Input: Cardiovascular effects of hypotension induced by adenosine triphosphate and sodium nitroprusside on dogs with denervated hearts. Adenosine triphosphate (ATP) and sodium nitroprusside (SNP) are administered to patients to induce and control hypotension during anesthesia. SNP is authorized for clinical use in USA and UK, and ATP is clinically used in other countries such as Japan. We investigated how these two drugs act on the cardiovascular systems of 20 dogs whose hearts had been denervated by a procedure we had devised. ATP (10 dogs) or SNP (10 dogs) was administered to reduce mean arterial pressure by 30% to 70% of control. Before, during and after induced hypotension, we measured major cardiovascular parameters. Hypotension induced by ATP was accompanied by significant decreases in mean pulmonary arterial pressure (p less than 0. 001), central venous pressure (p less than 0. 001), left ventricular end - diastolic pressure (p less than 0. 001), total peripheral resistance (p less than 0. 001), rate pressure product (p less than 0. 001), total body oxygen consumption (p less than 0. 05), and heart rate (p less than 0. 001); all these variables returned normal within 30 min after ATP was stopped. Cardiac output did not change. During hypotension produced by SNP similar decreases were observed in mean pulmonary arterial pressure (p less than 0. 01), central venous pressure (p less than 0. 001), left ventricular end - diastolic pressure (p less than 0. 01), total peripheral resistance (p less than 0. 001), rate pressure product (p less than 0. 001), and oxygen content difference between arterial and mixed venous blood (p less than 0. 05), while heart rate (p less than 0. 001) and cardiac output (p less than 0. 05) were increased. Recoveries of heart rate and left ventricular end - diastolic pressure were not shown within 60 min after SNP had been stopped. Both ATP and SNP should act on the pacemaker tissue of the heart.

hypotension

hypotension

hypotension

Hypotension

hypotension

adenosine triphosphate

sodium nitroprusside

Adenosine triphosphate

ATP

sodium nitroprusside

SNP

SNP

ATP

ATP

SNP

ATP

oxygen

ATP

SNP

oxygen

SNP

ATP

SNP

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

Hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

Hypotension

sodium nitroprusside

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

Hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

Hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

Hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

Hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

Hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

Hypotension

SNP

hypotension

adenosine triphosphate

hypotension

adenosine triphosphate

hypotension

adenosine triphosphate

hypotension

adenosine triphosphate

Hypotension

adenosine triphosphate

hypotension

Adenosine triphosphate

hypotension

Adenosine triphosphate

hypotension

Adenosine triphosphate

hypotension

Adenosine triphosphate

Hypotension

Adenosine triphosphate

hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

Hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

Hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

Hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

Hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

Hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

hypotension

ATP

Hypotension

ATP

hypotension


Input: Comparative study: Endografine (diatrizoate), Vasurix polyvidone (acetrizoate), Dimer - X (iocarmate) and Hexabrix (ioxaglate) in hysterosalpingography. Side effects of hysterosalpingography with Dimer - X, Hexabrix, Vasurix polyvidone and Endografine in 142 consecutive patients, receiving one of the four tested media were evaluated from replies to postal questionnaires. The Dimer - X group had a higher incidence of nausea and dizziness. The Endografine group had a higher incidence of abdominal pain. These differences occur especially in the age groups under 30 years. Hexabrix and Vasurix polyvidone are considered the best contrast media for hysterosalpingography and perhaps because of its low toxicity Hexabrix should be preferred.

Endografine

diatrizoate

Vasurix polyvidone

acetrizoate

Dimer - X

iocarmate

Hexabrix

ioxaglate

Dimer - X

Hexabrix

Vasurix polyvidone

Endografine

Dimer - X

Endografine

Hexabrix

Vasurix polyvidone

contrast media

Hexabrix

nausea

dizziness

abdominal pain

toxicity

Endografine

abdominal pain

Endografine

abdominal pain

Endografine

abdominal pain

Dimer - X

dizziness

iocarmate

dizziness

Dimer - X

dizziness

Dimer - X

dizziness

Dimer - X

nausea

iocarmate

nausea

Dimer - X

nausea

Dimer - X

nausea


Input: Post - suxamethonium pains in Nigerian surgical patients. Contrary to an earlier report by Coxon, scoline pain occurs in African negroes. Its incidence was determined in a prospective study involving a total of 100 Nigerian patients (50 out - patients and 50 in - patients). About 62% of the out - patients developed scoline pain as compared with about 26% among the in - patients. The abolition of muscle fasciculations (by 0. 075mg / kg dose of Fazadinium) did not influence the occurrence of scoline pain. Neither the type of induction agent (Althesin or Thiopentone) nor the salt preparation of suxamethonium used (chloride or bromide), affected the incidence of scoline pain.

suxamethonium

scoline

scoline

Fazadinium

scoline

Althesin

Thiopentone

suxamethonium

chloride

bromide

scoline

pains

pain

pain

fasciculations

pain

pain

suxamethonium

fasciculations

scoline

fasciculations

scoline

fasciculations

scoline

fasciculations

suxamethonium

fasciculations

scoline

fasciculations

suxamethonium

pains

suxamethonium

pain

suxamethonium

pain

suxamethonium

pain

suxamethonium

pain

scoline

pains

scoline

pain

scoline

pain

scoline

pain

scoline

pain

scoline

pains

scoline

pain

scoline

pain

scoline

pain

scoline

pain

scoline

pains

scoline

pain

scoline

pain

scoline

pain

scoline

pain

suxamethonium

pains

suxamethonium

pain

suxamethonium

pain

suxamethonium

pain

suxamethonium

pain

scoline

pains

scoline

pain

scoline

pain

scoline

pain

scoline

pain


Input: Medial changes in arterial spasm induced by L - norepinephrine. In normal rats, the media of small arteries (0. 4 - - 0. 2 mm in diameter) previously was shown to contain intracellular vacuoles, identified ultrastructurally as herniations of one smooth muscle cell into another. The hypothesis that intense vasoconstriction would increase the number of such vacuoles has been tested. In the media of the saphenous artery and its distal branch, vasoconstriction induced by L - norepinephrine produced many cell - to - cell hernias within 15 minutes. At 1 day their number was reduced to about 1 / 10 of the original number. By 7 days the vessel was almost restored to normal. Triple stimulation over 1 day induced more severe changes in the media. These findings suggest that smooth muscle cells are susceptible to damage in the course of their specific function. The experimental data are discussed in relation to medial changes observed in other instances of arterial spasm. Endothelial changes that developed in the same experimental model were described in a previous paper.

spasm

hernias

spasm

L - norepinephrine

L - norepinephrine

L - norepinephrine

spasm

L - norepinephrine

spasm

L - norepinephrine

spasm

L - norepinephrine

spasm


Input: Abnormalities of the pupil and visual - evoked potential in quinine amblyopia. Total blindness with a transient tonic pupillary response, denervation supersensitivity, and abnormal visual - evoked potentials developed in a 54 - year - old man after the use of quinine sulfate for leg cramps. He later recovered normal visual acuity. A transient tonic pupillary response, denervation supersensitivity, and abnormal visual - evoked potentials in quinine toxicity, to our knowledge, have not been previously reported.

quinine

quinine sulfate

quinine

amblyopia

blindness

tonic pupillary

leg cramps

tonic pupillary

toxicity

quinine

tonic pupillary

quinine

tonic pupillary

quinine sulfate

tonic pupillary

quinine sulfate

tonic pupillary

quinine

tonic pupillary

quinine

tonic pupillary

quinine

amblyopia

quinine sulfate

amblyopia

quinine

amblyopia

quinine

blindness

quinine sulfate

blindness

quinine

blindness


Input: Suxamethonium - induced jaw stiffness and myalgia associated with atypical cholinesterase: case report. An 11 - year - old boy was given halothane, nitrous oxide and oxygen, pancuronium 0. 4 mg and suxamethonium 100 mg for induction of anaesthesia. In response to this a marked jaw stiffness occurred which lasted for two minutes and the anaesthesia were terminated. Four hours of apnoea ensued and he suffered generalized severe myalgia lasting for one week. He was found to have atypical plasma cholinesterase with a dibucaine number of 12, indicating homozygocity. This was verified by study of the family. The case shows that prolonged jaw rigidity and myalgia may occur after suxamethonium in patients with atypical cholinesterase despite pretreatment with pancuronium.

Suxamethonium

halothane

nitrous oxide

oxygen

pancuronium

suxamethonium

dibucaine

suxamethonium

pancuronium

jaw stiffness

myalgia

jaw stiffness

apnoea

myalgia

prolonged jaw rigidity

myalgia

Suxamethonium

jaw stiffness

Suxamethonium

jaw stiffness

Suxamethonium

prolonged jaw rigidity

suxamethonium

jaw stiffness

suxamethonium

jaw stiffness

suxamethonium

prolonged jaw rigidity

suxamethonium

jaw stiffness

suxamethonium

jaw stiffness

suxamethonium

prolonged jaw rigidity

Suxamethonium

apnoea

suxamethonium

apnoea

suxamethonium

apnoea

Suxamethonium

myalgia

Suxamethonium

myalgia

Suxamethonium

myalgia

suxamethonium

myalgia

suxamethonium

myalgia

suxamethonium

myalgia

suxamethonium

myalgia

suxamethonium

myalgia

suxamethonium

myalgia


Input: Indomethacin - induced hyperkalemia in three patients with gouty arthritis. We describe three patients in whom severe, life - threatening hyperkalemia and renal insufficiency developed after treatment of acute gouty arthritis with indomethacin. This complication may result from an inhibition of prostaglandin synthesis and consequent hyporeninemic hypoaidosteronism. Careful attention to renal function and potassium balance in patients receiving indomethacin or other nonsteroidal anti - inflammatory agents, particularly in those patients with diabetes mellitus or preexisting renal disease, will help prevent this potentially serious complication.

