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When there is a change in H+ concentration, the *buffer systems* of the body fluids react within seconds to minimize these changes. Buffer systems do not eliminate H<sup>+</sup> from or add H+ to the body but only keep them tied up until balance can be re-established.
The second line of defense, the *respiratory sy... | {
"Header 1": "**Acid–Base Regulation**",
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Fortunately, the amount of $CO_2$ in the blood is a linear function of $Pco_2$ multiplied by the solubility coefficient for $CO_2$ ; under physiological conditions, the solubility coefficient for $CO_2$ is 0.03 mmol/mm Hg at body temperature. This means that 0.03 millimole of $H_2CO_3$ is present in the blood ... | {
"Header 1": "**Acid–Base Regulation**",
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When a strong acid such as HCl is added to a mixture of these two substances, the hydrogen is accepted by the base HPO4 = and converted to H2PO4 −:
$$HCl + Na_2HPO_4 \rightarrow NaH_2PO_4 + NaCl$$
The result of this reaction is that the strong acid, HCl, is replaced by an additional amount of a weak acid, NaH2PO4, ... | {
"Header 1": "**Acid–Base Regulation**",
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We have been discussing buffer systems as though they operate individually in the body fluids. However, they all work together because H<sup>+</sup> is common to the reactions of all these systems. Therefore, whenever there is a change in H<sup>+</sup> concentration in the extracellular fluid, the balance of all the bu... | {
"Header 1": "**Acid–Base Regulation**",
"Header 2": "Isohydric Principle: All Buffers in a Common Solution Are in Equilibrium With the Same H<sup>+</sup> Concentration",
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$\mathrm{CO}_2$ is formed continually in the body by intracellular metabolic processes. After it is formed, it diffuses from the cells into the interstitial fluids and blood, and the flowing blood transports it to the lungs, where it diffuses into the alveoli and then is transferred to the atmosphere by pulmonary vent... | {
"Header 1": "**Acid–Base Regulation**",
"Header 2": "PULMONARY EXPIRATION OF CO<sub>2</sub> BALANCES METABOLIC FORMATION OF CO<sub>2</sub>",
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If the metabolic formation of $CO_2$ remains constant, the only other factor that affects $PCO_2$ in extracellular fluid is the rate of alveolar ventilation. The higher the alveolar ventilation, the lower the $PCO_2$ . As discussed previously, when $CO_2$ concentration increases, the $H_2CO_3$ concentration an... | {
"Header 1": "INCREASING ALVEOLAR VENTILATION DECREASES EXTRACELLULAR FLUID H+ CONCENTRATION AND RAISES PH",
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Not only does the alveolar ventilation rate influence H<sup>+</sup> concentration by changing PCO<sub>2</sub> of the body fluids, but the H<sup>+</sup> concentration affects the rate of alveolar ventilation. Thus, **Figure 31-3** shows that alveolar ventilation rate increases four to five times normal as pH decreases f... | {
"Header 1": "INCREASING ALVEOLAR VENTILATION DECREASES EXTRACELLULAR FLUID H+ CONCENTRATION AND RAISES PH",
"Header 2": "INCREASED H+ CONCENTRATION STIMULATES ALVEOLAR VENTILATION",
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The kidneys control acid—base balance by excreting acidic or basic urine. Excreting acidic urine reduces the amount of acid in extracellular fluid, whereas excreting basic urine removes base from the extracellular fluid.
The overall mechanism whereby the kidneys excrete acidic or basic urine is as follows. Large amou... | {
"Header 1": "INCREASING ALVEOLAR VENTILATION DECREASES EXTRACELLULAR FLUID H+ CONCENTRATION AND RAISES PH",
"Header 2": "RENAL CONTROL OF ACID-BASE BALANCE",
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Hydrogen ion secretion and $HCO_3^-$ reabsorption occur in virtually all parts of the tubules except the descending and ascending thin limbs of the loop of Henle. **Figure 31-4** summarizes $HCO_3^-$ reabsorption along the tubule. Keep in mind that for *each* $HCO_3^-$ *reabsorbed, an* $H^+$ *must be secreted.*... | {
"Header 1": "INCREASING ALVEOLAR VENTILATION DECREASES EXTRACELLULAR FLUID H+ CONCENTRATION AND RAISES PH",
"Header 2": "SECRETION OF H<sup>+</sup> AND REABSORPTION OF HCO<sub>3</sub><sup>-</sup> BY THE RENAL TUBULES",
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Bicarbonate ions do not readily permeate the luminal membranes of the renal tubular cells; therefore, $HCO_3^-$ that is filtered by the glomerulus cannot be directly reabsorbed. Instead, $HCO_3^-$ is reabsorbed by a special process in which it first combines with $H^+$ to form $H_2CO_3$ , which eventually become... | {
"Header 1": "INCREASING ALVEOLAR VENTILATION DECREASES EXTRACELLULAR FLUID H+ CONCENTRATION AND RAISES PH",
"Header 2": "FILTERED HCO<sub>3</sub>- IS REABSORBED BY INTERACTION WITH H<sup>+</sup> IN THE TUBULES",
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Beginning in the late distal tubules and continuing through the remainder of the tubular system, the tubular epithelium secretes H<sup>+</sup> by *primary active transport*. The characteristics of this transport are different from those discussed for the proximal tubule, loop of Henle, and early distal tubule.
