziness

telmisartan

headache

telmisartan

headache

telmisartan

diarrhea

telmisartan

diarrhea

telmisartan

edema

telmisartan

edema

amlodipine

diarrhea

amlodipine

diarrhea

amlodipine

diarrhea

amlodipine

diarrhea

amlodipine

edema

amlodipine

edema

amlodipine

edema

amlodipine

edema

amlodipine

cough

amlodipine

cough

amlodipine

cough

amlodipine

cough

amlodipine

dizziness

amlodipine

dizziness

amlodipine

dizziness

amlodipine

dizziness

telmisartan

cough

telmisartan

cough


Input: Cutaneous leucocytoclastic vasculitis associated with oxacillin. A 67 - year - old man who was treated with oxacillin for one week because of Staphylococcus aureus bacteremia, developed renal failure and diffuse, symmetric, palpable purpuric lesions on his feet. Necrotic blisters were noted on his fingers. Skin biopsies showed findings diagnostic of leucocytoclastic vasculitis. Oxacillin was discontinued and patient was treated with corticosteroids. The rash disappeared after three weeks and renal function returned to normal. Leucocytoclastic vasculitis presents as palpable purpura of the lower extremities often accompanied by abdominal pain, arthralgia, and renal involvement. Etiologic factors or associated disorders include infections, medications, collagen vascular disease and neoplasia. However, in half of the cases no etiologic factor is identified. Usually it is a self - limited disorder, but corticosteroid therapy may be needed in life - threatening cases since early treatment with corticosteroids in severe cases can prevent complications. Oxacillin should be included among the drugs that can cause leucocytoclastic vasculitis.

Cutaneous leucocytoclastic vasculitis

Staphylococcus aureus bacteremia

Staphylococcus aureus bacteremia

bacteremia

renal failure

purpuric lesions

Necrotic blisters

Necrotic

blisters

leucocytoclastic vasculitis

rash

Leucocytoclastic vasculitis

purpura

abdominal pain

arthralgia

renal involvement

infections

collagen vascular disease

neoplasia

leucocytoclastic vasculitis

oxacillin

oxacillin

Oxacillin

corticosteroids

corticosteroid

corticosteroids

Oxacillin

corticosteroids

renal failure

corticosteroid

renal failure

corticosteroids

renal failure

oxacillin

renal failure

oxacillin

renal failure

Oxacillin

renal failure

Oxacillin

renal failure

oxacillin

Cutaneous leucocytoclastic vasculitis

oxacillin

leucocytoclastic vasculitis

oxacillin

Leucocytoclastic vasculitis

oxacillin

leucocytoclastic vasculitis

oxacillin

Cutaneous leucocytoclastic vasculitis

oxacillin

leucocytoclastic vasculitis

oxacillin

Leucocytoclastic vasculitis

oxacillin

leucocytoclastic vasculitis

Oxacillin

Cutaneous leucocytoclastic vasculitis

Oxacillin

leucocytoclastic vasculitis

Oxacillin

Leucocytoclastic vasculitis

Oxacillin

leucocytoclastic vasculitis

Oxacillin

Cutaneous leucocytoclastic vasculitis

Oxacillin

leucocytoclastic vasculitis

Oxacillin

Leucocytoclastic vasculitis

Oxacillin

leucocytoclastic vasculitis

corticosteroids

Cutaneous leucocytoclastic vasculitis

corticosteroids

leucocytoclastic vasculitis

corticosteroids

Leucocytoclastic vasculitis

corticosteroids

leucocytoclastic vasculitis

corticosteroid

Cutaneous leucocytoclastic vasculitis

corticosteroid

leucocytoclastic vasculitis

corticosteroid

Leucocytoclastic vasculitis

corticosteroid

leucocytoclastic vasculitis

corticosteroids

Cutaneous leucocytoclastic vasculitis

corticosteroids

leucocytoclastic vasculitis

corticosteroids

Leucocytoclastic vasculitis

corticosteroids

leucocytoclastic vasculitis


Input: Naloxazone pretreatment modifies cardiorespiratory, temperature, and behavioral effects of morphine. Behavioral and cardiorespiratory responses to a lethal dose of morphine were evaluated in rats pretreated with saline or naloxazone, an antagonist of high - affinity mu 1 opioid receptors. Pretreatment with naloxazone significantly blocked morphine analgesia, catalepsy and hypothermia at a dose which completely eliminated high - affinity binding in brain membranes. Moreover, naloxazone significantly attenuated the morphine - induced hypotension and respiratory depression, whereas morphine - induced bradycardia was less affected. Results indicate that subpopulations of mu receptors may mediate selective behavioral and cardiorespiratory responses to morphine.