Indomethacin

indomethacin

prostaglandin

potassium

indomethacin

hyperkalemia

gouty arthritis

hyperkalemia

renal insufficiency

gouty arthritis

hyporeninemic hypoaidosteronism

diabetes mellitus

renal disease

Indomethacin

hyperkalemia

Indomethacin

hyperkalemia

indomethacin

hyperkalemia

indomethacin

hyperkalemia

indomethacin

hyperkalemia

indomethacin

hyperkalemia

Indomethacin

renal insufficiency

indomethacin

renal insufficiency

indomethacin

renal insufficiency


Input: Etomidate: a foreshortened clinical trial. A clinical evaluation of etomidate for outpatient cystoscopy was embarked upon. Unpremedicated patients were given fentanyl 1 microgram / kg followed by etomidate 0. 3 mg / kg. Anaesthesia was maintained with intermittent etomidate in 2 - 4 mg doses. Patients were interviewed personally later the same day, and by questionnaire three to four weeks later. The trial was discontinued after 20 cases because of an unacceptable incidence of side effects. Venous pain occurred in 68% of patients and 50% had redness, pain or swelling related to the injection site, in some cases lasting up to three weeks after anaesthesia. Skeletal movements occurred in 50% of patients; 30% experienced respiratory upset, one sufficiently severe to necessitate abandoning the technique. Nausea and vomiting occurred in 40% and 25% had disturbing emergence psychoses.

Etomidate

etomidate

fentanyl

etomidate

etomidate

pain

pain

swelling

respiratory upset

Nausea

vomiting

psychoses

Etomidate

Nausea

etomidate

Nausea

etomidate

Nausea

etomidate

Nausea

Etomidate

vomiting

etomidate

vomiting

etomidate

vomiting

etomidate

vomiting

Etomidate

pain

Etomidate

pain

etomidate

pain

etomidate

pain

etomidate

pain

etomidate

pain

etomidate

pain

etomidate

pain

Etomidate

respiratory upset

etomidate

respiratory upset

etomidate

respiratory upset

etomidate

respiratory upset

Etomidate

psychoses

etomidate

psychoses

etomidate

psychoses

etomidate

psychoses


Input: Levodopa - induced dyskinesias are improved by fluoxetine. We evaluated the severity of motor disability and dyskinesias in seven levodopa - responsive patients with Parkinson' s disease after an acute challenge with the mixed dopamine agonist, apomorphine, before and after the administration of fluoxetine (20 mg twice per day) for 11 + / - 1 days. After fluoxetine treatment, there was a significant 47% improvement (p < 0. 05) of apomorphine - induced dyskinesias without modification of parkinsonian motor disability. The dyskinesias were reduced predominantly in the lower limbs during the onset and disappearance of dystonic dyskinesias (onset - and end - of - dose dyskinesias) and in the upper limbs during choreic mid - dose dyskinesias. The results suggest that increased brain serotoninergic transmission with fluoxetine may reduce levodopa - or dopamine agonist - induced dyskinesias without aggravating parkinsonian motor disability.

Levodopa

fluoxetine

levodopa

dopamine

apomorphine

fluoxetine

fluoxetine

apomorphine

fluoxetine

levodopa

dopamine

dyskinesias

motor disability

dyskinesias

Parkinson' s disease

dyskinesias

parkinsonian

motor disability

dyskinesias

dystonic dyskinesias

dystonic

dyskinesias

dyskinesias

choreic mid - dose dyskinesias

choreic

mid - dose dyskinesias

dyskinesias

parkinsonian

motor disability

apomorphine

dyskinesias

apomorphine

dyskinesias

apomorphine

dyskinesias

apomorphine

dyskinesias

apomorphine

dystonic dyskinesias

apomorphine

dyskinesias

apomorphine

dyskinesias

apomorphine

choreic mid - dose dyskinesias

apomorphine

dyskinesias

apomorphine

dyskinesias

apomorphine

dyskinesias

apomorphine

dyskinesias

apomorphine

dyskinesias

apomorphine

dystonic dyskinesias

apomorphine

dyskinesias

apomorphine

dyskinesias

apomorphine

choreic mid - dose dyskinesias

apomorphine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dystonic dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

choreic mid - dose dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dystonic dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

choreic mid - dose dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dystonic dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

choreic mid - dose dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

dystonic dyskinesias

fluoxetine

dyskinesias

fluoxetine

dyskinesias

fluoxetine

choreic mid - dose dyskinesias

fluoxetine

dyskinesias


Input: A large population - based follow - up study of trimethoprim - sulfamethoxazole, trimethoprim, and cephalexin for uncommon serious drug toxicity. We conducted a population - based 45 - day follow - up study of 232, 390 people who were prescribed trimethoprim - sulfamethoxazole (TMP - SMZ), 266, 951 prescribed trimethoprim alone, and 196, 397 prescribed cephalexin, to estimate the risk of serious liver, blood, skin, and renal disorders resulting in referral or hospitalization associated with these drugs. The results were based on information recorded on office computers by selected general practitioners in the United Kingdom, together with a review of clinical records. The risk of clinically important idiopathic liver disease was similar for persons prescribed TMP - SMZ (5. 2 / 100, 000) and those prescribed trimethoprim alone (3. 8 / 100, 000). The risk for those prescribed cephalexin was somewhat lower (2. 0 / 100, 000). Only five patients experienced blood disorders, one of whom was exposed to TMP - SMZ; of seven with erythema multiforme and Stevens - Johnson syndrome, four were exposed to TMP - SMZ. The one case of toxic epidermal necrolysis occurred in a patient who took cephalexin. Finally, only five cases of acute parenchymal renal disease occurred, none likely to be caused by a study drug. We conclude that the risk of the serious diseases studied is small for the three agents, and compares reasonably with the risk for many other antibiotics.

trimethoprim - sulfamethoxazole

trimethoprim

cephalexin

trimethoprim - sulfamethoxazole

TMP - SMZ

trimethoprim

cephalexin

TMP - SMZ

trimethoprim

cephalexin

TMP - SMZ

TMP - SMZ

cephalexin

drug toxicity

liver, blood, skin, and renal disorders

liver, blood, skin, and renal disorders

blood, skin, and renal disorders

skin, and renal disorders

renal disorders

liver disease

erythema multiforme

Stevens - Johnson syndrome

toxic epidermal necrolysis

renal disease

trimethoprim

liver, blood, skin, and renal disorders

trimethoprim

liver, blood, skin, and renal disorders

trimethoprim

liver disease

trimethoprim

liver, blood, skin, and renal disorders

trimethoprim

liver, blood, skin, and renal disorders

trimethoprim

liver disease

trimethoprim

liver, blood, skin, and renal disorders

trimethoprim

liver, blood, skin, and renal disorders

trimethoprim

liver disease

trimethoprim - sulfamethoxazole

liver, blood, skin, and renal disorders

trimethoprim - sulfamethoxazole

liver, blood, skin, and renal disorders

trimethoprim - sulfamethoxazole

liver disease

trimethoprim - sulfamethoxazole

liver, blood, skin, and renal disorders

trimethoprim - sulfamethoxazole

liver, blood, skin, and renal disorders

trimethoprim - sulfamethoxazole

liver disease

TMP - SMZ

liver, blood, skin, and renal disorders

TMP - SMZ

liver, blood, skin, and renal disorders

TMP - SMZ

liver disease

TMP - SMZ

liver, blood, skin, and renal disorders

TMP - SMZ

liver, blood, skin, and renal disorders

TMP - SMZ

liver disease

TMP - SMZ

liver, blood, skin, and renal disorders

TMP - SMZ

liver, blood, skin, and renal disorders

TMP - SMZ

liver disease

TMP - SMZ

liver, blood, skin, and renal disorders

TMP - SMZ

liver, blood, skin, and renal disorders

TMP - SMZ

liver disease

cephalexin

liver, blood, skin, and renal disorders

cephalexin

liver, blood, skin, and renal disorders

cephalexin

liver disease

cephalexin

liver, blood, skin, and renal disorders

cephalexin

liver, blood, skin, and renal disorders

cephalexin

liver disease

cephalexin

liver, blood, skin, and renal disorders

cephalexin

liver, blood, skin, and renal disorders

cephalexin

liver disease

cephalexin

liver, blood, skin, and renal disorders

cephalexin

liver, blood, skin, and renal disorders

cephalexin

liver disease

cephalexin

Stevens - Johnson syndrome

cephalexin

toxic epidermal necrolysis

cephalexin

Stevens - Johnson syndrome

cephalexin

toxic epidermal necrolysis

cephalexin

Stevens - Johnson syndrome

cephalexin

toxic epidermal necrolysis

cephalexin

Stevens - Johnson syndrome

cephalexin

toxic epidermal necrolysis

trimethoprim - sulfamethoxazole

Stevens - Johnson syndrome

trimethoprim - sulfamethoxazole

toxic epidermal necrolysis

trimethoprim - sulfamethoxazole

Stevens - Johnson syndrome

trimethoprim - sulfamethoxazole

toxic epidermal necrolysis

TMP - SMZ

Stevens - Johnson syndrome

TMP - SMZ

toxic epidermal necrolysis

TMP - SMZ

Stevens - Johnson syndrome

TMP - SMZ

toxic epidermal necrolysis

TMP - SMZ

Stevens - Johnson syndrome

TMP - SMZ

toxic epidermal necrolysis

TMP - SMZ

Stevens - Johnson syndrome

TMP - SMZ

toxic epidermal necrolysis


Input: Clinical safety of lidocaine in patients with cocaine - associated myocardial infarction. STUDY OBJECTIVE: To evaluate the safety of lidocaine in the setting of cocaine - induced myocardial infarction (MI). DESIGN: A retrospective, multicenter study. SETTING: Twenty - nine university, university - affiliated, or community hospitals during a 6 - year period (total of 117 cumulative hospital - years). PARTICIPANTS: Patients with cocaine - associated MI who received lidocaine in the emergency department. RESULTS: Of 29 patients who received lidocaine in the setting of cocaine - associated MI, no patient died; exhibited bradydysrhythmias, ventricular tachycardia, or ventricular fibrillation; or experienced seizures after administration of lidocaine (95% confidence interval, 0% to 11%). CONCLUSION: Despite theoretical concerns that lidocaine may enhance cocaine toxicity, the use of lidocaine in patients with cocaine - associated MI was not associated with significant cardiovascular or central nervous system toxicity.

lidocaine

cocaine

lidocaine

cocaine

cocaine

lidocaine

lidocaine

cocaine

lidocaine

lidocaine

cocaine

lidocaine

cocaine

myocardial infarction

myocardial infarction

MI

MI

MI

bradydysrhythmias

ventricular tachycardia

ventricular fibrillation

seizures

toxicity

MI

cardiovascular or central nervous system toxicity

cardiovascular or central nervous system toxicity

central nervous system toxicity

cocaine

myocardial infarction

cocaine

myocardial infarction

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

myocardial infarction

cocaine

myocardial infarction

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

myocardial infarction

cocaine

myocardial infarction

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

myocardial infarction

cocaine

myocardial infarction

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

myocardial infarction

cocaine

myocardial infarction

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

myocardial infarction

cocaine

myocardial infarction

cocaine

MI

cocaine

MI

cocaine

MI

cocaine

MI


Input: Paclitaxel 3 - hour infusion given alone and combined with carboplatin: preliminary results of dose - escalation trials. Paclitaxel (Taxol; Bristol - Myers Squibb Company, Princeton, NJ) by 3 - hour infusion was combined with carboplatin in a phase I / II study directed to patients with non - small cell lung cancer. Carboplatin was given at a fixed target area under the concentration - time curve of 6. 0 by the Calvert formula, whereas paclitaxel was escalated in patient cohorts from 150 mg / m2 (dose level I) to 175, 200, 225, and 250 mg / m2. The 225 mg / m2 level was expanded for the phase II study since the highest level achieved (250 mg / m2) required modification because of nonhematologic toxicities (arthralgia and sensory neuropathy). Therapeutic effects were noted at all dose levels, with objective responses in 17 (two complete and 15 partial regressions) of 41 previously untreated patients. Toxicities were compared with a cohort of patients in a phase I trial of paclitaxel alone at identical dose levels. Carboplatin did not appear to add to the hematologic toxicities observed, and the paclitaxel / carboplatin combination could be dosed every 3 weeks.