The me... | {
"Header 1": "PRIMARY ACTIVE SECRETION OF H<sup>+</sup> IN THE INTERCALATED CELLS OF LATE DISTAL AND COLLECTING TUBULES",
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When $H^+$ is secreted in excess of the $HCO_3^-$ filtered into the tubular fluid, only a small part of the excess $H^+$ can be excreted in the ionic form $(H^+)$ in the urine.
This is because the minimal urine pH is about 4.5, corresponding to an H $^+$ concentration of $10^{-4.5}$ mEq/L, or 0.03 mEq/L. T... | {
"Header 1": "COMBINATION OF EXCESS H+ WITH PHOSPHATE AND AMMONIA BUFFERS IN THE TUBULE GENERATES \"NEW\" HCO<sub>3</sub>-",
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The phosphate buffer system is composed of $HPO_4$ <sup>=</sup>. Both become concentrated in the tubular fluid because water is normally reabsorbed to a greater extent than phosphate by the renal tubules. Therefore, although phosphate is not an important extracellular fluid buffer, it is much more effective as a buffe... | {
"Header 1": "PHOSPHATE BUFFER SYSTEM CARRIES EXCESS H+ INTO THE URINE AND GENERATES NEW HCO<sub>3</sub>-",
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A second buffer system in the tubular fluid that is even more important quantitatively than the phosphate buffer system is composed of ammonia (NH<sub>3</sub>) and the ammonium ion (NH<sub>4</sub>+). Ammonium ion is synthesized from glutamine, which comes mainly from metabolism of amino acids in the liver. The glutamin... | {
"Header 1": "EXCRETION OF EXCESS H+ AND GENERATION OF NEW HCO<sub>3</sub>- BY AMMONIA BUFFER SYSTEM",
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Based on the principles discussed earlier, we can quantify the kidneys' net excretion of acid or net addition or elimination of $HCO_3^-$ from the blood as follows.
Bicarbonate excretion is calculated as urine flow rate multiplied by the urinary $HCO_3^-$ concentration and indicates how rapidly the kidneys are re... | {
"Header 1": "EXCRETION OF EXCESS H+ AND GENERATION OF NEW HCO<sub>3</sub>- BY AMMONIA BUFFER SYSTEM",
"Header 2": "QUANTIFYING RENAL ACID-BASE EXCRETION",
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As discussed earlier, $H^+$ secretion by the tubular epithelium is necessary for $HCO_3^-$ reabsorption and generation of new $HCO_3^-$ associated with titratable acid formation. Therefore, the rate of $H^+$ secretion must be carefully regulated if the kidneys are to perform their functions in acid—base homeost... | {
"Header 1": "EXCRETION OF EXCESS H+ AND GENERATION OF NEW HCO<sub>3</sub>- BY AMMONIA BUFFER SYSTEM",
"Header 2": "REGULATION OF RENAL TUBULAR H\\* SECRETION",
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**Table 31-3** Extracellular Fluid Characteristics of Primary Acid–Base Disturbances[a](#page-399-1)
| | pH | H+ | Pco2 | −<br>HCO3 |
|--------------------------|-----|----------|----------|-----------|
| Normal | 7.4 | 40 mEq/L | 40 mm Hg | 24 mEq/L |
| Respir... | {
"Header 1": "EXCRETION OF EXCESS H+ AND GENERATION OF NEW HCO<sub>3</sub>- BY AMMONIA BUFFER SYSTEM",
"Header 2": "REGULATION OF RENAL TUBULAR H\\* SECRETION",
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The gastrointestinal secretions normally contain large amounts of bicarbonate, and diarrhea results in the loss of HCO3 − from the body, which has the same effect as losing large amounts of bicarbonate in the urine. This form of metabolic acidosis can be serious and can cause death, especially in young children.
**Vo... | {
"Header 1": "EXCRETION OF EXCESS H+ AND GENERATION OF NEW HCO<sub>3</sub>- BY AMMONIA BUFFER SYSTEM",
"Header 2": "REGULATION OF RENAL TUBULAR H\\* SECRETION",
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The appropriate therapy of acid–base disorders requires proper diagnosis. The simple acid–base disorders described previously can be diagnosed by analyzing three measurements from an arterial blood sample: pH, plasma $HCO_3$ -concentration, and $PCO_2$ .
The diagnosis of simple acid–base disorders involves several ... | {
"Header 1": "EXCRETION OF EXCESS H+ AND GENERATION OF NEW HCO<sub>3</sub>- BY AMMONIA BUFFER SYSTEM",
"Header 2": "Clinical Measurements and Analysis of Acid–Base Disorders",
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In some cases, acid—base disorders are not accompanied by appropriate compensatory responses. When this situation occurs, the abnormality is referred to as a *mixed acid—base disorder*, which means that there are two or more underlying causes for the acid—base disturbance. For example, a patient with a low pH would be ... | {
"Header 1": "EXCRETION OF EXCESS H+ AND GENERATION OF NEW HCO<sub>3</sub>- BY AMMONIA BUFFER SYSTEM",
"Header 2": "Complex Acid–Base Disorders and Use of Acid–Base Nomogram for Diagnosis",
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Clin J Am Soc Nephrol 10:2232, 2015.