Naloxazone

morphine

morphine

naloxazone

naloxazone

morphine

naloxazone

morphine

morphine

morphine

analgesia

catalepsy

hypothermia

hypotension

respiratory depression

bradycardia

morphine

hypotension

morphine

hypotension

morphine

hypotension

morphine

hypotension

morphine

hypotension

morphine

hypotension

morphine

hypothermia

morphine

hypothermia

morphine

hypothermia

morphine

hypothermia

morphine

hypothermia

morphine

hypothermia

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

bradycardia

morphine

bradycardia

morphine

bradycardia

morphine

bradycardia

morphine

bradycardia

morphine

bradycardia


Input: Dexrazoxane protects against myelosuppression from the DNA cleavage - enhancing drugs etoposide and daunorubicin but not doxorubicin. PURPOSE: The anthracyclines daunorubicin and doxorubicin and the epipodophyllotoxin etoposide are potent DNA cleavage - enhancing drugs that are widely used in clinical oncology; however, myelosuppression and cardiac toxicity limit their use. Dexrazoxane (ICRF - 187) is recommended for protection against anthracycline - induced cardiotoxicity. EXPERIMENTAL DESIGN: Because of their widespread use, the hematologic toxicity following coadministration of dexrazoxane and these three structurally different DNA cleavage enhancers was investigated: Sensitivity of human and murine blood progenitor cells to etoposide, daunorubicin, and doxorubicin + / - dexrazoxane was determined in granulocyte - macrophage colony forming assays. Likewise, in vivo, B6D2F1 mice were treated with etoposide, daunorubicin, and doxorubicin, with or without dexrazoxane over a wide range of doses: posttreatment, a full hematologic evaluation was done. RESULTS: Nontoxic doses of dexrazoxane reduced myelosuppression and weight loss from daunorubicin and etoposide in mice and antagonized their antiproliferative effects in the colony assay; however, dexrazoxane neither reduced myelosuppression, weight loss, nor the in vitro cytotoxicity from doxorubicin. CONCLUSION: Although our findings support the observation that dexrazoxane reduces neither hematologic activity nor antitumor activity from doxorubicin clinically, the potent antagonism of daunorubicin activity raises concern; a possible interference with anticancer efficacy certainly would call for renewed attention. Our data also suggest that significant etoposide dose escalation is perhaps possible by the use of dexrazoxane. Clinical trials in patients with brain metastases combining dexrazoxane and high doses of etoposide is ongoing with the aim of improving efficacy without aggravating hematologic toxicity. If successful, this represents an exciting mechanism for pharmacologic regulation of side effects from cytotoxic chemotherapy.

Dexrazoxane

etoposide

daunorubicin

doxorubicin

anthracyclines

daunorubicin

doxorubicin

epipodophyllotoxin

etoposide

Dexrazoxane

ICRF - 187

anthracycline

dexrazoxane

etoposide

daunorubicin

doxorubicin

dexrazoxane

etoposide

daunorubicin

doxorubicin

dexrazoxane

dexrazoxane

daunorubicin

etoposide

dexrazoxane

doxorubicin

dexrazoxane

doxorubicin

daunorubicin

etoposide

dexrazoxane

dexrazoxane

etoposide

myelosuppression

myelosuppression

cardiac toxicity

cardiotoxicity

hematologic toxicity

myelosuppression

weight loss

myelosuppression

weight loss

cytotoxicity

metastases

hematologic toxicity

daunorubicin

weight loss

daunorubicin

weight loss

daunorubicin

weight loss

daunorubicin

weight loss

daunorubicin

weight loss

daunorubicin

weight loss

daunorubicin

weight loss

daunorubicin

weight loss

daunorubicin

weight loss

daunorubicin

weight loss

daunorubicin

weight loss

daunorubicin

weight loss

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

doxorubicin

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

etoposide

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

daunorubicin

hematologic toxicity

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

etoposide

weight loss

doxorubicin

weight loss

doxorubicin

weight loss

doxorubicin

weight loss

doxorubicin

weight loss

doxorubicin

weight loss

doxorubicin

weight loss

doxorubicin

weight loss

doxorubicin

weight loss

doxorubicin

weight loss

doxorubicin

weight loss

doxorubicin

weight loss

doxorubicin

weight loss


Input: Effects of the novel compound aniracetam (Ro 13 - 5057) upon impaired learning and memory in rodents. The effect of aniracetam (Ro 13 - 5057, 1 - anisoyl - 2 - pyrrolidinone) was studied on various forms of experimentally impaired cognitive functions (learning and memory) in rodents and produced the following effects: (1) almost complete prevention of the incapacity to learn a discrete escape response in rats exposed to sublethal hypercapnia immediately before the acquisition session; (2) partial (rats) or complete (mice) prevention of the scopolamine - induced short - term amnesia for a passive avoidance task; (3) complete protection against amnesia for a passive avoidance task in rats submitted to electroconvulsive shock immediately after avoidance acquisition; (4) prevention of the long - term retention - or retrieval - deficit for a passive avoidance task induced in rats and mice by chloramphenicol or cycloheximide administered immediately after acquisition; (5) reversal, when administered as late as 1 h before the retention test, of the deficit in retention or retrieval of a passive avoidance task induced by cycloheximide injected 2 days previously; (6) prevention of the deficit in the retrieval of an active avoidance task induced in mice by subconvulsant electroshock or hypercapnia applied immediately before retrieval testing (24 h after acquisition). These improvements or normalizations of impaired cognitive functions were seen at oral aniracetam doses of 10 - 100 mg / kg. Generally, the dose - response curves were bell - shaped. The mechanisms underlying the activity of aniracetam and its' therapeutic window' are unknown. Piracetam, another pyrrolidinone derivative was used for comparison. It was active only in six of nine tests and had about one - tenth the potency of aniracetam. The results indicate that aniracetam improves cognitive functions which are impaired by different procedure and in different phases of the learning and memory process.

aniracetam

Ro 13 - 5057

aniracetam

Ro 13 - 5057

1 - anisoyl - 2 - pyrrolidinone

scopolamine

chloramphenicol

cycloheximide

cycloheximide

aniracetam

aniracetam

Piracetam

pyrrolidinone

aniracetam

aniracetam

impaired learning and memory

impaired learning

impaired learning and memory

impaired cognitive functions

hypercapnia

amnesia

amnesia

hypercapnia

impaired cognitive functions

scopolamine

amnesia

scopolamine

amnesia

cycloheximide

impaired learning and memory

cycloheximide

impaired learning and memory

cycloheximide

impaired learning and memory

cycloheximide

impaired learning and memory

chloramphenicol

impaired learning and memory

chloramphenicol

impaired learning and memory


Input: Nicotine potentiation of morphine - induced catalepsy in mice. In the present study, effects of nicotine on catalepsy induced by morphine in mice have been investigated. Morphine but not nicotine induced a dose - dependent catalepsy. The response of morphine was potentiated by nicotine. Intraperitoneal administration of atropine, naloxone, mecamylamine, and hexamethonium to mice reduced catalepsy induced by a combination of morphine with nicotine. Intracerebroventricular injection of atropine, hexamethonium, and naloxone also decreased catalepsy induced by morphine plus nicotine. Intraperitoneal administration of atropine, but not intraperitoneal or intracerebroventricular injection of hexamethonium, decreased the effect of a single dose of morphine. It was concluded that morphine catalepsy can be elicited by opioid and cholinergic receptors, and the potentiation of morphine induced by nicotine may also be mediated through cholinergic receptor mechanisms.