Paclitaxel

carboplatin

Paclitaxel

Taxol

carboplatin

Carboplatin

paclitaxel

paclitaxel

Carboplatin

paclitaxel

carboplatin

non - small cell lung cancer

toxicities

arthralgia

sensory neuropathy

Toxicities

hematologic toxicities

Paclitaxel

sensory neuropathy

Paclitaxel

sensory neuropathy

Taxol

sensory neuropathy

paclitaxel

sensory neuropathy

paclitaxel

sensory neuropathy

paclitaxel

sensory neuropathy

Paclitaxel

hematologic toxicities

Paclitaxel

hematologic toxicities

Taxol

hematologic toxicities

paclitaxel

hematologic toxicities

paclitaxel

hematologic toxicities

paclitaxel

hematologic toxicities

Paclitaxel

arthralgia

Paclitaxel

arthralgia

Taxol

arthralgia

paclitaxel

arthralgia

paclitaxel

arthralgia

paclitaxel

arthralgia


Input: The dose - dependent effect of misoprostol on indomethacin - induced renal dysfunction in well compensated cirrhosis. Misoprostol (200 micrograms) has been shown to acutely counteract the indomethacin - induced renal dysfunction in well compensated cirrhotic patients. The aim of this study was to determine if the prophylactic value of misoprostol was dose - dependent. Parameters of renal hemodynamics and tubular sodium and water handling were assessed by clearance techniques in 26 well compensated cirrhotic patients before and after an oral combination of 50 mg of indomethacin and various doses of misoprostol. The 200 - micrograms dose was able to totally abolish the deleterious renal effects of indomethacin, whereas the 800 - micrograms dose resulted in significant worsening of renal hemodynamics and sodium retention. These changes were maximal in the hour immediately after medications and slowly returned toward base - line levels thereafter. These results suggest that the renal protective effects of misoprostol is dose - dependent. However, until this apparent ability of 200 micrograms of misoprostol to prevent the adverse effects of indomethacin on renal function is confirmed with chronic frequent dosing, it would be prudent to avoid nonsteroidal anti - inflammatory therapy in patients with cirrhosis.

misoprostol

indomethacin

Misoprostol

indomethacin

misoprostol

sodium

indomethacin

misoprostol

indomethacin

sodium

misoprostol

misoprostol

indomethacin

renal dysfunction

cirrhosis

renal dysfunction

cirrhotic

cirrhotic

cirrhosis

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal dysfunction


Input: Increased frequency and severity of angio - oedema related to long - term therapy with angiotensin - converting enzyme inhibitor in two patients. Adverse reactions to drugs are well recognized as a cause of acute or chronic urticaria, and angio - oedema. Angiotensin - converting enzyme (ACE) inhibitors, used to treat hypertension and congestive heart failure, were introduced in Europe in the middle of the eighties, and the use of these drugs has increased progressively. Soon after the introduction of ACE inhibitors, acute bouts of angio - oedema were reported in association with the use of these drugs. We wish to draw attention to the possibility of adverse reactions to ACE inhibitors after long - term use and in patients with pre - existing angio - oedema.

angio - oedema

urticaria

angio - oedema

hypertension

congestive heart failure

angio - oedema

angio - oedema

angiotensin - converting enzyme inhibitor

Angiotensin - converting enzyme (ACE) inhibitors

ACE inhibitors

ACE inhibitors

angiotensin - converting enzyme inhibitor

angio - oedema

angiotensin - converting enzyme inhibitor

angio - oedema

angiotensin - converting enzyme inhibitor

angio - oedema

angiotensin - converting enzyme inhibitor

angio - oedema

Angiotensin - converting enzyme (ACE) inhibitors

angio - oedema

Angiotensin - converting enzyme (ACE) inhibitors

angio - oedema

Angiotensin - converting enzyme (ACE) inhibitors

angio - oedema

Angiotensin - converting enzyme (ACE) inhibitors

angio - oedema

ACE inhibitors

angio - oedema

ACE inhibitors

angio - oedema

ACE inhibitors

angio - oedema

ACE inhibitors

angio - oedema

ACE inhibitors

angio - oedema

ACE inhibitors

angio - oedema

ACE inhibitors

angio - oedema

ACE inhibitors

angio - oedema


Input: Myoclonus associated with lorazepam therapy in very - low - birth - weight infants. Lorazepam is being used with increasing frequency as a sedative in the newborn and the young infant. Concern has been raised with regard to the safety of lorazepam in this age group, especially in very - low - birth - weight (VLBW; < 1, 500 g) infants. Three young infants, all of birth weight < 1, 500 g, experienced myoclonus following the intravenous administration of lorazepam. The potential neurotoxic effects of the drug (and its vehicle) in this population are discussed. Injectable lorazepam should be used with caution in VLBW infants.

Myoclonus

myoclonus

neurotoxic

lorazepam

Lorazepam

lorazepam

lorazepam

lorazepam

lorazepam

Myoclonus

lorazepam

myoclonus

Lorazepam

Myoclonus

Lorazepam

myoclonus

lorazepam

Myoclonus

lorazepam

myoclonus

lorazepam

Myoclonus

lorazepam

myoclonus

lorazepam

Myoclonus

lorazepam

myoclonus


Input: Transvenous right ventricular pacing during cardiopulmonary resuscitation of pediatric patients with acute cardiomyopathy. We describe the cardiopulmonary resuscitation efforts on five patients who presented in acute circulatory failure from myocardial dysfunction. Three patients had acute viral myocarditis, one had a carbamazepine - induced acute eosinophilic myocarditis, and one had cardiac hemosiderosis resulting in acute cardiogenic shock. All patients were continuously monitored with central venous and arterial catheters in addition to routine noninvasive monitoring. An introducer sheath, a pacemaker, and sterile pacing wires were made readily available for the patients, should the need arise to terminate resistant cardiac dysrhythmias. All patients developed cardiocirculatory arrest associated with extreme hypotension and dysrhythmias within the first 48 hours of their admission to the pediatric intensive care unit (PICU). Right ventricular pacemaker wires were inserted in all of them during cardiopulmonary resuscitation (CPR). In four patients, cardiac pacing was used, resulting in a temporary captured rhythm and restoration of their cardiac output. These patients had a second event of cardiac arrest, resulting in death, within 10 to 60 minutes. In one patient, cardiac pacing was not used, because he converted to normal sinus rhythm by electrical defibrillation within three minutes of initiating CPR. We conclude that cardiac pacing during resuscitative efforts in pediatric patients suffering from acute myocardial dysfunction may not have long - term value in and of itself; however, if temporary hemodynamic stability is achieved by this procedure, it may provide additional time needed to institute other therapeutic modalities.

cardiomyopathy

circulatory failure

myocardial dysfunction

myocarditis

eosinophilic myocarditis

eosinophilic

myocarditis

cardiogenic shock

dysrhythmias

hypotension

dysrhythmias

cardiac arrest

myocardial dysfunction

carbamazepine

carbamazepine

eosinophilic myocarditis

carbamazepine

eosinophilic

carbamazepine

myocarditis

carbamazepine

myocarditis


Input: Efficacy and safety of granisetron, a selective 5 - hydroxytryptamine - 3 receptor antagonist, in the prevention of nausea and vomiting induced by high - dose cisplatin. PURPOSE: To assess the antiemetic effects and safety profile of four different doses of granisetron (Kytril; SmithKline Beecham Pharmaceuticals, Philadelphia, PA) when administered as a single intravenous (IV) dose for prophylaxis of cisplatin - induced nausea and vomiting. PATIENTS AND METHODS: One hundred eighty - four chemotherapy - naive patients receiving high - dose cisplatin (81 to 120 mg / m2) were randomized to receive one of four granisetron doses (5, 10, 20, or 40 micrograms / kg) administered before chemotherapy. Patients were observed on an inpatient basis for 18 to 24 hours, and vital signs, nausea, vomiting, retching, and appetite were assessed. Safety analyses included incidence of adverse experiences and laboratory parameter changes. RESULTS: After granisetron doses of 5, 10, 20, and 40 micrograms / kg, a major response (< or = two vomiting or retching episodes, and no antiemetic rescue) was recorded in 23%, 57%, 58%, and 60% of patients, respectively, and a complete response (no vomiting or retching, and no antiemetic rescue) in 18%, 41%, 40%, and 47% of patients, respectively. There was a statistically longer time to first episode of nausea (P =. 0015) and vomiting (P =. 0001), and fewer patients were administered additional antiemetic medication in the 10 - micrograms / kg dosing groups than in the 5 - micrograms / kg dosing group. As granisetron dose increased, appetite return increased (P =. 040). Headache was the most frequently reported adverse event (20%). CONCLUSION: A single 10 -, 20 -, or 40 - micrograms / kg dose of granisetron was effective in controlling vomiting in 57% to 60% of patients who received cisplatin at doses greater than 81 mg / m2 and totally prevented vomiting in 40% to 47% of patients. There were no statistically significant differences in efficacy between the 10 - micrograms / kg dose and the 20 - and 40 - micrograms / kg doses. Granisetron was well tolerated at all doses.