- Kamel KS, Halperin ML: Acid-base problems in diabetic ketoacidosis. N Engl J Med 372:546, 2015.
- Kraut JA, Madias NE: Differential diagnosis of nongap metabolic acidosis: value of a systematic approach. Clin J Am Soc Nephrol 7:671, 2012.
- Kurtz I: Renal tubular acidosis: H+/base... | {
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"Header 2": "Complex Acid–Base Disorders and Use of Acid–Base Nomogram for Diagnosis",
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#### DIURETICS AND THEIR MECHANISMS OF ACTION
Diuretics increase the rate of urine volume output, as the name implies. Most diuretics also increase the urinary excretion of solutes, especially sodium and chloride. In fact, most diuretics that are used clinically act by decreasing renal tubular sodium reabsorption, wh... | {
"Header 1": "**Diuretics and Kidney Diseases**",
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| Table 32-1 Classes of Diuretics, Their Mechanisms of Action, and Tubular Sites of Action | | |
|------------------------------------------------------------------------------------------|--|--|
|------------------------------------------------------------------------------------------|--|--|
| Class of Diuretic... | {
"Header 1": "**Diuretics and Kidney Diseases**",
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If the cause of prerenal AKI is not corrected, and ischemia of the kidney persists longer than a few hours, this type of renal failure can evolve into intrarenal AKI, as discussed later. Acute reduction of renal blood flow is a common cause of AKI in hospitalized patients, especially those who have sustained severe i... | {
"Header 1": "**Diuretics and Kidney Diseases**",
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**Table 32-4** Some Causes of Chronic Kidney Disease
| Metabolic Disorders<br>Diabetes mellitus |
|----------------------------------------------------------------------|
| Obesity |
| Amyloidosis ... | {
"Header 1": "**Diuretics and Kidney Diseases**",
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Many types of vascular lesions can lead to renal ischemia and death of kidney tissue. The most common of these lesions are the following: (1) *atherosclerosis* of the larger renal arteries, with progressive sclerotic constriction of the vessels; (2) *fibromuscular hyperplasia* of one or more of the large arteries, whic... | {
"Header 1": "**Diuretics and Kidney Diseases**",
"Header 2": "INJURY TO RENAL BLOOD VESSELS AS A CAUSE OF CHRONIC KIDNEY DISEASE",
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Chronic glomerulonephritis can be caused by several diseases that cause inflammation and damage to the glomerular capillary loops of the kidneys. In contrast to the acute form of this disease, chronic glomerulonephritis is a
slowly progressive disease that often leads to irreversible renal failure. It may be a primar... | {
"Header 1": "INJURY TO THE GLOMERULI AS A CAUSE OF CHRONIC KIDNEY DISEASE—GLOMERULONEPHRITIS",
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In the case of sodium and chloride ions, their plasma concentrations are maintained virtually constant, even with severe decreases in GFR (see curve C of Figure 32-5). This maintenance is accomplished by greatly decreasing tubular reabsorption of these electrolytes.
For example, with a 75% loss of functional nephro... | {
"Header 1": "INJURY TO THE GLOMERULI AS A CAUSE OF CHRONIC KIDNEY DISEASE—GLOMERULONEPHRITIS",
"token_count": 2040,
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#### **Hypertension and Kidney Disease**
As discussed earlier in this chapter, hypertension can exacerbate injury to the glomeruli and blood vessels of the kidneys and is a major cause of ESRD. Abnormalities of kidney function can also cause hypertension, as discussed in Chapter 19. Thus, the relationship between h... | {
"Header 1": "INJURY TO THE GLOMERULI AS A CAUSE OF CHRONIC KIDNEY DISEASE—GLOMERULONEPHRITIS",
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However, when adequate quantities of water are not available, the person rapidly becomes dehydrated.
**Fanconi Syndrome—Generalized Reabsorptive Defect of the Renal Tubules.** Fanconi syndrome is usually associated with increased urinary excretion of virtually all amino acids, glucose, and phosphate. In severe cases,... | {
"Header 1": "INJURY TO THE GLOMERULI AS A CAUSE OF CHRONIC KIDNEY DISEASE—GLOMERULONEPHRITIS",
"token_count": 2005,
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The total amount of blood in the artificial kidney at any one time is usually less than 500 milliliters, the rate of flow may be several hundred milliliters per minute, and the total diffusion surface area is between 0.6 and 2.5 m2. To prevent coagulation of the blood in the artificial kidney, a small amount of heparin... | {
"Header 1": "INJURY TO THE GLOMERULI AS A CAUSE OF CHRONIC KIDNEY DISEASE—GLOMERULONEPHRITIS",
"token_count": 1678,
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In this chapter, we begin discussing the *blood cells* and cells of the *macrophage system* and *lymphatic system*. We first present the functions of red blood cells (RBCs), which are the most abundant cells of the blood and are necessary for the delivery of oxygen to the tissues.