Nicotine

morphine

nicotine

morphine

Morphine

nicotine

morphine

nicotine

atropine

naloxone

mecamylamine

hexamethonium

morphine

nicotine

atropine

hexamethonium

naloxone

morphine

nicotine

atropine

hexamethonium

morphine

morphine

morphine

nicotine

catalepsy

catalepsy

catalepsy

catalepsy

catalepsy

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

Morphine

catalepsy

Morphine

catalepsy

Morphine

catalepsy

Morphine

catalepsy

Morphine

catalepsy

Morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

morphine

catalepsy

Nicotine

catalepsy

Nicotine

catalepsy

Nicotine

catalepsy

Nicotine

catalepsy

Nicotine

catalepsy

Nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy

nicotine

catalepsy


Input: Reduced cardiotoxicity and preserved antitumor efficacy of liposome - encapsulated doxorubicin and cyclophosphamide compared with conventional doxorubicin and cyclophosphamide in a randomized, multicenter trial of metastatic breast cancer. PURPOSE: To determine whether Myocet (liposome - encapsulated doxorubicin; The Liposome Company, Elan Corporation, Princeton, NJ) in combination with cyclophosphamide significantly reduces doxorubicin cardiotoxicity while providing comparable antitumor efficacy in first - line treatment of metastatic breast cancer (MBC). PATIENTS AND METHODS: Two hundred ninety - seven patients with MBC and no prior chemotherapy for metastatic disease were randomized to receive either 60 mg / m (2) of Myocet (M) or conventional doxorubicin (A), in combination with 600 mg / m (2) of cyclophosphamide (C), every 3 weeks until disease progression or unacceptable toxicity. Cardiotoxicity was defined by reductions in left - ventricular ejection fraction, assessed by serial multigated radionuclide angiography scans, or congestive heart failure (CHF). Antitumor efficacy was assessed by objective tumor response rates (World Health Organization criteria), time to progression, and survival. RESULTS: Six percent of MC patients versus 21% (including five cases of CHF) of AC patients developed cardiotoxicity (P =. 0002). Median cumulative doxorubicin dose at onset was more than 2, 220 mg / m (2) for MC versus 480 mg / m (2) for AC (P =. 0001, hazard ratio, 5. 04). MC patients also experienced less grade 4 neutropenia. Antitumor efficacy of MC versus AC was comparable: objective response rates, 43% versus 43%; median time to progression, 5. 1% versus 5. 5 months; median time to treatment failure, 4. 6 versus 4. 4 months; and median survival, 19 versus 16 months. CONCLUSION: Myocet improves the therapeutic index of doxorubicin by significantly reducing cardiotoxicity and grade 4 neutropenia and provides comparable antitumor efficacy, when used in combination with cyclophosphamide as first - line therapy for MBC.

cardiotoxicity

breast cancer

cardiotoxicity

breast cancer

MBC

MBC

toxicity

Cardiotoxicity

congestive heart failure

CHF

tumor

CHF

cardiotoxicity

neutropenia

cardiotoxicity

neutropenia

MBC

doxorubicin

cyclophosphamide

doxorubicin

cyclophosphamide

Myocet

doxorubicin

cyclophosphamide

doxorubicin

Myocet

doxorubicin

cyclophosphamide

doxorubicin

Myocet

doxorubicin

cyclophosphamide

cyclophosphamide

neutropenia

cyclophosphamide

neutropenia

cyclophosphamide

neutropenia

cyclophosphamide

neutropenia

cyclophosphamide

neutropenia

cyclophosphamide

neutropenia

cyclophosphamide

neutropenia

cyclophosphamide

neutropenia

cyclophosphamide

neutropenia

cyclophosphamide

neutropenia

doxorubicin

neutropenia

doxorubicin

neutropenia

doxorubicin

neutropenia

doxorubicin

neutropenia

Myocet

neutropenia

Myocet

neutropenia

doxorubicin

neutropenia

doxorubicin

neutropenia

doxorubicin

neutropenia

doxorubicin

neutropenia

Myocet

neutropenia

Myocet

neutropenia

doxorubicin

neutropenia

doxorubicin

neutropenia

doxorubicin

neutropenia

doxorubicin

neutropenia

Myocet

neutropenia

Myocet

neutropenia

doxorubicin

neutropenia

doxorubicin

neutropenia

cyclophosphamide

congestive heart failure

cyclophosphamide

CHF

cyclophosphamide

CHF

cyclophosphamide

congestive heart failure

cyclophosphamide

CHF

cyclophosphamide

CHF

cyclophosphamide

congestive heart failure

cyclophosphamide

CHF

cyclophosphamide

CHF

cyclophosphamide

congestive heart failure

cyclophosphamide

CHF

cyclophosphamide

CHF

cyclophosphamide

congestive heart failure

cyclophosphamide

CHF

cyclophosphamide

CHF

doxorubicin

congestive heart failure

doxorubicin

CHF

doxorubicin

CHF

doxorubicin

congestive heart failure

doxorubicin

CHF

doxorubicin

CHF

Myocet

congestive heart failure

Myocet

CHF

Myocet

CHF

doxorubicin

congestive heart failure

doxorubicin

CHF

doxorubicin

CHF

doxorubicin

congestive heart failure

doxorubicin

CHF

doxorubicin

CHF

Myocet

congestive heart failure

Myocet

CHF

Myocet

CHF

doxorubicin

congestive heart failure

doxorubicin

CHF

doxorubicin

CHF

doxorubicin

congestive heart failure

doxorubicin

CHF

doxorubicin

CHF

Myocet

congestive heart failure

Myocet

CHF

Myocet

CHF

doxorubicin

congestive heart failure

doxorubicin

CHF

doxorubicin

CHF


Input: Protective effect of a specific platelet - activating factor antagonist, BN 52021, on bupivacaine - induced cardiovascular impairments in rats. Administration of the local anaesthetic bupivacaine (1. 5 or 2 mg / kg, i. v.) to rats elicited a marked decrease of mean arterial blood pressure (MBP) and heart rate (HR) leading to death (in 67% or 90% of animals respectively). Intravenous injection of the specific platelet - activating factor (PAF) antagonist BN 52021 (10 mg / kg), 30 min before bupivacaine administration (2 mg / kg i. v.) suppressed both the decrease of MBP and HR. In contrast, doses of 1 mg / kg BN 52021 given 30 min before or 10 mg / kg administered 5 min before i. v. injection of bupivacaine were ineffective. When BN 52021 (20 mg / kg i. v.) was injected immediately after bupivacaine (2 mg / kg), a partial reversion of the decrease of MBP and HR was observed, whereas the dose of 10 mg / kg was ineffective. A partial recovery of bupivacaine - induced ECG alterations was observed after pretreatment of the rats with BN 52021. Since the administration of BN 52021, at all doses studied, did not alter MBP and HR at the doses used, the bulk of these results clearly demonstrate a protective action of BN 52021, a specific antagonist of PAF, against bupivacaine - induced cardiovascular toxicity. Thus, consistent with its direct effect on heart, PAF appears to be implicated in bupivacaine - induced cardiovascular alterations.