granisetron

5 - hydroxytryptamine

cisplatin

granisetron

Kytril

cisplatin

cisplatin

granisetron

granisetron

granisetron

granisetron

cisplatin

Granisetron

nausea

vomiting

nausea

vomiting

nausea

vomiting

vomiting

vomiting

nausea

vomiting

Headache

vomiting

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

cisplatin

vomiting

granisetron

Headache

granisetron

Headache

Kytril

Headache

granisetron

Headache

granisetron

Headache

granisetron

Headache

granisetron

Headache

Granisetron

Headache

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea

cisplatin

nausea


Input: Adverse interaction between clonidine and verapamil. OBJECTIVE: To report two cases of a possible adverse interaction between clonidine and verapamil resulting in atrioventricular (AV) block in both patients and severe hypotension in one patient. CASE SUMMARIES: A 54 - year - old woman with hyperaldosteronism was treated with verapamil 480 mg / d and spironolactone 100 mg / d. After the addition of a minimal dose of clonidine (0. 15 mg bid), she developed complete AV block and severe hypotension, which resolved upon cessation of all medications. A 65 - year - old woman was treated with extended - release verapamil 240 mg / d. After the addition of clonidine 0. 15 mg bid she developed complete AV block, which resolved after all therapy was stopped. DISCUSSION: An adverse interaction between clonidine and verapamil has not been reported previously. We describe two such cases and discuss the various mechanisms that might cause such an interaction. Clinicians should be acquainted with this possibly fatal interaction between two commonly used antihypertensive drugs. CONCLUSIONS: Caution is recommended in combining clonidine and verapamil therapy, even in patients who do not have sinus or AV node dysfunction. The two drugs may act synergistically on both the AV node and the peripheral circulation.

clonidine

verapamil

clonidine

verapamil

verapamil

spironolactone

clonidine

verapamil

clonidine

clonidine

verapamil

clonidine

verapamil

atrioventricular (AV) block

hypotension

hyperaldosteronism

AV block

hypotension

AV block

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

verapamil

atrioventricular (AV) block

verapamil

AV block

verapamil

AV block

verapamil

atrioventricular (AV) block

verapamil

AV block

verapamil

AV block

verapamil

atrioventricular (AV) block

verapamil

AV block

verapamil

AV block

verapamil

atrioventricular (AV) block

verapamil

AV block

verapamil

AV block

verapamil

atrioventricular (AV) block

verapamil

AV block

verapamil

AV block

verapamil

atrioventricular (AV) block

verapamil

AV block

verapamil

AV block

clonidine

atrioventricular (AV) block

clonidine

AV block

clonidine

AV block

clonidine

atrioventricular (AV) block

clonidine

AV block

clonidine

AV block

clonidine

atrioventricular (AV) block

clonidine

AV block

clonidine

AV block

clonidine

atrioventricular (AV) block

clonidine

AV block

clonidine

AV block

clonidine

atrioventricular (AV) block

clonidine

AV block

clonidine

AV block

clonidine

atrioventricular (AV) block

clonidine

AV block

clonidine

AV block

clonidine

hypotension

clonidine

hypotension

clonidine

hypotension

clonidine

hypotension

clonidine

hypotension

clonidine

hypotension

clonidine

hypotension

clonidine

hypotension

clonidine

hypotension

clonidine

hypotension

clonidine

hypotension

clonidine

hypotension


Input: Pharmacological studies on a new dihydrothienopyridine calcium antagonist, S - 312 - d. 5th communication: anticonvulsant effects in mice. S - 312, S - 312 - d, but not S - 312 - l, L - type calcium channel antagonists, showed anticonvulsant effects on the audiogenic tonic convulsions in DBA / 2 mice; and their ED50 values were 18. 4 (12. 8 - 27. 1) mg / kg, p. o. and 15. 0 (10. 2 - 23. 7) mg / kg, p. o., respectively, while that of flunarizine was 34. 0 (26. 0 - 44. 8) mg / kg, p. o. Although moderate anticonvulsant effects of S - 312 - d in higher doses were observed against the clonic convulsions induced by pentylenetetrazole (85 mg / kg, s. c.) or bemegride (40 mg / kg, s. c.), no effects were observed in convulsions induced by N - methyl - D - aspartate, picrotoxin, or electroshock in Slc: ddY mice. S - 312 - d may be useful in the therapy of certain types of human epilepsy.

dihydrothienopyridine calcium

S - 312 - d

S - 312

S - 312 - d

S - 312 - l

calcium

flunarizine

S - 312 - d

pentylenetetrazole

bemegride

N - methyl - D - aspartate

picrotoxin

S - 312 - d

audiogenic tonic convulsions

convulsions

convulsions

epilepsy

picrotoxin

convulsions

picrotoxin

convulsions

pentylenetetrazole

convulsions

pentylenetetrazole

convulsions

bemegride

convulsions

bemegride

convulsions


Input: Transmural myocardial infarction with sumatriptan. For sumatriptan, tightness in the chest caused by an unknown mechanism has been reported in 3 - 5% of users. We describe a 47 - year - old woman with an acute myocardial infarction after administration of sumatriptan 6 mg subcutaneously for cluster headache. The patient had no history of underlying ischaemic heart disease or Prinzmetal' s angina. She recovered without complications.

myocardial infarction

myocardial infarction

cluster headache

ischaemic heart disease

Prinzmetal' s angina

sumatriptan

sumatriptan

sumatriptan

sumatriptan

myocardial infarction

sumatriptan

myocardial infarction

sumatriptan

myocardial infarction

sumatriptan

myocardial infarction

sumatriptan

myocardial infarction

sumatriptan

myocardial infarction


Input: Flumazenil induces seizures and death in mixed cocaine - diazepam intoxications. STUDY HYPOTHESIS: Administration of the benzodiazepine antagonist flumazenil may unmask seizures in mixed cocaine - benzodiazepine intoxication. DESIGN: Male Sprague - Dawley rats received 100 mg / kg cocaine IP alone, 5 mg / kg diazepam alone, or a combination of diazepam and cocaine. Three minutes later, groups were challenged with vehicle or flumazenil 5 or 10 mg / kg IP. Animal behavior, seizures (time to and incidence), death (time to and incidence), and cortical EEG tracings were recorded. INTERVENTIONS: Administration of flumazenil to animals after they had received a combination dose of cocaine and diazepam. RESULTS: In group 1, animals received cocaine followed by vehicle. This resulted in 100% developing seizures and death. Group 2 received diazepam alone followed by vehicle. Animals became somnolent and none died. Group 3 received diazepam followed by 5 mg / kg flumazenil. Animals became somnolent after diazepam and then active after flumazenil administration. In group 4, a combination of cocaine and diazepam was administered simultaneously. This resulted in no overt or EEG - detectable seizures and a 50% incidence of death. Group 5 received a similar combination of cocaine and diazepam, followed later by 5 mg / kg flumazenil. This resulted in an increased incidence of seizures, 90% (P <. 01), and death, 100% (P < or =. 01), compared with group 4. Group 6 received cocaine and diazepam followed by 10 mg / kg flumazenil. This also resulted in an increased incidence of seizures, 90% (P < or =. 01), and death, 90% (P < or =. 05), compared with group 4. CONCLUSION: Flumazenil can unmask seizures and increase the incidence of death in a model of combined cocaine - diazepam intoxications.

Flumazenil

cocaine

diazepam

benzodiazepine

flumazenil

cocaine

benzodiazepine

cocaine

diazepam

diazepam

cocaine

flumazenil

flumazenil

cocaine

diazepam

cocaine

diazepam

diazepam

flumazenil

diazepam

flumazenil

cocaine

diazepam

cocaine

diazepam

flumazenil

cocaine

diazepam

flumazenil

Flumazenil

cocaine

diazepam

seizures

seizures

seizures

seizures

seizures

seizures

seizures

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

diazepam

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

Flumazenil

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

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cocaine

seizures

cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

seizures

cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

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cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

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cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures

cocaine

seizures


Input: Mechanisms for protective effects of free radical scavengers on gentamicin - mediated nephropathy in rats. Studies were performed to examine the mechanisms for the protective effects of free radical scavengers on gentamicin (GM) - mediated nephropathy. Administration of GM at 40 mg / kg sc for 13 days to rats induced a significant reduction in renal blood flow (RBF) and inulin clearance (CIn) as well as marked tubular damage. A significant reduction in urinary guanosine 3', 5' - cyclic monophosphate (cGMP) excretion and a significant increase in renal cortical renin and endothelin - 1 contents were also observed in GM - mediated nephropathy. Superoxide dismutase (SOD) or dimethylthiourea (DMTU) significantly lessened the GM - induced decrement in CIn. The SOD - induced increase in glomerular filtration rate was associated with a marked improvement in RBF, an increase in urinary cGMP excretion, and a decrease in renal renin and endothelin - 1 content. SOD did not attenuate the tubular damage. In contrast, DMTU significantly reduced the tubular damage and lipid peroxidation, but it did not affect renal hemodynamics and vasoactive substances. Neither SOD nor DMTU affected the renal cortical GM content in GM - treated rats. These results suggest that 1) both SOD and DMTU have protective effects on GM - mediated nephropathy, 2) the mechanisms for the protective effects differ for SOD and DMTU, and 3) superoxide anions play a critical role in GM - induced renal vasoconstriction.