#### RED BLOOD CELLS (ERYTHROCYTES) ... | {
"Header 1": "**Red Blood Cells, Anemia, and Polycythemia**",
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The first-generation cells are called *basophil erythroblasts* because they stain with basic dyes. Hemoglobin first appears in *polychromatophil erythroblasts*. In the succeeding generations, as shown in **[Figure 33](#page-421-0)**-3, the cells become filled with hemoglobin to a concentration of about 34%, the nucleus... | {
"Header 1": "**Red Blood Cells, Anemia, and Polycythemia**",
"token_count": 2001,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
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The parietal cells of the gastric glands secrete a glycoprotein called *intrinsic factor*, which combines with vitamin B12 in food and makes the B12 available for absorption by the gut in the following way:
- 1. Intrinsic factor binds tightly with the vitamin B12. In this bound state, vitamin B12 is protected from di... | {
"Header 1": "**Red Blood Cells, Anemia, and Polycythemia**",
"token_count": 2044,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
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When the quantity of iron in the plasma falls low, some of the iron in the ferritin storage pool is removed easily and transported in the form of transferrin in the plasma to the areas of the body where it is needed. A unique characteristic of the transferrin molecule is that it binds strongly with receptors in the c... | {
"Header 1": "**Red Blood Cells, Anemia, and Polycythemia**",
"token_count": 2033,
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When this hemoglobin is exposed to low concentrations of oxygen, it precipitates into long crystals inside the RBC. These crystals elongate the cell and give it the appearance of a sickle rather than a biconcave disc. The precipitated hemoglobin also damages the cell membrane, so the cells become highly fragile, leadin... | {
"Header 1": "**Red Blood Cells, Anemia, and Polycythemia**",
"token_count": 2040,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
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Our bodies are exposed continually to bacteria, viruses, fungi, and parasites, all of which occur normally and to varying degrees in the skin, mouth, respiratory passageways, intestinal tract, lining membranes of the eyes, and even the urinary tract. Many of these infectious agents are capable of causing serious abnorm... | {
"Header 1": "**Red Blood Cells, Anemia, and Polycythemia**",
"Header 2": "**Resistance of the Body to Infection: I. Leukocytes, Granulocytes, the Monocyte-Macrophage System, and Inflammation**",
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These cells are now called *macrophages*, and they are extremely capable of combating disease agents in the tissues.
**White Blood Cells Enter the Tissue Spaces by Diapedesis.** Neutrophils and monocytes can squeeze through gaps between endothelial cells of the blood capillaries and postcapillary venules by *diapedes... | {
"Header 1": "**Red Blood Cells, Anemia, and Polycythemia**",
"Header 2": "**Resistance of the Body to Infection: I. Leukocytes, Granulocytes, the Monocyte-Macrophage System, and Inflammation**",
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The total combination of monocytes, mobile macrophages, fixed tissue macrophages, and a few specialized endothelial cells in the bone marrow, spleen, and lymph nodes is called the *reticuloendothelial system*. However, all or almost all these cells originate from monocytic stem
**Fig... | {
"Header 1": "**Red Blood Cells, Anemia, and Polycythemia**",
"Header 2": "**Resistance of the Body to Infection: I. Leukocytes, Granulocytes, the Monocyte-Macrophage System, and Inflammation**",
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This invasion is caused by inflammatory cytokines (e.g., tumor necrosis factor and interleukin-1) and other biochemical products produced by the inflamed tissues that initiate the following reactions:
**Figure 34-7.** Migration of neutrophils from the blood into inflamed tissue. Cytoki... | {
"Header 1": "**Red Blood Cells, Anemia, and Polycythemia**",
"Header 2": "**Resistance of the Body to Infection: I. Leukocytes, Granulocytes, the Monocyte-Macrophage System, and Inflammation**",
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Although more than two dozen factors have been implicated in control of the macrophage response to inflammation, five of these are believed to play dominant roles. They are shown in **Figure 34-8** and consist of the following: (1) tumor necrosis factor (TNF); (2) interleukin-1 (IL-1), (3) granulocyte-monocyte colony-s... | {
"Header 1": "Feedback Control of Macrophage and Neutrophil Responses",
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#### **Effects of Leukemia on the Body**
The first effect of leukemia is metastatic growth of leukemic cells in abnormal areas of the body. Leukemic cells from the bone marrow may reproduce so much that they invade the surrounding bone, causing pain and, eventually, a tendency for bones to fracture easily.