BN 52021

bupivacaine

bupivacaine

BN 52021

bupivacaine

BN 52021

bupivacaine

BN 52021

bupivacaine

bupivacaine

BN 52021

BN 52021

BN 52021

bupivacaine

bupivacaine

cardiovascular impairments

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

decrease of mean arterial blood pressure (MBP)

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

decrease of MBP and HR

decrease of MBP

decrease of MBP and HR

decrease of MBP and HR

decrease of MBP

decrease of MBP and HR

cardiovascular toxicity

cardiovascular alterations

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of mean arterial blood pressure (MBP) and heart rate (HR)

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of MBP and HR

bupivacaine

decrease of mean arterial blood pressure (MBP)

bupivacaine

decrease of MBP

bupivacaine

decrease of MBP

bupivacaine

decrease of mean arterial blood pressure (MBP)

bupivacaine

decrease of MBP

bupivacaine

decrease of MBP

bupivacaine

decrease of mean arterial blood pressure (MBP)

bupivacaine

decrease of MBP

bupivacaine

decrease of MBP

bupivacaine

decrease of mean arterial blood pressure (MBP)

bupivacaine

decrease of MBP

bupivacaine

decrease of MBP

bupivacaine

decrease of mean arterial blood pressure (MBP)

bupivacaine

decrease of MBP

bupivacaine

decrease of MBP

bupivacaine

decrease of mean arterial blood pressure (MBP)

bupivacaine

decrease of MBP

bupivacaine

decrease of MBP

bupivacaine

decrease of mean arterial blood pressure (MBP)

bupivacaine

decrease of MBP

bupivacaine

decrease of MBP

bupivacaine

decrease of mean arterial blood pressure (MBP)

bupivacaine

decrease of MBP

bupivacaine

decrease of MBP


Input: Benzylacyclouridine reverses azidothymidine - induced marrow suppression without impairment of anti - human immunodeficiency virus activity. Increased extracellular concentrations of uridine (Urd) have been reported to reduce, in vitro, azidothymidine (AZT) - induced inhibition of human granulocyte - macrophage progenitor cells without impairment of its antihuman immunodeficiency virus (HIV) activity. Because of the clinical toxicities associated with chronic Urd administration, the ability of benzylacyclouridine (BAU) to effect, in vivo, AZT - induced anemia and leukopenia was assessed. This agent inhibits Urd catabolism and, in vivo, increases the plasma concentration of Urd in a dose - dependent manner, without Urd - related toxicity. In mice rendered anemic and leukopenic by the administration of AZT for 28 days in drinking water (1. 5 mg / mL), the continued administration of AZT plus daily BAU (300 mg / kg, orally) partially reversed AZT - induced anemia and leukopenia (P less than. 05), increased peripheral reticulocytes (to 4. 9%, P less than. 01), increased cellularity in the marrow, and improved megaloblastosis. When coadministered with AZT from the onset of drug administration, BAU reduced AZT - induced marrow toxicity. In vitro, at a concentration of 100 mumol / L, BAU possesses minimal anti - HIV activity and has no effect on the ability of AZT to reverse the HIV - induced cytopathic effect in MT4 cells. The clinical and biochemical implications of these findings are discussed.