gentamicin

gentamicin

GM

GM

guanosine 3', 5' - cyclic monophosphate

cGMP

GM

Superoxide

dimethylthiourea

DMTU

GM

cGMP

DMTU

DMTU

GM

GM

DMTU

GM

DMTU

superoxide

GM

nephropathy

nephropathy

tubular damage

nephropathy

tubular damage

tubular damage

nephropathy

gentamicin

nephropathy

gentamicin

nephropathy

gentamicin

tubular damage

gentamicin

nephropathy

gentamicin

tubular damage

gentamicin

tubular damage

gentamicin

nephropathy

gentamicin

nephropathy

gentamicin

nephropathy

gentamicin

tubular damage

gentamicin

nephropathy

gentamicin

tubular damage

gentamicin

tubular damage

gentamicin

nephropathy

GM

nephropathy

GM

nephropathy

GM

tubular damage

GM

nephropathy

GM

tubular damage

GM

tubular damage

GM

nephropathy

GM

nephropathy

GM

nephropathy

GM

tubular damage

GM

nephropathy

GM

tubular damage

GM

tubular damage

GM

nephropathy

GM

nephropathy

GM

nephropathy

GM

tubular damage

GM

nephropathy

GM

tubular damage

GM

tubular damage

GM

nephropathy

GM

nephropathy

GM

nephropathy

GM

tubular damage

GM

nephropathy

GM

tubular damage

GM

tubular damage

GM

nephropathy

GM

nephropathy

GM

nephropathy

GM

tubular damage

GM

nephropathy

GM

tubular damage

GM

tubular damage

GM

nephropathy

GM

nephropathy

GM

nephropathy

GM

tubular damage

GM

nephropathy

GM

tubular damage

GM

tubular damage

GM

nephropathy

GM

nephropathy

GM

nephropathy

GM

tubular damage

GM

nephropathy

GM

tubular damage

GM

tubular damage

GM

nephropathy

GM

nephropathy

GM

nephropathy

GM

tubular damage

GM

nephropathy

GM

tubular damage

GM

tubular damage

GM

nephropathy


Input: Assessment of cardiomyocyte DNA synthesis during hypertrophy in adult mice. The ability of cardiomyocytes to synthesize DNA in response to experimentally induced cardiac hypertrophy was assessed in adult mice. Isoproterenol delivered by osmotic minipump implantation in adult C3Heb / FeJ mice resulted in a 46% increase in heart weight and a 19. 3% increase in cardiomyocyte area. No DNA synthesis, as assessed by autoradiographic analysis of isolated cardiomyocytes, was observed in control or hypertrophic hearts. A survey of 15 independent inbred strains of mice revealed that ventricular cardiomyocyte nuclear number ranged from 3 to 13% mononucleate, suggesting that cardiomyocyte terminal differentiation is influenced directly or indirectly by genetic background. To determine whether the capacity for reactive DNA synthesis was also subject to genetic regulation, cardiac hypertrophy was induced in the strains of mice comprising the extremes of the nuclear number survey. These data indicate that adult mouse atrial and ventricular cardiomyocytes do not synthesize DNA in response to isoproterenol - induced cardiac hypertrophy.

hypertrophy

cardiac hypertrophy

hypertrophic hearts

cardiac hypertrophy

cardiac hypertrophy

Isoproterenol

isoproterenol

Isoproterenol

cardiac hypertrophy

Isoproterenol

hypertrophic hearts

Isoproterenol

cardiac hypertrophy

Isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

isoproterenol

hypertrophic hearts

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy


Input: Central cardiovascular effects of AVP and ANP in normotensive and spontaneously hypertensive rats. The purpose of the present study was to compare influence of central arginine vasopressin (AVP) and of atrial natriuretic peptide (ANP) on control of arterial blood pressure (MAP) and heart rate (HR) in normotensive (WKY) and spontaneously hypertensive (SHR) rats. Three series of experiments were performed on 30 WKY and 30 SHR, chronically instrumented with guide tubes in the lateral ventricle (LV) and arterial and venous catheters. MAP and HR were monitored before and after i. v. injections of either vehicle or 1, 10 and 50 ng of AVP and 25, 125 and 500 ng of ANP. Sensitivity of cardiac component of baroreflex (CCB), expressed as a slope of the regression line was determined from relationships between systolic arterial pressure (SAP) and HR period (HRp) during phenylephrine (Phe) - induced hypertension and sodium nitroprusside (SN) - induced hypotension. CCB was measured before and after administration of either vehicle, AVP, ANP, or both peptides together. Increases of MAP occurred after LV administration of 1, 10 and 50 ng of AVP in WKY and of 10 and 50 ng in SHR. ANP did not cause significant changes in MAP in both strains as compared to vehicle, but it abolished AVP - induced MAP increase in WKY and SHR. CCB was reduced in WKY and SHR after LV administration of AVP during SN - induced hypotension. In SHR but not in WKY administration of ANP, AVP and ANP + AVP decreased CCB during Phe - induced MAP elevation. The results indicate that centrally applied AVP and ANP exert differential effects on blood pressure and baroreflex control of heart rate in WKY and SHR and suggest interaction of these two peptides in blood pressure regulation at the level of central nervous system.

AVP

arginine vasopressin

AVP

AVP

phenylephrine

Phe

sodium nitroprusside

SN

AVP

AVP

AVP

AVP

SN

AVP

AVP

Phe

AVP

hypertensive

hypertensive

hypertension

hypotension

hypotension

phenylephrine

hypertensive

phenylephrine

hypertensive

phenylephrine

hypertension

Phe

hypertensive

Phe

hypertensive

Phe

hypertension

Phe

hypertensive

Phe

hypertensive

Phe

hypertension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

SN

hypotension

SN

hypotension

SN

hypotension

SN

hypotension

AVP

hypertensive

AVP

hypertensive

AVP

hypertension

arginine vasopressin

hypertensive

arginine vasopressin

hypertensive

arginine vasopressin

hypertension

AVP

hypertensive

AVP

hypertensive

AVP

hypertension

AVP

hypertensive

AVP

hypertensive

AVP

hypertension

AVP

hypertensive

AVP

hypertensive

AVP

hypertension

AVP

hypertensive

AVP

hypertensive

AVP

hypertension

AVP

hypertensive

AVP

hypertensive

AVP

hypertension

AVP

hypertensive

AVP

hypertensive

AVP

hypertension

AVP

hypertensive

AVP

hypertensive

AVP

hypertension

AVP

hypertensive

AVP

hypertensive

AVP

hypertension

AVP

hypertensive

AVP

hypertensive

AVP

hypertension


Input: Cutaneous exposure to warfarin - like anticoagulant causing an intracerebral hemorrhage: a case report. A case of intercerebral hematoma due to warfarin - induced coagulopathy is presented. The 39 - year - old woman had spread a warfarin - type rat poison around her house weekly using her bare hands, with no washing post application. Percutaneous absorption of warfarin causing coagulopathy, reported three times in the past, is a significant risk if protective measures, such as gloves, are not used. An adverse drug interaction with piroxicam, which she took occasionally, may have exacerbated the coagulopathy.

warfarin

warfarin

warfarin

warfarin

piroxicam

intracerebral hemorrhage

hematoma

coagulopathy

coagulopathy

coagulopathy

warfarin

intracerebral hemorrhage

warfarin

intracerebral hemorrhage

warfarin

intracerebral hemorrhage

warfarin

intracerebral hemorrhage


Input: Pediatric heart transplantation without chronic maintenance steroids. From 1986 to February 1993, 40 children aged 2 months to 18 years (average age 10. 4 + / - 5. 8 years) underwent heart transplantation. Indications for transplantation were idiopathic cardiomyopathy (52%), congenital heart disease (35%) with and without prior repair (71% and 29%, respectively), hypertrophic cardiomyopathy (5%), valvular heart disease (3%), and doxorubicin cardiomyopathy (5%). Patients were managed with cyclosporine and azathioprine. No prophylaxis with antilymphocyte globulin was used. Steroids were given to 39% of patients for refractory rejection, but weaning was always attempted and generally successful (64%). Five patients (14%) received maintenance steroids. Four patients died in the perioperative period and one died 4 months later. There have been no deaths related to rejection or infection. Average follow - up was 36 + / - 19 months (range 1 to 65 months). Cumulative survival is 88% at 5 years. In patients less than 7 years of age, rejection was monitored noninvasively. In the first postoperative month, 89% of patients were treated for rejection. Freedom from serious infections was 83% at 1 month and 65% at 1 year. Cytomegalovirus infections were treated successfully with ganciclovir in 11 patients. No impairment of growth was observed in children who underwent transplantation compared with a control population. Twenty - one patients (60%) have undergone annual catheterizations and no sign of graft atherosclerosis has been observed. Seizures occurred in five patients (14%) and hypertension was treated in 10 patients (28%). No patient was disabled and no lymphoproliferative disorder was observed. (ABSTRACT TRUNCATED AT 250 WORDS)

steroids

doxorubicin

cyclosporine

azathioprine

Steroids

steroids

ganciclovir

idiopathic cardiomyopathy

congenital heart disease

hypertrophic cardiomyopathy

valvular heart disease

cardiomyopathy

infection

infections

Cytomegalovirus infections

atherosclerosis

Seizures

hypertension

lymphoproliferative disorder

doxorubicin

cardiomyopathy


Input: Delirium during fluoxetine treatment. A case report. The correlation between high serum tricyclic antidepressant concentrations and central nervous system side effects has been well established. Only a few reports exist, however, on the relationship between the serum concentrations of selective serotonin reuptake inhibitors (SSRIs) and their toxic effects. In some cases, a high serum concentration of citalopram (> 600 nmol / L) in elderly patients has been associated with increased somnolence and movement difficulties. Widespread cognitive disorders, such as delirium, have not been previously linked with high blood levels of SSRIs. In this report, we describe a patient with acute hyperkinetic delirium connected with a high serum total fluoxetine (fluoxetine plus desmethylfluoxetine) concentration.

Delirium

somnolence

movement difficulties

cognitive disorders

delirium

hyperkinetic

delirium

fluoxetine

serotonin

citalopram

fluoxetine

fluoxetine

desmethylfluoxetine

fluoxetine

hyperkinetic

fluoxetine

hyperkinetic

fluoxetine

hyperkinetic

fluoxetine

Delirium

fluoxetine

delirium

fluoxetine

delirium

fluoxetine

Delirium

fluoxetine

delirium

fluoxetine

delirium

fluoxetine

Delirium

fluoxetine

delirium

fluoxetine

delirium


Input: Pulmonary edema and shock after high - dose aracytine - C for lymphoma; possible role of TNF - alpha and PAF. Four out of 23 consecutive patients treated with high - dose Ara - C for lymphomas in our institution developed a strikingly similar syndrome during the perfusion. It was characterized by the onset of fever, diarrhea, shock, pulmonary edema, acute renal failure, metabolic acidosis, weight gain and leukocytosis. Thorough bacteriological screening failed to provide evidence of infection. Sequential biological assays of IL - 1, IL - 2, TNF and PAF were performed during Ara - C infusion to ten patients, including the four who developed the syndrome. TNF and PAF activity was found in the serum of respectively two and four of the cases, but not in the six controls. As TNF and PAF are thought to be involved in the development of septic shock and adult respiratory distress syndrome, we hypothesize that high - dose Ara - C may be associated with cytokine release.