Almost... | {
"Header 1": "Feedback Control of Macrophage and Neutrophil Responses",
"token_count": 967,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
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The human body has the ability to resist almost all types of organisms or toxins that tend to damage the tissues and organs. This capability is called *immunity*. Much of the immunity is *acquired immunity* that does not develop until after the body is first attacked by a bacterium, virus, or toxin; often, weeks or mon... | {
"Header 1": "**Resistance of the Body to Infection: II. Immunity and Allergy**",
"token_count": 977,
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Acquired immunity is the product of the body's lymphocytes. In people who have a genetic lack of lymphocytes or whose lymphocytes have been destroyed by radiation or chemicals, no acquired immunity can develop. Within days after birth, such a person dies of fulminating bacterial infection unless he or she is treated by... | {
"Header 1": "**Resistance of the Body to Infection: II. Immunity and Allergy**",
"Header 2": "LYMPHOCYTES ARE RESPONSIBLE FOR ACQUIRED IMMUNITY",
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Millions of different clones of lymphocytes exist (shown as *B1, B2*, and *B3*). When the lymphocyte clone (*B2* in this example) is activated by its antigen, it reproduces to form large numbers of duplicate lymphocytes, which then secrete antibodies.
the respective T- and B-cell lymphocytes, these gene segments beco... | {
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"Header 2": "LYMPHOCYTES ARE RESPONSIBLE FOR ACQUIRED IMMUNITY",
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**Specificity of Antibodies.** Each antibody is specific for a particular antigen; this characteristic is a result of the unique structural organization of amino acids in the variable portions of the light and heavy chains. The amino acid organization has a different steric shape for each antigen specificity, so when... | {
"Header 1": "**Resistance of the Body to Infection: II. Immunity and Allergy**",
"Header 2": "LYMPHOCYTES ARE RESPONSIBLE FOR ACQUIRED IMMUNITY",
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Therefore, on subsequent exposure to the same antigen anywhere in the body, release of activated T cells occurs far more rapidly and much more powerfully than during first exposure.
**Antigen-Presenting Cells, Major Histocompatibility Complex Proteins, and Antigen Receptors on T Lymphocytes.** T-cell responses are ex... | {
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"Header 2": "LYMPHOCYTES ARE RESPONSIBLE FOR ACQUIRED IMMUNITY",
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#### **Regulatory T Cells**
Much less is known about the regulatory T cells than about the others, but they are capable of suppressing the functions of both cytotoxic and T-helper cells. These suppressor functions of the CD4+ regulatory T cells are believed to prevent the cytotoxic cells from causing excessive immu... | {
"Header 1": "**Resistance of the Body to Infection: II. Immunity and Allergy**",
"Header 2": "LYMPHOCYTES ARE RESPONSIBLE FOR ACQUIRED IMMUNITY",
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This reaction is called *anaphylaxis*. Histamine is released into the circulation and causes body-wide vasodilation, as well as increased permeability of the capillaries, with a resultant marked loss of plasma from the circulation. Occasionally, a person who experiences this reaction dies of circulatory shock within a ... | {
"Header 1": "**Resistance of the Body to Infection: II. Immunity and Allergy**",
"Header 2": "LYMPHOCYTES ARE RESPONSIBLE FOR ACQUIRED IMMUNITY",
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#### ANTIGENICITY CAUSES IMMUNE REACTIONS OF BLOOD
When blood transfusions from one person to another were first attempted, immediate or delayed agglutination and hemolysis of the red blood cells (RBCs) often occurred, resulting in typical transfusion reactions that frequently led to death. Soon it was discovered tha... | {
"Header 1": "**Blood Types; Transfusion; and T[issue](#page-451-0) and Organ Transplantation**",
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In this case, the antibodies cause lysis of the RBCs by activating the complement system and forming a *membrane attack complex* (also called *cytolytic complex*) that inserts itself into the lipid bilayer of the cell membranes; this insertion creates membrane pores that are permeable to ions and causes osmotic lysis o... | {
"Header 1": "**Blood Types; Transfusion; and T[issue](#page-451-0) and Organ Transplantation**",
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} |
By the time these transfused Rh-negative cells are replaced with the infant's own Rh-positive cells, a process that requires 6 weeks or more, the anti-Rh agglutinins that had come from the mother will have been destroyed.
**Prevention of Erythroblastosis Fetalis.** The D antigen of the Rh blood group system is the pr... | {
"Header 1": "**Blood Types; Transfusion; and T[issue](#page-451-0) and Organ Transplantation**",
"token_count": 2034,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
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These drugs inhibit genes that code for several cytokines, especially interleukin-2 (IL-2). IL-2 is an essential factor that induces T-cell proliferation and antibody formation.
- 2. Various drugs that have a toxic effect on the lymphoid system and therefore block formation of antibodies and T cells, especially the dru... | {
"Header 1": "**Blood Types; Transfusion; and T[issue](#page-451-0) and Organ Transplantation**",
"token_count": 907,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
#### HEMOSTASIS EVENTS
The term *hemostasis* means prevention of blood loss. Whenever a vessel is severed or ruptured, hemostasis is achieved by several mechanisms: (1) vascular constriction; (2) formation of a platelet plug; (3) formation of a blood clot as a result of blood coagulation; and (4) eventual growth of f... | {
"Header 1": "**Hemostasis and Blood Coagulation**",
"token_count": 1947,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
#### **FIBROUS ORGANIZATION OR DISSOLUTION OF BLOOD CLOTS**
Once a blood clot has formed, it can follow one of two courses: (1) it can become invaded by *fibroblasts*, which
**Table 37-1** Clotting Factors in Blood and Their Synonyms[a](#page-458-2)
| Clotting Factor | Synonym(s) ... | {
"Header 1": "**Hemostasis and Blood Coagulation**",
"token_count": 2019,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
This activated substance then operates as an enzyme to form *covalent bonds* between more and more of the fibrin monomer molecules, as well as multiple cross-linkages between adjacent fibrin fibers, thus adding tremendously to the three-dimensional strength of the fibrin meshwork.