Benzylacyclouridine

azidothymidine

uridine

Urd

azidothymidine

AZT

Urd

benzylacyclouridine

BAU

AZT

Urd

Urd

Urd

AZT

AZT

BAU

AZT

AZT

BAU

AZT

BAU

AZT

marrow suppression

immunodeficiency

immunodeficiency

toxicities

anemia

leukopenia

toxicity

anemic

leukopenic

anemia

leukopenia

megaloblastosis

marrow toxicity

azidothymidine

marrow suppression

azidothymidine

marrow toxicity

azidothymidine

marrow suppression

azidothymidine

marrow toxicity

AZT

marrow suppression

AZT

marrow toxicity

AZT

marrow suppression

AZT

marrow toxicity

AZT

marrow suppression

AZT

marrow toxicity

AZT

marrow suppression

AZT

marrow toxicity

AZT

marrow suppression

AZT

marrow toxicity

AZT

marrow suppression

AZT

marrow toxicity

AZT

marrow suppression

AZT

marrow toxicity

AZT

marrow suppression

AZT

marrow toxicity

azidothymidine

anemia

azidothymidine

anemic

azidothymidine

anemia

azidothymidine

anemia

azidothymidine

anemic

azidothymidine

anemia

AZT

anemia

AZT

anemic

AZT

anemia

AZT

anemia

AZT

anemic

AZT

anemia

AZT

anemia

AZT

anemic

AZT

anemia

AZT

anemia

AZT

anemic

AZT

anemia

AZT

anemia

AZT

anemic

AZT

anemia

AZT

anemia

AZT

anemic

AZT

anemia

AZT

anemia

AZT

anemic

AZT

anemia

AZT

anemia

AZT

anemic

AZT

anemia

azidothymidine

leukopenia

azidothymidine

leukopenic

azidothymidine

leukopenia

azidothymidine

leukopenia

azidothymidine

leukopenic

azidothymidine

leukopenia

AZT

leukopenia

AZT

leukopenic

AZT

leukopenia

AZT

leukopenia

AZT

leukopenic

AZT

leukopenia

AZT

leukopenia

AZT

leukopenic

AZT

leukopenia

AZT

leukopenia

AZT

leukopenic

AZT

leukopenia

AZT

leukopenia

AZT

leukopenic

AZT

leukopenia

AZT

leukopenia

AZT

leukopenic

AZT

leukopenia

AZT

leukopenia

AZT

leukopenic

AZT

leukopenia

AZT

leukopenia

AZT

leukopenic

AZT

leukopenia


Input: Cyclophosphamide - induced cystitis in freely - moving conscious rats: behavioral approach to a new model of visceral pain. PURPOSE: To develop a model of visceral pain in rats using a behavioral approach. Cyclophosphamide (CP), an antitumoral agent known to produce toxic effects on the bladder wall through its main toxic metabolite acrolein, was used to induce cystitis. MATERIALS AND METHODS: CP was administered at doses of 50, 100 and 200 mg. / kg. i. p. to male rats, and their behavior observed and scored. The effects of morphine (0. 5 to 4 mg. / kg. i. v.) on CP - induced behavioral modifications were tested administered alone and after naloxone (1 mg. / kg. s. c.). In addition, 90 minutes after CP injection, that is, at the time of administration of morphine, the bladder was removed in some rats for histological examination. Finally, to show that the bladder is essential for the CP - induced behavioral modifications, female rats also received CP at doses of 200 mg. / kg. i. p. and of 20 mg. by the intravesical route, and acrolein at doses of 0. 5 mg. by the intravesical route and of 5 mg. / kg. i. v. RESULTS: CP dose - relatedly induced marked behavioral modifications in male rats: breathing rate decrease, closing of the eyes and occurrence of specific postures. Morphine dose - dependently reversed these behavioral disorders. A dose of 0. 5 mg. / kg. produced a reduction of almost 50% of the behavioral score induced by CP 200 mg. / kg. This effect was completely prevented by pretreatment with naloxone. At the time of administration of morphine, histological modifications of the bladder wall, such as chorionic and muscle layer edema, were observed. In female rats, CP 200 mg. / kg. i. p. produced the same marked behavioral modifications as those observed in male rats. Administered at the dose of 20 mg. intravesically, CP did not produce any behavioral effects, whereas acrolein at 0. 5 mg. intravesically induced behavioral modifications identical to those under CP 200 mg. / kg. i. p., with the same maximal levels. Conversely, acrolein 5 mg. / kg. i. v. did not produce any behavioral effects at all. CONCLUSIONS: Overall, these results indicate that this experimental model of CP - induced cystitis may be an interesting new behavioral model of inflammatory visceral pain, allowing a better understanding of these painful syndromes and thus a better therapeutic approach to them.

Cyclophosphamide

Cyclophosphamide

CP

acrolein

CP

morphine

CP

naloxone

CP

morphine

CP

CP

acrolein

CP

Morphine

CP

naloxone

morphine

CP

CP

acrolein

CP

acrolein

CP

cystitis

visceral pain

visceral pain

cystitis

behavioral disorders

edema

cystitis

visceral pain

painful syndromes

Cyclophosphamide

cystitis

Cyclophosphamide

cystitis

Cyclophosphamide

cystitis

Cyclophosphamide

cystitis

Cyclophosphamide

cystitis

Cyclophosphamide

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

CP

cystitis

Cyclophosphamide

painful syndromes

Cyclophosphamide

painful syndromes

CP

painful syndromes

CP

painful syndromes

CP

painful syndromes

CP

painful syndromes

CP

painful syndromes

CP

painful syndromes

CP

painful syndromes

CP

painful syndromes

CP

painful syndromes

CP

painful syndromes

CP

painful syndromes

CP

painful syndromes

acrolein

painful syndromes

acrolein

painful syndromes

acrolein

painful syndromes

acrolein

painful syndromes


Input: Hyperalgesia and myoclonus in terminal cancer patients treated with continuous intravenous morphine. Eight cancer patients in the terminal stages of the disease treated with high doses of intravenous morphine developed hyperalgesia. All cases were retrospectively sampled from three different hospitals in Copenhagen. Five patients developed universal hyperalgesia and hyperesthesia which in 2 cases were accompanied by myoclonus. In 3 patients a pre - existing neuralgia increased to excruciating intensity and in 2 of these cases myoclonus occurred simultaneously. Although only few clinical descriptions of the relationship between hyperalgesia / myoclonus and high doses of morphine are available, experimental support from animal studies indicates that morphine, or its metabolites, plays a causative role for the observed behavioural syndrome. The possible mechanisms are discussed and treatment proposals given suggesting the use of more efficacious opioids with less excitatory potency in these situations.

Hyperalgesia

myoclonus

cancer

cancer

hyperalgesia

hyperalgesia

hyperesthesia

myoclonus

neuralgia

myoclonus

hyperalgesia

myoclonus

morphine

morphine

morphine

morphine

morphine

Hyperalgesia

morphine

hyperalgesia

morphine

hyperalgesia

morphine

hyperalgesia

morphine

Hyperalgesia

morphine

hyperalgesia

morphine

hyperalgesia

morphine

hyperalgesia

morphine

Hyperalgesia

morphine

hyperalgesia

morphine

hyperalgesia

morphine

hyperalgesia

morphine

Hyperalgesia

morphine

hyperalgesia

morphine

hyperalgesia

morphine

hyperalgesia

morphine

hyperesthesia

morphine

hyperesthesia

morphine

hyperesthesia

morphine

hyperesthesia

morphine

neuralgia

morphine

neuralgia

morphine

neuralgia

morphine

neuralgia

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus

morphine

myoclonus


Input: A prospective study of adverse reactions associated with vancomycin therapy. A prospective evaluation of the efficacy and safety of vancomycin was conducted in 54 consecutive patients over a 16 - month period. Vancomycin was curative in 95% of 43 patients with proven infection. Drugs were ceased in six patients because of adverse reactions; in three of these vancomycin was considered the likely cause. Reactions included thrombophlebitis (20 of 54 patients), rash (4 of 54), nephrotoxicity (4 of 50), proteinuria (1 of 50) and ototoxicity (1 of 11 patients tested by audiometry). Thrombophlebitis occurred only with infusion through peripheral cannulae; nephrotoxicity and ototoxicity were confined to patients receiving an aminoglycoside plus vancomycin. We conclude that vancomycin, administered appropriately, constitutes safe, effective therapy for infections caused by susceptible bacteria.