Pulmonary edema

shock

lymphoma

lymphomas

fever

diarrhea

shock

pulmonary edema

acute renal failure

metabolic acidosis

weight gain

leukocytosis

infection

shock

adult respiratory distress syndrome

aracytine - C

Ara - C

Ara - C

Ara - C

aracytine - C

diarrhea

Ara - C

diarrhea

Ara - C

diarrhea

Ara - C

diarrhea

aracytine - C

fever

Ara - C

fever

Ara - C

fever

Ara - C

fever

aracytine - C

Pulmonary edema

aracytine - C

pulmonary edema

Ara - C

Pulmonary edema

Ara - C

pulmonary edema

Ara - C

Pulmonary edema

Ara - C

pulmonary edema

Ara - C

Pulmonary edema

Ara - C

pulmonary edema

aracytine - C

acute renal failure

Ara - C

acute renal failure

Ara - C

acute renal failure

Ara - C

acute renal failure

aracytine - C

weight gain

Ara - C

weight gain

Ara - C

weight gain

Ara - C

weight gain

aracytine - C

shock

aracytine - C

shock

aracytine - C

shock

Ara - C

shock

Ara - C

shock

Ara - C

shock

Ara - C

shock

Ara - C

shock

Ara - C

shock

Ara - C

shock

Ara - C

shock

Ara - C

shock

aracytine - C

leukocytosis

Ara - C

leukocytosis

Ara - C

leukocytosis

Ara - C

leukocytosis

aracytine - C

metabolic acidosis

Ara - C

metabolic acidosis

Ara - C

metabolic acidosis

Ara - C

metabolic acidosis


Input: Protective effect of clentiazem against epinephrine - induced cardiac injury in rats. We investigated the effects of clentiazem, a 1, 5 - benzothiazepine calcium antagonist, on epinephrine - induced cardiomyopathy in rats. With 2 - week chronic epinephrine infusion, 16 of 30 rats died within 4 days, and severe ischemic lesions and fibrosis of the left ventricles were observed. In epinephrine - treated rats, left atrial and left ventricular papillary muscle contractile responses to isoproterenol were reduced, but responses to calcium were normal or enhanced compared to controls. Left ventricular alpha and beta adrenoceptor densities were also reduced compared to controls. Treatment with clentiazem prevented epinephrine - induced death (P <. 05), and attenuated the ventricular ischemic lesions and fibrosis, in a dose - dependent manner. Left atrial and left ventricular papillary muscle contractile responses to isoproterenol were reduced compared to controls in groups treated with clentiazem alone, but combined with epinephrine, clentiazem restored left atrial responses and enhanced left ventricular papillary responses to isoproterenol. On the other hand clentiazem did not prevent epinephrine - induced down - regulation of alpha and beta adrenoceptors. Interestingly, clentiazem, infused alone, resulted in decreased adrenergic receptor densities in the left ventricle. Clentiazem also did not prevent the enhanced responses to calcium seen in the epinephrine - treated animals, although the high dose of clentiazem partially attenuated the maximal response to calcium compared to epinephrine - treated animals. In conclusion, clentiazem attenuated epinephrine - induced cardiac injury, possibly through its effect on the adrenergic pathway.

clentiazem

epinephrine

clentiazem

1, 5 - benzothiazepine

calcium

epinephrine

epinephrine

epinephrine

isoproterenol

calcium

clentiazem

epinephrine

isoproterenol

clentiazem

epinephrine

clentiazem

isoproterenol

clentiazem

epinephrine

clentiazem

Clentiazem

calcium

epinephrine

clentiazem

calcium

epinephrine

clentiazem

epinephrine

cardiac injury

cardiomyopathy

ischemic lesions

fibrosis

ischemic lesions

fibrosis

cardiac injury

epinephrine

cardiomyopathy

epinephrine

cardiomyopathy

epinephrine

cardiomyopathy

epinephrine

cardiomyopathy

epinephrine

cardiomyopathy

epinephrine

cardiomyopathy

epinephrine

cardiomyopathy

epinephrine

cardiomyopathy

epinephrine

cardiomyopathy

epinephrine

cardiomyopathy


Input: Cocaine induced myocardial ischemia. We report a case of myocardial ischemia induced by cocaine. The ischemia probably induced by coronary artery spasm was reversed by nitroglycerin and calcium blocking agents.

Cocaine

cocaine

nitroglycerin

calcium

myocardial ischemia

myocardial ischemia

ischemia

coronary artery spasm

Cocaine

myocardial ischemia

Cocaine

myocardial ischemia

cocaine

myocardial ischemia

cocaine

myocardial ischemia

Cocaine

coronary artery spasm

cocaine

coronary artery spasm


Input: Doxorubicin - induced cardiotoxicity monitored by ECG in freely moving mice. A new model to test potential protectors. In laboratory animals, histology is most commonly used to study doxorubicin - induced cardiotoxicity. However, for monitoring during treatment, large numbers of animals are needed. Recently we developed a new method to measure ECG values in freely moving mice by telemetry. With this model we investigated the effect of chronic doxorubicin administration on the ECG of freely moving BALB / c mice and the efficacy of ICRF - 187 as a protective agent. The ST interval significantly widened from 15. 0 + / - 1. 5 to 56. 8 + / - 11. 8 ms in week 10 (7 weekly doses of 4 mg / kg doxorubicin given i. v. plus 3 weeks of observation). The ECG of the control animals did not change during the entire study. After sacrifice the hearts of doxorubicin - treated animals were enlarged and the atria were hypertrophic. As this schedule exerted more toxicity than needed to investigate protective agents, the protection of ICRF - 187 was determined using a dose schedule with lower general toxicity (6 weekly doses of 4 mg / kg doxorubicin given i. v. plus 2 weeks of observation). On this schedule, the animals' hearts appeared normal after sacrifice and ICRF - 187 (50 mg / kg given i. p. 1 h before doxorubicin) provided almost full protection. These data were confirmed by histology. The results indicate that this new model is very sensitive and enables monitoring of the development of cardiotoxicity with time. These findings result in a model that allows the testing of protectors against doxorubicin - induced cardiotoxicity as demonstrated by the protection provided by ICRF - 187.

Doxorubicin

doxorubicin

doxorubicin

ICRF - 187

doxorubicin

doxorubicin

ICRF - 187

doxorubicin

ICRF - 187

doxorubicin

doxorubicin

ICRF - 187

cardiotoxicity

cardiotoxicity

hypertrophic

toxicity

toxicity

cardiotoxicity

cardiotoxicity

Doxorubicin

cardiotoxicity

Doxorubicin

cardiotoxicity

Doxorubicin

cardiotoxicity

Doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity


Input: Epinephrine dysrhythmogenicity is not enhanced by subtoxic bupivacaine in dogs. Since bupivacaine and epinephrine may both precipitate dysrhythmias, circulating bupivacaine during regional anesthesia could potentiate dysrhythmogenic effects of epinephrine. We therefore examined whether bupivacaine alters the dysrhythmogenicity of subsequent administration of epinephrine in conscious, healthy dogs and in anesthetized dogs with myocardial infarction. Forty - one conscious dogs received 10 micrograms. kg - 1. min - 1 epinephrine. Seventeen animals responded with ventricular tachycardia (VT) within 3 min. After 3 h, these responders randomly received 1 or 2 mg / kg bupivacaine or saline over 5 min, followed by 10 micrograms. kg - 1. min - 1 epinephrine. In the bupivacaine groups, epinephrine caused fewer prodysrhythmic effects than without bupivacaine. VT appeared in fewer dogs and at a later time, and there were more sinoatrial beats and less ectopies. Epinephrine shortened QT less after bupivacaine than in control animals. One day after experimental myocardial infarction, six additional halothane - anesthetized dogs received 4 micrograms. kg - 1. min - 1 epinephrine until VT appeared. After 45 min, 1 mg / kg bupivacaine was injected over 5 min, again followed by 4 micrograms. kg - 1. min - 1 epinephrine. In these dogs, the prodysrhythmic response to epinephrine was also mitigated by preceding bupivacaine. Bupivacaine antagonizes epinephrine dysrhythmogenicity in conscious dogs susceptible to VT and in anesthetized dogs with spontaneous postinfarct dysrhythmias. There is no evidence that systemic subtoxic bupivacaine administration enhances the dysrhythmogenicity of subsequent epinephrine.

Epinephrine

bupivacaine

bupivacaine

epinephrine

bupivacaine

epinephrine

bupivacaine

epinephrine

epinephrine

bupivacaine

epinephrine

bupivacaine

epinephrine

bupivacaine

Epinephrine

bupivacaine

halothane

epinephrine

bupivacaine

epinephrine

epinephrine

bupivacaine

Bupivacaine

epinephrine

bupivacaine

epinephrine

dysrhythmias

myocardial infarction

ventricular tachycardia

VT

VT

myocardial infarction

VT

VT

dysrhythmias

Epinephrine

ventricular tachycardia

Epinephrine

VT

Epinephrine

VT

Epinephrine

VT

Epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT

Epinephrine

ventricular tachycardia

Epinephrine

VT

Epinephrine

VT

Epinephrine

VT

Epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

ventricular tachycardia

epinephrine

VT

epinephrine

VT

epinephrine

VT

epinephrine

VT


Input: Milk - alkali syndrome induced by 1, 25 (OH) 2D in a patient with hypoparathyroidism. Milk - alkali syndrome was first described 70 years ago in the context of the treatment of peptic ulcer disease with large amounts of calcium and alkali. Although with current ulcer therapy (H - 2 blockers, omeprazole, and sucralfate), the frequency of milk - alkali syndrome has decreased significantly, the classic triad of hypercalcemia, alkalosis, and renal impairment remains the hallmark of the syndrome. Milk - alkali syndrome can present serious and occasionally life - threatening illness unless diagnosed and treated appropriately. This article presents a patient with hypoparathyroidism who was treated with calcium carbonate and calcitriol resulting in two admissions to the hospital for milk - alkali syndrome. The patient was successfully treated with intravenous pamidronate on his first admission and with hydrocortisone on the second. This illustrates intravenous pamidronate as a valuable therapeutic tool when milk - alkali syndrome presents as hypercalcemic emergency.