**Blood Clot.** The clot is composed... | {
"Header 1": "**Hemostasis and Blood Coagulation**",
"token_count": 487,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
Once a blood clot starts to develop, it normally extends within minutes into the surrounding blood—that is, the clot initiates a positive feedback to promote more clotting. One of the most important causes of this clot promotion is that the proteolytic action of thrombin allows it to act on many of the other blood-clot... | {
"Header 1": "**Hemostasis and Blood Coagulation**",
"Header 2": "POSITIVE FEEDBACK OF CLOT FORMATION",
"token_count": 203,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
Now that we have discussed the clotting process, the more complex mechanisms that initiate clotting in the first place will be described. These mechanisms are set into play by the following: (1) trauma to the vascular wall and adjacent tissues; (2) trauma to the blood; or (3) contact of the blood with damaged endotheli... | {
"Header 1": "INITIATION OF COAGULATION: FORMATION OF PROTHROMBIN ACTIVATOR",
"token_count": 2014,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
When the endothelial wall is damaged, its smoothness and glycocalyx-thrombomodulin layer are lost, which activates both factor XII and the platelets, thus setting off the intrinsic pathway of clotting. If factor XII and platelets come into contact with the subendothelial collagen, the activation is even more powerful... | {
"Header 1": "INITIATION OF COAGULATION: FORMATION OF PROTHROMBIN ACTIVATOR",
"token_count": 1998,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
If one of her X chromosomes is deficient, she will be a *hemophilia carrier;* her male offspring will have a 50% chance of inheriting the illness, and her female offspring will have a 50% chance of inheriting the carrier status.
Although female carriers have one normal allele and usually do not develop symptomatic he... | {
"Header 1": "INITIATION OF COAGULATION: FORMATION OF PROTHROMBIN ACTIVATOR",
"token_count": 2033,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The ones most clinically useful are *heparin* and the *coumarins*.
#### **HEPARIN—INTRAVENOUS ANTICOAGULANT**
Commercial heparin is extracted from several different animal tissues and prepared in almost pure form. Injection of relatively small quantities, about 0.5 to 1 mg/kg of body weight, causes the blood-clotti... | {
"Header 1": "INITIATION OF COAGULATION: FORMATION OF PROTHROMBIN ACTIVATOR",
"token_count": 2039,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
N Engl J Med 359:938, 2008.
Gupta S, Shapiro AD: Optimizing bleed prevention throughout the lifespan: womb to tomb. Haemophilia 24 Suppl 6:76, 2018.
Hess CN, Hiatt WR: Antithrombotic therapy for peripheral artery disease in 2018. JAMA 319:2329, 2018.
Hunt BJ: Bleeding and coagulopathies in critical care. N Engl J... | {
"Header 1": "INITIATION OF COAGULATION: FORMATION OF PROTHROMBIN ACTIVATOR",
"token_count": 848,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The main functions of respiration are to provide oxygen to the tissues and remove carbon dioxide. The four major components of respiration are the following: (1) *pulmonary ventilation*, which means the inflow and outflow of air between the atmosphere and the lung alveoli; (2) *diffusion of oxygen* (O2) *and carbon dio... | {
"Header 1": "**Pulmonary Ventilation**",
"token_count": 2032,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The two curves are called, respectively, the *inspiratory compliance curve* and the *expiratory compliance curve*, and the entire diagram is called the *compliance diagram of the lungs*.
The characteristics of the compliance diagram are determined by the elastic forces of the lungs. These forces can be divided into t... | {
"Header 1": "**Pulmonary Ventilation**",
"token_count": 492,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
Principle of Surface Tension. When water forms a surface with air, the water molecules on the surface of the water have an especially strong attraction for one another. As a result, the water surface is always attempting to contract. This is what holds raindrops together—a tight contractile membrane of water molecules ... | {
"Header 1": "**Pulmonary Ventilation**",
"Header 2": "Surfactant, Surface Tension, and Collapse of the Alveoli",
"token_count": 1845,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
**Table 38-1** Average Pulmonary Volumes and Capacities for Healthy, Young Adult Men and Women
| Pulmonary Volumes and Capacities | Men | Women |
|----------------------------------|------|-------|
| Volume (ml) | | |
| Tidal volume | 500 | 400 |
| Inspiratory... | {
"Header 1": "**Pulmonary Ventilation**",
"Header 2": "Surfactant, Surface Tension, and Collapse of the Alveoli",
"token_count": 2045,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The *minute respiratory volume* is the total amount of new air moved into the respiratory passages each minute and is equal to the *tidal volume* times the *respiratory rate per minute*. The normal tidal volume is about 500 ml, and the normal respiratory rate is about 12 breaths/min. Therefore, the *minute respiratory ... | {
"Header 1": "MINUTE RESPIRATORY VOLUME EQUALS RESPIRATORY RATE TIMES TIDAL VOLUME",
"token_count": 353,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
Some of the air a person breathes never reaches the gas exchange areas but simply fills respiratory passages, such as the nose, pharynx, and trachea, where gas exchange does not occur. This air is called *dead space air* because it is not useful for gas exchange.