vancomycin

vancomycin

Vancomycin

vancomycin

aminoglycoside

vancomycin

vancomycin

infection

thrombophlebitis

rash

nephrotoxicity

proteinuria

ototoxicity

Thrombophlebitis

nephrotoxicity

ototoxicity

infections

vancomycin

thrombophlebitis

vancomycin

Thrombophlebitis

vancomycin

thrombophlebitis

vancomycin

Thrombophlebitis

Vancomycin

thrombophlebitis

Vancomycin

Thrombophlebitis

vancomycin

thrombophlebitis

vancomycin

Thrombophlebitis

vancomycin

thrombophlebitis

vancomycin

Thrombophlebitis

vancomycin

thrombophlebitis

vancomycin

Thrombophlebitis

vancomycin

rash

vancomycin

rash

Vancomycin

rash

vancomycin

rash

vancomycin

rash

vancomycin

rash

vancomycin

proteinuria

vancomycin

proteinuria

Vancomycin

proteinuria

vancomycin

proteinuria

vancomycin

proteinuria

vancomycin

proteinuria

vancomycin

ototoxicity

vancomycin

ototoxicity

vancomycin

ototoxicity

vancomycin

ototoxicity

Vancomycin

ototoxicity

Vancomycin

ototoxicity

vancomycin

ototoxicity

vancomycin

ototoxicity

vancomycin

ototoxicity

vancomycin

ototoxicity

vancomycin

ototoxicity

vancomycin

ototoxicity


Input: Blockade of both D - 1 and D - 2 dopamine receptors may induce catalepsy in mice. 1. The catalepsy induced by dopamine antagonists has been tested and the possible dopamine subtypes involved in catalepsy was determined. 2. Dopamine antagonist fluphenazine, D - 1 antagonist SCH 23390 or D - 2 antagonist sulpiride induced catalepsy. The effect of fluphenazine and sulpiride was dose - dependent. Combination of SCH 23390 with sulpiride did not induce catalepsy potentiation. 3. D - 1 agonist SKF 38393 or D - 2 agonist quinpirole decreased the catalepsy induced by fluphenazine, SCH 23390 or sulpiride. 4. Combination of SKF 38393 with quinpirole did not cause potentiated inhibitory effect on catalepsy induced by dopamine antagonists. 5. The data may indicate that although D - 2 receptor blockade is involved in catalepsy, the D - 1 receptor may plan a role.

dopamine

dopamine

dopamine

Dopamine

fluphenazine

SCH 23390

sulpiride

fluphenazine

sulpiride

SCH 23390

sulpiride

SKF 38393

quinpirole

fluphenazine

SCH 23390

sulpiride

SKF 38393

quinpirole

dopamine

catalepsy

catalepsy

catalepsy

catalepsy

catalepsy

catalepsy

catalepsy

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

fluphenazine

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

sulpiride

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy

SCH 23390

catalepsy


Input: Dextran - etodolac conjugates: synthesis, in vitro and in vivo evaluation. Etodolac (E), is a non - narcotic analgesic and antiinflammatory drug. A biodegradable polymer dextran has been utilized as a carrier for synthesis of etodolac - dextran conjugates (ED) to improve its aqueous solubility and reduce gastrointestinal side effects. An activated moiety, i. e. N - acylimidazole derivative of etodolac (EAI), was condensed with the polysaccharide polymer dextran of different molecular weights (40000, 60000, 110000 and 200000). IR spectral data confirmed formation of ester bonding in the conjugates. Etodolac contents were evaluated by UV - spectrophotometric analysis. The molecular weights were determined by measuring viscosity using the Mark - Howink - Sakurada equation. In vitro hydrolysis of ED was done in aqueous buffers (pH 1. 2, 7. 4, 9) and in 80% (v / v) human plasma (pH 7. 4). At pH 9, a higher rate of etodolac release from ED was observed as compared to aqueous buffer of pH 7. 4 and 80% human plasma (pH 7. 4), following first - order kinetics. In vivo investigations were performed in animals. Acute analgesic and antiinflammatory activities were ascertained using acetic acid induced writhing model (mice) and carrageenan - induced rat paw edema model, respectively. In comparison to control, E and ED1 - ED4 showed highly significant analgesic and antiinflammatory activities (p < 0. 001). Biological evaluation suggested that conjugates (ED1 - ED4) retained comparable analgesic and antiinflammatory activities with remarkably reduced ulcerogenicity as compared to their parent drug - - etodolac.

Dextran

etodolac

Etodolac

E

dextran

etodolac

dextran

N - acylimidazole

etodolac

EAI

dextran

Etodolac

etodolac

acetic acid

carrageenan

E

etodolac

writhing

edema

carrageenan

edema

carrageenan

writhing


Input: Hypersensitivity myocarditis complicating hypertrophic cardiomyopathy heart. The present report describes a case of eosinophilic myocarditis complicating hypertrophic cardiomyopathy. The 47 - year - old female patient, known to have hypertrophic cardiomyopathy, was admitted with biventricular failure and managed aggressively with dobutamine infusion and other drugs while being assessed for heart transplantation. On transthoracic echocardiogram, she had moderate left ventricular dysfunction with regional variability and moderate mitral regurgitation. The recipient' s heart showed the features of apical hypertrophic cardiomyopathy and myocarditis with abundant eosinophils. Myocarditis is rare and eosinophilic myocarditis is rarer. It is likely that the hypersensitivity (eosinophilic) myocarditis was related to dobutamine infusion therapy. Eosinophilic myocarditis has been reported with an incidence of 2. 4% to 7. 2% in explanted hearts and may be related to multidrug therapy.