Milk - alkali syndrome

hypoparathyroidism

Milk - alkali syndrome

peptic ulcer disease

ulcer

milk - alkali syndrome

hypercalcemia

alkalosis

renal impairment

Milk - alkali syndrome

hypoparathyroidism

milk - alkali syndrome

milk - alkali syndrome

hypercalcemic emergency

1, 25 (OH) 2D

calcium

alkali

omeprazole

sucralfate

calcium carbonate

calcitriol

pamidronate

hydrocortisone

pamidronate

1, 25 (OH) 2D

renal impairment

calcitriol

renal impairment

sucralfate

peptic ulcer disease

calcium

alkalosis

alkali

renal impairment

alkali

alkalosis

calcium carbonate

alkalosis

omeprazole

peptic ulcer disease

1, 25 (OH) 2D

Milk - alkali syndrome

1, 25 (OH) 2D

Milk - alkali syndrome

1, 25 (OH) 2D

milk - alkali syndrome

1, 25 (OH) 2D

hypercalcemia

1, 25 (OH) 2D

Milk - alkali syndrome

1, 25 (OH) 2D

milk - alkali syndrome

1, 25 (OH) 2D

milk - alkali syndrome

1, 25 (OH) 2D

hypercalcemic emergency

calcitriol

Milk - alkali syndrome

calcitriol

Milk - alkali syndrome

calcitriol

milk - alkali syndrome

calcitriol

hypercalcemia

calcitriol

Milk - alkali syndrome

calcitriol

milk - alkali syndrome

calcitriol

milk - alkali syndrome

calcitriol

hypercalcemic emergency

alkali

Milk - alkali syndrome

alkali

Milk - alkali syndrome

alkali

milk - alkali syndrome

alkali

hypercalcemia

alkali

Milk - alkali syndrome

alkali

milk - alkali syndrome

alkali

milk - alkali syndrome

alkali

hypercalcemic emergency

1, 25 (OH) 2D

alkalosis

calcitriol

alkalosis

calcium

Milk - alkali syndrome

calcium

Milk - alkali syndrome

calcium

milk - alkali syndrome

calcium

hypercalcemia

calcium

Milk - alkali syndrome

calcium

milk - alkali syndrome

calcium

milk - alkali syndrome

calcium

hypercalcemic emergency

calcium carbonate

Milk - alkali syndrome

calcium carbonate

Milk - alkali syndrome

calcium carbonate

milk - alkali syndrome

calcium carbonate

hypercalcemia

calcium carbonate

Milk - alkali syndrome

calcium carbonate

milk - alkali syndrome

calcium carbonate

milk - alkali syndrome

calcium carbonate

hypercalcemic emergency

calcium carbonate

renal impairment

calcium

renal impairment


Input: Encephalopathy during amitriptyline therapy: are neuroleptic malignant syndrome and serotonin syndrome spectrum disorders? This report describes a case of encephalopathy developed in the course of amitriptyline therapy, during a remission of unipolar depression. This patient could have been diagnosed as having either neuroleptic malignant syndrome (NMS) or serotonin syndrome (SS). The major determinant of the symptoms may have been dopamine / serotonin imbalance in the central nervous system. The NMS - like encephalopathy that develops in association with the use of antidepressants indicates that NMS and SS are spectrum disorders induced by drugs with both antidopaminergic and serotonergic effects.

Encephalopathy

neuroleptic malignant syndrome

serotonin syndrome

encephalopathy

unipolar depression

neuroleptic malignant syndrome

NMS

serotonin syndrome

SS

NMS

encephalopathy

NMS

SS

amitriptyline

amitriptyline

dopamine

serotonin

amitriptyline

Encephalopathy

amitriptyline

encephalopathy

amitriptyline

encephalopathy

amitriptyline

Encephalopathy

amitriptyline

encephalopathy

amitriptyline

encephalopathy


Input: Genetic separation of tumor growth and hemorrhagic phenotypes in an estrogen - induced tumor. Chronic administration of estrogen to the Fischer 344 (F344) rat induces growth of large, hemorrhagic pituitary tumors. Ten weeks of diethylstilbestrol (DES) treatment caused female F344 rat pituitaries to grow to an average of 109. 2 + / - 6. 3 mg (mean + / - SE) versus 11. 3 + / - 1. 4 mg for untreated rats, and to become highly hemorrhagic. The same DES treatment produced no significant growth (8. 9 + / - 0. 5 mg for treated females versus 8. 7 + / - 1. 1 for untreated females) or morphological changes in Brown Norway (BN) rat pituitaries. An F1 hybrid of F344 and BN exhibited significant pituitary growth after 10 weeks of DES treatment with an average mass of 26. 3 + / - 0. 7 mg compared with 8. 6 + / - 0. 9 mg for untreated rats. Surprisingly, the F1 hybrid tumors were not hemorrhagic and had hemoglobin content and outward appearance identical to that of BN. Expression of both growth and morphological changes is due to multiple genes. However, while DES - induced pituitary growth exhibited quantitative, additive inheritance, the hemorrhagic phenotype exhibited recessive, epistatic inheritance. Only 5 of the 160 F2 pituitaries exhibited the hemorrhagic phenotype; 36 of the 160 F2 pituitaries were in the F344 range of mass, but 31 of these were not hemorrhagic, indicating that the hemorrhagic phenotype is not merely a consequence of extensive growth. The hemorrhagic F2 pituitaries were all among the most massive, indicating that some of the genes regulate both phenotypes.

tumor

hemorrhagic

tumor

hemorrhagic

pituitary tumors

hemorrhagic

tumors

hemorrhagic

hemorrhagic

hemorrhagic

hemorrhagic

hemorrhagic

hemorrhagic

estrogen

estrogen

diethylstilbestrol

DES

DES

DES

DES

diethylstilbestrol

pituitary tumors

DES

pituitary tumors

DES

pituitary tumors

DES

pituitary tumors

DES

pituitary tumors


Input: Increased expression of neuronal nitric oxide synthase in bladder afferent pathways following chronic bladder irritation. Immunocytochemical techniques were used to examine alterations in the expression of neuronal nitric oxide synthase (NOS) in bladder pathways following acute and chronic irritation of the urinary tract of the rat. Chemical cystitis was induced by cyclophosphamide (CYP) which is metabolized to acrolein, an irritant eliminated in the urine. Injection of CYP (n = 10, 75 mg / kg, i. p.) 2 hours prior to perfusion (acute treatment) of the animals increased Fos - immunoreactivity (IR) in neurons in the dorsal commissure, dorsal horn, and autonomic regions of spinal segments (L1 - L2 and L6 - S1) which receive afferent inputs from the bladder, urethra, and ureter. Fos - IR in the spinal cord was not changed in rats receiving chronic CYP treatment (n = 15, 75 mg / kg, i. p., every 3rd day for 2 weeks). In control animals and in animals treated acutely with CYP, only small numbers of NOS - IR cells (0. 5 - 0. 7 cell profiles / sections) were detected in the L6 - S1 dorsal root ganglia (DRG). Chronic CYP administration significantly (P < or =. 002) increased bladder weight by 60% and increased (7 - to 11 - fold) the numbers of NOS - immunoreactive (IR) afferent neurons in the L6 - S1 DRG. A small increase (1. 5 - fold) also occurred in the L1 DRG, but no change was detected in the L2 and L5 DRG. Bladder afferent cells in the L6 - S1 DRG labeled by Fluorogold (40 microliters) injected into the bladder wall did not exhibit NOS - IR in control animals; however, following chronic CYP administration, a significant percentage of bladder afferent neurons were NOS - IR: L6 (19. 8 + / - 4. 6%) and S1 (25. 3 + / - 2. 9%). These results indicate that neuronal gene expression in visceral sensory pathways can be upregulated by chemical irritation of afferent receptors in the urinary tract and / or that pathological changes in the urinary tract can initiate chemical signals that alter the chemical properties of visceral afferent neurons.

nitric oxide

nitric oxide

cyclophosphamide

CYP

acrolein

CYP

CYP

CYP

CYP

CYP

bladder irritation

irritation of the urinary tract

cystitis

cyclophosphamide

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis


Input: Effects of a new calcium antagonist, CD - 832, on isoproterenol - induced myocardial ischemia in dogs with partial coronary stenosis. Effects of CD - 832 on isoproterenol (ISO) - induced myocardial ischemia were studied in dogs with partial coronary stenosis of the left circumflex coronary artery and findings were compared with those for nifedipine or diltiazem. In the presence of coronary artery stenosis, 3 - min periods of intracoronary ISO infusion (10 ng / kg / min) increased heart rate and maximal rate of left ventricular pressure rise, which resulted in a decrease in percentage segmental shortening and ST - segment elevation of the epicardial electrocardiogram. After the control ISO infusion with stenosis was performed, equihypotensive doses of CD - 832 (3 and 10 micrograms / kg / min, n = 7), nifedipine (1 and 3 micrograms / kg / min, n = 9) or diltiazem (10 and 30 micrograms / kg / min, n = 7) were infused 5 min before and during the second and third ISO infusion. Both CD - 832 and diltiazem, but not nifedipine, significantly reduced the increase in heart rate induced by ISO infusion. In contrast to nifedipine, CD - 832 (10 micrograms / kg / min) prevented the decrease in percentage segmental shortening from 32 + / - 12% to 115 + / - 26% of the control value (P <. 01) and ST - segment elevation from 5. 6 + / - 1. 0 mV to 1. 6 + / - 1. 3 mV (P <. 01) at 3 min after ISO infusion with stenosis. Diltiazem (30 micrograms / kg / min) also prevented the decrease in percentage segmental shortening from 34 + / - 14% to 63 + / - 18% of the control value (P <. 05) and ST - segment elevation from 4. 7 + / - 0. 7 mV to 2. 1 + / - 0. 7 mV (P <. 01) at 3 min after ISO infusion with stenosis. These data show that CD - 832 improves myocardial ischemia during ISO infusion with stenosis and suggest that the negative chronotropic property of CD - 832 plays a major role in the beneficial effects of CD - 832.