On expiration, the air in the dead space is expired fi... | {
"Header 1": "MINUTE RESPIRATORY VOLUME EQUALS RESPIRATORY RATE TIMES TIDAL VOLUME",
"Header 2": "DEAD SPACE AND ITS EFFECT ON ALVEOLAR VENTILATION",
"token_count": 2041,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
Also, a bronchiolar constrictor reflex often occurs when microemboli occlude small pulmonary arteries.
#### **Local Secretory Factors May Cause Bronchiolar Constric-**
**tion.** Several substances formed in the lungs are often active in causing bronchiolar constriction. Two of the most important of these are *hista... | {
"Header 1": "MINUTE RESPIRATORY VOLUME EQUALS RESPIRATORY RATE TIMES TIDAL VOLUME",
"Header 2": "DEAD SPACE AND ITS EFFECT ON ALVEOLAR VENTILATION",
"token_count": 2031,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The pitch of the vibration is determined mainly by the degree of stretch of the cords, but also by how tightly the cords are approximated to one another and by the mass of their edges.
**[Figure 38-9](#page-478-0)***A* shows a dissected view of the vocal folds after removal of the mucous epithelial lining. Immediatel... | {
"Header 1": "MINUTE RESPIRATORY VOLUME EQUALS RESPIRATORY RATE TIMES TIDAL VOLUME",
"Header 2": "DEAD SPACE AND ITS EFFECT ON ALVEOLAR VENTILATION",
"token_count": 1276,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The lung has two circulations, *a high-pressure, low-flow circulation* and *a low-pressure, high-flow circulation*. The *high-pressure, low-flow circulation* supplies systemic arterial blood to the trachea, bronchial tree (including the terminal bronchioles), supporting tissues of the lung, and outer coats (adventitia)... | {
"Header 1": "**Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid**",
"token_count": 2044,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
with decreasing pressure. For adequate aeration of the blood to occur, the blood must be distributed to the segments of the lungs where the alveoli are best oxygenated. This distribution is achieved by the following mechanism.
**Decreased Alveolar Oxygen Reduces Local Alveolar Blood Flow and Regulates Pulmonary Blo... | {
"Header 1": "**Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid**",
"token_count": 2039,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
This extra flow is accommodated in the lungs in three ways: (1) by increasing the number of open capillaries, sometimes as much as threefold; (2) by distending all the capillaries and increasing the rate of flow through each capillary more than twofold; and (3) by increasing the pulmonary arterial pressure. Normally, t... | {
"Header 1": "**Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid**",
"token_count": 2045,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
In these experiments, as soon as the left atrial pressure rose above 23 mm Hg (causing the pulmonary capillary pressure to rise above 25 mm Hg), fluid began to accumulate in the lungs. This fluid accumulation increased even more rapidly with
**Figure 39-8.** Rate of fluid loss into the ... | {
"Header 1": "**Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid**",
"token_count": 1823,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
After the alveoli are ventilated with fresh air, the next step in respiration is *diffusion* of oxygen (O2) from the alveoli into the pulmonary blood and diffusion of carbon dioxide (CO2) in the opposite direction, out of the blood into the alveoli. The process of diffusion is simply the random motion of molecules in a... | {
"Header 1": "**Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid**",
"Header 2": "**Principles of Gas Exchange; Diffusion of Oxygen and Carbon Dioxide Through the Respiratory Membrane**",
"token_count": 1123,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
When partial pressure is expressed in atmospheres (1 atmosphere [1 atm] pressure equals 760 mm Hg) and concentration is expressed in volume of gas dissolved in each volume of water, the solubility coefficients for important respiratory gases at body temperature are the following:
| Oxygen: | 0.024 |
|-------... | {
"Header 1": "Partial pressure = $\\frac{\\text{Concentration of dissolved gas}}{\\text{Solubility coefficient}}$",
"token_count": 728,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
From the preceding discussion, it is clear that when the partial pressure of a gas is greater in one area than in another area, there will be net diffusion from the high-pressure area toward the low-pressure area. For example, returning to Figure 40-1, one can readily see that the molecules in the area of high pressure... | {
"Header 1": "Partial pressure = $\\frac{\\text{Concentration of dissolved gas}}{\\text{Solubility coefficient}}$",
"Header 2": "Pressure Difference Causes Net Diffusion of Gases Through Fluids",
"token_count": 2011,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
This makes the respiratory control mechanism much more stable than it would be otherwise, and it helps prevent excessive increases and decreases in tissue oxygenation, tissue $CO_2$ concentration, and tissue pH when respiration is temporarily interrupted.