Hypersensitivity

myocarditis

hypertrophic cardiomyopathy

eosinophilic myocarditis

eosinophilic

myocarditis

hypertrophic cardiomyopathy

hypertrophic cardiomyopathy

biventricular failure

left ventricular dysfunction

mitral regurgitation

hypertrophic cardiomyopathy

myocarditis

Myocarditis

eosinophilic myocarditis

eosinophilic

myocarditis

hypersensitivity

eosinophilic

myocarditis

Eosinophilic myocarditis

Eosinophilic

myocarditis

dobutamine

dobutamine

dobutamine

eosinophilic myocarditis

dobutamine

eosinophilic

dobutamine

eosinophilic myocarditis

dobutamine

eosinophilic

dobutamine

eosinophilic

dobutamine

Eosinophilic myocarditis

dobutamine

Eosinophilic

dobutamine

eosinophilic myocarditis

dobutamine

eosinophilic

dobutamine

eosinophilic myocarditis

dobutamine

eosinophilic

dobutamine

eosinophilic

dobutamine

Eosinophilic myocarditis

dobutamine

Eosinophilic

dobutamine

Hypersensitivity

dobutamine

hypersensitivity

dobutamine

Hypersensitivity

dobutamine

hypersensitivity

dobutamine

myocarditis

dobutamine

myocarditis

dobutamine

myocarditis

dobutamine

Myocarditis

dobutamine

myocarditis

dobutamine

myocarditis

dobutamine

myocarditis

dobutamine

myocarditis

dobutamine

myocarditis

dobutamine

myocarditis

dobutamine

Myocarditis

dobutamine

myocarditis

dobutamine

myocarditis

dobutamine

myocarditis


Input: All - trans - retinoic acid - induced erythema nodosum in patients with acute promyelocytic leukemia. Erythema nodosum associated with all - trans - retinoic acid (ATRA) for acute promyelocytic leukemia (APL) is very rare. We describe four patients with classic APL who developed erythema nodosum during ATRA therapy. Fever and subsequent multiple painful erythematous nodules over extremities developed on D11, D16, D17, and D19, respectively, after ATRA therapy. The skin biopsy taken from each patient was consistent with erythema nodosum. All patients received short course of steroids. Fever subsided rapidly and the skin lesions regressed completely. All patients achieved complete remission without withdrawal of ATRA. ATRA seemed to be the most possible etiology of erythema nodosum in our patients. Short - term use of steroid is very effective in ATRA - induced erythema nodosum.

All - trans - retinoic acid

all - trans - retinoic acid

ATRA

ATRA

ATRA

steroids

ATRA

ATRA

steroid

ATRA

erythema nodosum

acute promyelocytic leukemia

Erythema nodosum

acute promyelocytic leukemia

APL

APL

erythema nodosum

Fever

painful

erythematous nodules

erythema nodosum

Fever

erythema nodosum

erythema nodosum

All - trans - retinoic acid

erythema nodosum

All - trans - retinoic acid

Erythema nodosum

All - trans - retinoic acid

erythema nodosum

All - trans - retinoic acid

erythematous nodules

All - trans - retinoic acid

erythema nodosum

All - trans - retinoic acid

erythema nodosum

All - trans - retinoic acid

erythema nodosum

all - trans - retinoic acid

erythema nodosum

all - trans - retinoic acid

Erythema nodosum

all - trans - retinoic acid

erythema nodosum

all - trans - retinoic acid

erythematous nodules

all - trans - retinoic acid

erythema nodosum

all - trans - retinoic acid

erythema nodosum

all - trans - retinoic acid

erythema nodosum

ATRA

erythema nodosum

ATRA

Erythema nodosum

ATRA

erythema nodosum

ATRA

erythematous nodules

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

Erythema nodosum

ATRA

erythema nodosum

ATRA

erythematous nodules

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

Erythema nodosum

ATRA

erythema nodosum

ATRA

erythematous nodules

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

Erythema nodosum

ATRA

erythema nodosum

ATRA

erythematous nodules

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

Erythema nodosum

ATRA

erythema nodosum

ATRA

erythematous nodules

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

Erythema nodosum

ATRA

erythema nodosum

ATRA

erythematous nodules

ATRA

erythema nodosum

ATRA

erythema nodosum

ATRA

erythema nodosum

All - trans - retinoic acid

Fever

All - trans - retinoic acid

Fever

all - trans - retinoic acid

Fever

all - trans - retinoic acid

Fever

ATRA

Fever

ATRA

Fever

ATRA

Fever

ATRA

Fever

ATRA

Fever

ATRA

Fever

ATRA

Fever

ATRA

Fever

ATRA

Fever

ATRA

Fever

ATRA

Fever

ATRA

Fever


Input: Delayed - onset heparin - induced thrombocytopenia. BACKGROUND: Heparin - induced thrombocytopenia presents 5 to 12 days after heparin exposure, with or without arterial or venous thromboemboli. Delayed recognition and treatment of heparin - induced thrombocytopenia contribute to poor patient outcomes. OBJECTIVE: To describe and increase awareness of a clinical scenario in which the onset or manifestations of heparin - induced thrombocytopenia are delayed. DESIGN: Retrospective case series. SETTING: Three large urban hospitals (with active cardiovascular surgery programs). PATIENTS: 14 patients seen over a 3 - year period in whom heparin - induced thrombocytopenia became apparent on delayed presentation with thromboembolic complications. MEASUREMENTS: Platelet counts, onset of objectively determined thromboembolism, results of heparin - induced platelet factor 4 antibody tests, and outcomes. RESULTS: Patients went home after hospitalizations that had included heparin exposure - - in most cases, with no thrombocytopenia recognized - - only to return to the hospital (median, day 14) with thromboembolic complications. Thromboemboli were venous (12 patients, 7 with pulmonary emboli) or arterial (4 patients) or both. Platelet counts were mildly decreased in all but 2 patients on second presentation. On readmission, 11 patients received therapeutic heparin, which worsened the patients' clinical condition and, in all 11 cases, decreased the platelet count (mean at readmission, 143 x 10 (9) cells / L; mean nadir after heparin re - exposure, 39 x 10 (9) cells / L). Results of serologic tests for heparin - induced antibodies were positive in all patients. Subsequent treatments included alternative anticoagulants (11 patients), thrombolytic drugs (3 patients), inferior vena cava filters (3 patients) and, eventually, warfarin (11 patients). Three patients died. CONCLUSIONS: Delayed - onset heparin - induced thrombocytopenia is increasingly being recognized. To avoid disastrous outcomes, physicians must consider heparin - induced thrombocytopenia whenever a recently hospitalized patient returns with thromboembolism; therapy with alternative anticoagulants, not heparin, should be initiated.