calcium

CD - 832

isoproterenol

CD - 832

isoproterenol

ISO

nifedipine

diltiazem

ISO

ISO

CD - 832

nifedipine

diltiazem

ISO

CD - 832

diltiazem

nifedipine

ISO

nifedipine

CD - 832

ISO

Diltiazem

ISO

CD - 832

ISO

CD - 832

CD - 832

myocardial ischemia

coronary stenosis

myocardial ischemia

coronary stenosis

coronary artery stenosis

stenosis

stenosis

stenosis

myocardial ischemia

stenosis

isoproterenol

myocardial ischemia

isoproterenol

myocardial ischemia

isoproterenol

myocardial ischemia

isoproterenol

myocardial ischemia

isoproterenol

myocardial ischemia

isoproterenol

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia

ISO

myocardial ischemia


Input: The effect of recombinant human insulin - like growth factor - I on chronic puromycin aminonucleoside nephropathy in rats. We recently demonstrated that recombinant hGH exacerbates renal functional and structural injury in chronic puromycin aminonucleoside (PAN) nephropathy, an experimental model of glomerular disease. Therefore, we examined whether recombinant human (rh) IGF - I is a safer alternative for the treatment of growth failure in rats with chronic PAN nephropathy. The glomerulopathy was induced by seven serial injections of PAN over 12 wk. Experimental animals (n = 6) received rhIGF - I, 400 micrograms / d, whereas control rats (n = 6) received the vehicle. rhIGF - I improved weight gain by 14% (p < 0. 05), without altering hematocrit or blood pressure in rats with renal disease. Urinary protein excretion was unaltered by rhIGF - I treatment in rats with chronic PAN nephropathy. After 12 wk, the inulin clearance was higher in rhIGF - I - treated rats, 0. 48 + / - 0. 08 versus 0. 24 + / - 0. 06 mL / min / 100 g of body weight in untreated PAN nephropathy animals, p < 0. 05. The improvement in GFR was not associated with enhanced glomerular hypertrophy or increased segmental glomerulosclerosis, tubulointerstitial injury, or renal cortical malondialdehyde content. In rats with PAN nephropathy, administration of rhIGF - I increased IGF - I and GH receptor gene expression, without altering the steady state level of IGF - I receptor mRNA. In normal rats with intact kidneys, rhIGF - I administration (n = 4) did not alter weight gain, blood pressure, proteinuria, GFR, glomerular planar area, renal cortical malondialdehyde content, or glomerular or tubulointerstitial damage, compared with untreated animals (n = 4). rhIGF - I treatment reduced the steady state renal IGF - I mRNA level but did not modify gene expression of the IGF - I or GH receptors. We conclude that: 1) administration of rhIGF - I improves growth and GFR in rats with chronic PAN nephropathy and 2) unlike rhGH, long - term use of rhIGF - I does not worsen renal functional and structural injury in this disease model.

puromycin aminonucleoside

puromycin aminonucleoside

PAN

PAN

PAN

PAN

PAN

malondialdehyde

PAN

malondialdehyde

PAN

nephropathy

nephropathy

glomerular disease

growth failure

nephropathy

glomerulopathy

renal disease

nephropathy

nephropathy

glomerular hypertrophy

glomerulosclerosis

tubulointerstitial injury

nephropathy

proteinuria

tubulointerstitial damage

nephropathy

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

glomerular disease

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

glomerulopathy

puromycin aminonucleoside

renal disease

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

glomerular hypertrophy

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

tubulointerstitial damage

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

glomerular disease

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

glomerulopathy

puromycin aminonucleoside

renal disease

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

glomerular hypertrophy

puromycin aminonucleoside

nephropathy

puromycin aminonucleoside

tubulointerstitial damage

puromycin aminonucleoside

nephropathy

PAN

nephropathy

PAN

nephropathy

PAN

glomerular disease

PAN

nephropathy

PAN

glomerulopathy

PAN

renal disease

PAN

nephropathy

PAN

nephropathy

PAN

glomerular hypertrophy

PAN

nephropathy

PAN

tubulointerstitial damage

PAN

nephropathy

PAN

nephropathy

PAN

nephropathy

PAN

glomerular disease

PAN

nephropathy

PAN

glomerulopathy

PAN

renal disease

PAN

nephropathy

PAN

nephropathy

PAN

glomerular hypertrophy

PAN

nephropathy

PAN

tubulointerstitial damage

PAN

nephropathy

PAN

nephropathy

PAN

nephropathy

PAN

glomerular disease

PAN

nephropathy

PAN

glomerulopathy

PAN

renal disease

PAN

nephropathy

PAN

nephropathy

PAN

glomerular hypertrophy

PAN

nephropathy

PAN

tubulointerstitial damage

PAN

nephropathy

PAN

nephropathy

PAN

nephropathy

PAN

glomerular disease

PAN

nephropathy

PAN

glomerulopathy

PAN

renal disease

PAN

nephropathy

PAN

nephropathy

PAN

glomerular hypertrophy

PAN

nephropathy

PAN

tubulointerstitial damage

PAN

nephropathy

PAN

nephropathy

PAN

nephropathy

PAN

glomerular disease

PAN

nephropathy

PAN

glomerulopathy

PAN

renal disease

PAN

nephropathy

PAN

nephropathy

PAN

glomerular hypertrophy

PAN

nephropathy

PAN

tubulointerstitial damage

PAN

nephropathy

PAN

nephropathy

PAN

nephropathy

PAN

glomerular disease

PAN

nephropathy

PAN

glomerulopathy

PAN

renal disease

PAN

nephropathy

PAN

nephropathy

PAN

glomerular hypertrophy

PAN

nephropathy

PAN

tubulointerstitial damage

PAN

nephropathy

PAN

nephropathy

PAN

nephropathy

PAN

glomerular disease

PAN

nephropathy

PAN

glomerulopathy

PAN

renal disease

PAN

nephropathy

PAN

nephropathy

PAN

glomerular hypertrophy

PAN

nephropathy

PAN

tubulointerstitial damage

PAN

nephropathy


Input: Nefiracetam (DM - 9384) reverses apomorphine - induced amnesia of a passive avoidance response: delayed emergence of the memory retention effects. Nefiracetam is a novel pyrrolidone derivative which attenuates scopolamine - induced learning and post - training consolidation deficits. Given that apomorphine inhibits passive avoidance retention when given during training or in a defined 10 - 12h post - training period, we evaluated the ability of nefiracetam to attenuate amnesia induced by dopaminergic agonism. A step - down passive avoidance paradigm was employed and nefiracetam (3 mg / kg) and apomorphine (0. 5 mg / kg) were given alone or in combination during training and at the 10 - 12h post - training period of consolidation. Co - administration of nefiracetam and apomorphine during training or 10h thereafter produced no significant anti - amnesic effect. However, administration of nefiracetam during training completely reversed the amnesia induced by apomorphine at the 10h post - training time and the converse was also true. These effects were not mediated by a dopaminergic mechanism as nefiracetam, at millimolar concentrations, failed to displace either [3H] SCH 23390 or [3H] spiperone binding from D1 or D2 dopamine receptor subtypes, respectively. It is suggested that nefiracetam augments molecular processes in the early stages of events which ultimately lead to consolidation of memory.

Nefiracetam

DM - 9384

apomorphine

Nefiracetam

pyrrolidone

scopolamine

apomorphine

nefiracetam

nefiracetam

apomorphine

nefiracetam

apomorphine

nefiracetam

apomorphine

nefiracetam

SCH 23390

spiperone

dopamine

nefiracetam

amnesia

learning and post - training consolidation deficits

amnesia

amnesia

scopolamine

learning and post - training consolidation deficits

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia

apomorphine

amnesia


Input: Human corticotropin - releasing hormone and thyrotropin - releasing hormone modulate the hypercapnic ventilatory response in humans. Human corticotropin - releasing hormone (hCRH) and thyrotropin - releasing hormone (TRH) are known to stimulate ventilation after i. v. administration in humans. In a placebo - controlled, single - blind study we aimed to clarify if both peptides act by altering central chemosensitivity. Two subsequent CO2 - rebreathing tests were performed in healthy young volunteers. During the first test 0. 9% NaCl was given i. v.; during the second test 200 micrograms of hCRH (n = 12) or 400 micrograms of TRH (n = 6) was administered i. v. Nine subjects received 0. 9% NaCl i. v. during both rebreathing manoeuvres. The CO2 - response curves for the two tests were compared within the same subject. In the hCRH group a marked parallel shift of the CO2 - response curve to the left was observed after hCRH (P < 0. 01). The same effect occurred following TRH but was less striking (P = 0. 05). hCRH and TRH caused a reduction in the CO2 threshold. The CO2 - response curves in the control group were nearly identical. The results indicate an additive effect of both releasing hormones on the hypercapnic ventilatory response in humans, presumably independent of central chemosensitivity.

corticotropin

thyrotropin

corticotropin

thyrotropin

NaCl

NaCl

hypercapnic

hypercapnic

hypercapnic

hypercapnic

hypercapnic

hypercapnic

hypercapnic

hypercapnic

hypercapnic

hypercapnic

hypercapnic

hypercapnic


Input: Lamivudine is effective in suppressing hepatitis B virus DNA in Chinese hepatitis B surface antigen carriers: a placebo - controlled trial. Lamivudine is a novel 2', 3' - dideoxy cytosine analogue that has potent inhibitory effects on hepatitis B virus replication in vitro and in vivo. We performed a single - blind, placebo - controlled study to assess its effectiveness and safety in Chinese hepatitis B surface antigen (HBsAg) carriers. Forty - two Chinese HBsAg carriers were randomized to receive placebo (6 patients) or lamivudine orally in dosages of 25 mg, 100 mg, or 300 mg daily (12 patients for each dosage). The drug was given for 4 weeks. The patients were closely monitored clinically, biochemically, and serologically up to 4 weeks after drug treatment. All 36 patients receiving lamivudine had a decrease in hepatitis B virus (HBV) DNA values of > 90% (P <. 001 compared with placebo). Although 25 mg of lamivudine was slightly less effective than 100 mg (P =. 011) and 300 mg (P =. 005), it still induced 94% suppression of HBV DNA after the fourth week of therapy. HBV DNA values returned to pretreatment levels within 4 weeks of cessation of therapy. There was no change in the hepatitis B e antigen status or in aminotransferase levels. No serious adverse events were observed. In conclusion, a 4 - week course of lamivudine was safe and effective in suppression of HBV DNA in Chinese HBsAg carriers. The suppression was > 90% but reversible. Studies with long - term lamivudine administration should be performed to determine if prolonged suppression of HBV DNA can be achieved.

Lamivudine

hepatitis B surface antigen

Lamivudine

2', 3' - dideoxy cytosine

hepatitis B surface antigen

HBsAg

HBsAg

lamivudine

lamivudine

lamivudine

lamivudine

HBsAg

lamivudine

hepatitis B

hepatitis B

hepatitis B

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

hepatitis B surface antigen

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B

HBsAg

hepatitis B