heparin

Heparin

heparin

heparin

heparin

heparin

heparin

heparin

heparin

heparin

heparin

warfarin

heparin

heparin

heparin

thrombocytopenia

thrombocytopenia

arterial or venous thromboemboli

arterial or venous thromboemboli

venous thromboemboli

thrombocytopenia

thrombocytopenia

thrombocytopenia

thromboembolic

thromboembolism

thrombocytopenia

thromboembolic

Thromboemboli

pulmonary emboli

thrombocytopenia

thrombocytopenia

thromboembolism

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

Heparin

arterial or venous thromboemboli

Heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

venous thromboemboli

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

arterial or venous thromboemboli

Heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

arterial or venous thromboemboli

heparin

pulmonary emboli

Heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli

heparin

pulmonary emboli


Input: Valsartan, a new angiotensin II antagonist for the treatment of essential hypertension: a comparative study of the efficacy and safety against amlodipine. OBJECTIVE: To compare the antihypertensive efficacy of a new angiotensin II antagonist, valsartan, with a reference therapy, amlodipine. METHODS: One hundred sixty - eight adult outpatients with mild to moderate hypertension were randomly allocated in double - blind fashion and equal number to receive 80 mg valsartan or 5 mg amlodipine for 12 weeks. After 8 weeks of therapy, in patients whose blood pressure remained uncontrolled, 5 mg amlodipine was added to the initial therapy. Patients were assessed at 4, 8, and 12 weeks. The primary efficacy variable was change from baseline in mean sitting diastolic blood pressure at 8 weeks. Secondary variables included change in sitting systolic blood pressure and responder rates. RESULTS: Both valsartan and amlodipine were effective at lowering blood pressure at 4, 8, and 12 weeks. Similar decreases were observed in both groups, with no statistically significant differences between the groups for any variable analyzed. For the primary variable the difference was 0. 5 mm Hg in favor of valsartan (p = 0. 68; 95% confidence interval, - 2. 7 to 1. 7). Responder rates at 8 weeks were 66. 7% for valsartan and 60. 2% for amlodipine (p = 0. 39). Both treatments were well tolerated. The incidence of drug - related dependent edema was somewhat higher in the amlodipine group, particularly at a dose of 10 mg per day (2. 4% for 80 mg valsartan; 3. 6% for 5 mg amlodipine; 0% for valsartan plus 5 mg amlodipine; 14. 3% for 10 mg amlodipine). CONCLUSIONS: The data show that valsartan is at least as effective as amlodipine in the treatment of mild to moderate hypertension. The results also show valsartan to be well tolerated and suggest that it is not associated with side effects characteristic of this comparator class, dihydropyridine calcium antagonists.

Valsartan

angiotensin II

amlodipine

angiotensin II

valsartan

amlodipine

valsartan

amlodipine

amlodipine

valsartan

amlodipine

valsartan

valsartan

amlodipine

amlodipine

valsartan

amlodipine

valsartan

amlodipine

amlodipine

valsartan

amlodipine

valsartan

dihydropyridine

calcium

hypertension

hypertension

edema

hypertension

Valsartan

edema

valsartan

edema

valsartan

edema

valsartan

edema

valsartan

edema

valsartan

edema

valsartan

edema

valsartan

edema

valsartan

edema

valsartan

edema

amlodipine

edema

amlodipine

edema

amlodipine

edema

amlodipine

edema

amlodipine

edema

amlodipine

edema

amlodipine

edema

amlodipine

edema

amlodipine

edema

amlodipine

edema

amlodipine

edema


Input: KF17837: a novel selective adenosine A2A receptor antagonist with anticataleptic activity. KF17837 is a novel selective adenosine A2A receptor antagonist. Oral administration of KF17837 (2. 5, 10. 0 and 30. 0 mg / kg) significantly ameliorated the cataleptic responses induced by intracerebroventricular administration of an adenosine A2A receptor agonist, CGS 21680 (10 micrograms), in a dose - dependent manner. KF17837 also reduced the catalepsy induced by haloperidol (1 mg / kg i. p.) and by reserpine (5 mg / kg i. p.). These anticataleptic effects were exhibited dose dependently at doses from 0. 625 and 2. 5 mg / kg p. o., respectively. Moreover, KF17837 (0. 625 mg / kg p. o.) potentiated the anticataleptic effects of a subthreshold dose of L - 3, 4 - dihydroxyphenylalanine (L - DOPA; 25 mg / kg i. p.) plus benserazide (6. 25 mg / kg i. p.). These results suggested that KF17837 is a centrally active adenosine A2A receptor antagonist and that the dopaminergic function of the nigrostriatal pathway is potentiated by adenosine A2A receptor antagonists. Furthermore, KF17837 may be a useful drug in the treatment of parkinsonism.

adenosine

adenosine

adenosine

CGS 21680

haloperidol

reserpine

L - 3, 4 - dihydroxyphenylalanine

L - DOPA

benserazide

adenosine

adenosine

cataleptic

catalepsy

parkinsonism

reserpine

cataleptic

reserpine

catalepsy

CGS 21680

cataleptic

CGS 21680

catalepsy

haloperidol

cataleptic

haloperidol

catalepsy


Input: Some central effects of repeated treatment with fluvoxamine. We investigated the effect of repeated treatment with fluvoxamine, a selective serotonin uptake inhibitor, on behavioral effects of dopaminomimetics and methoxamine and on the animal behavior in the " behavioral despair " test. A repeated treatment with fluvoxamine (twice daily for 14 days) potentiated in mice and in rats (weaker) the amphetamine - induced hyperactivity. The hyperactivity induced by nomifensine in mice remained unaffected by fluvoxamine. The stimulation of locomotor activity by intracerebroventricularly administered methoxamine was not affected by repeated treatment with fluvoxamine. Given three times fluvoxamine had no effect on the immobilization time in the " behavioral despair " test in rats. The results indicate that fluvoxamine given repeatedly acts differently than citalopram, another selective serotonin uptake inhibitor, and differs also from other antidepressant drugs.

fluvoxamine

fluvoxamine

serotonin

methoxamine

fluvoxamine

amphetamine

nomifensine

fluvoxamine

methoxamine

fluvoxamine

fluvoxamine

fluvoxamine

citalopram

serotonin

hyperactivity

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

fluvoxamine

hyperactivity

methoxamine

hyperactivity

methoxamine

hyperactivity

methoxamine

hyperactivity

methoxamine

hyperactivity

nomifensine

hyperactivity

nomifensine

hyperactivity

amphetamine

hyperactivity

amphetamine

hyperactivity