#### Oxygen Concentration and Partial Pressure in Alveoli
... | {
"Header 1": "Partial pressure = $\\frac{\\text{Concentration of dissolved gas}}{\\text{Solubility coefficient}}$",
"Header 2": "Pressure Difference Causes Net Diffusion of Gases Through Fluids",
"token_count": 735,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
Carbon dioxide is continually formed in the body and then carried in the blood to the alveoli; it is continually removed from the alveoli by ventilation. Figure 40-5 shows the effects on the alveolar partial pressure of PCO<sub>2</sub> of both alveolar ventilation and two rates of CO<sub>2</sub> excretion, 200 and 800 ... | {
"Header 1": "Partial pressure = $\\frac{\\text{Concentration of dissolved gas}}{\\text{Solubility coefficient}}$",
"Header 2": "CO<sub>2</sub> Concentration and Partial Pressure in Alveoli",
"token_count": 2032,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The *diffusion coefficient* for transfer of each gas through the respiratory membrane depends on the gas's *solubility* in the membrane and, inversely, on the *square root* of the gas's *molecular weight*. The rate of diffusion in the respiratory membrane is almost exactly the same as that in water, for reasons expla... | {
"Header 1": "Partial pressure = $\\frac{\\text{Concentration of dissolved gas}}{\\text{Solubility coefficient}}$",
"Header 2": "CO<sub>2</sub> Concentration and Partial Pressure in Alveoli",
"token_count": 1377,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
Earlier in this chapter, we learned that two factors determine the Po<sub>2</sub> and Pco<sub>2</sub> in the alveoli: (1) the rate of alveolar ventilation; and (2) the rate of transfer of O<sub>2</sub> and CO<sub>2</sub> through the respiratory membrane. This discussion made the assumption that all the alveoli are vent... | {
"Header 1": "Partial pressure = $\\frac{\\text{Concentration of dissolved gas}}{\\text{Solubility coefficient}}$",
"Header 2": "CO<sub>2</sub> Concentration and Partial Pressure in Alveoli",
"Header 3": "Effect of Ventilation-Perfusion Ratio on Alveolar Gas Concentration",
"token_count": 2012,
"source_pdf":... |
#### **Concept of Physiological Dead Space When V**˙**A/Q**˙ **Greater Than Normal**
When ventilation of some of the alveoli is great but alveolar blood flow is low, there is far more available oxygen in the alveoli than can be transported away from the alveoli by the flowing blood. Thus, the ventilation of these a... | {
"Header 1": "Partial pressure = $\\frac{\\text{Concentration of dissolved gas}}{\\text{Solubility coefficient}}$",
"Header 2": "CO<sub>2</sub> Concentration and Partial Pressure in Alveoli",
"Header 3": "Effect of Ventilation-Perfusion Ratio on Alveolar Gas Concentration",
"token_count": 1553,
"source_pdf":... |
Once *oxygen* (O2) has diffused from the alveoli into the pulmonary blood, it is transported to the tissue capillaries almost entirely in combination with hemoglobin. The presence of hemoglobin in the red blood cells allows the blood to transport 30 to 100 times as much O2 as could be transported in the form of dissolv... | {
"Header 1": "**Transport of Oxygen and Carbon Dioxide in Blood and Tissue Fluids**",
"token_count": 1161,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
About 98% of the blood that enters the left atrium from the lungs has just passed through the alveolar capillaries and has become oxygenated up to a Po2 of about 104 mm Hg. Another 2% of the blood has passed from the aorta through the bronchial circulation, which supplies mainly the deep tissues of the lungs and is not... | {
"Header 1": "**Transport of Oxygen and Carbon Dioxide in Blood and Tissue Fluids**",
"Header 2": "TRANSPORT OF OXYGEN IN ARTERIAL BLOOD",
"token_count": 364,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
When the arterial blood reaches the peripheral tissues, its $Po_2$ in the capillaries is still 95 mm Hg. Yet, as shown in **Figure 41-3**, the $Po_2$ in the *interstitial fluid* that surrounds the tissue cells averages only 40 mm Hg. Thus, there is a large initial pressure difference that causes $O_2$ to diffuse ... | {
"Header 1": "DIFFUSION OF OXYGEN FROM THE PERIPHERAL CAPILLARIES INTO THE TISSUE FLUID",
"token_count": 1726,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The chemistry of hemoglobin is presented in Chapter 33, where we pointed out that the $O_2$ molecule combines loosely and reversibly with the heme portion of hemoglobin. When $Po_2$ is high, as in the pulmonary capillaries, $O_2$ binds with hemoglobin, but when $Po_2$ is low, as in the tissue capillaries, $O_2... | {
"Header 1": "Reversible Combination of O<sub>2</sub> With Hemoglobin",
"token_count": 2040,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
Consequently, the level of alveolar O2 may vary greatly—from 60 to more than 500 mm Hg Po2—and still the Po2 in the peripheral tissues does not vary more than a few milliliters from normal, *demonstrating beautifully the tissue "oxygen buffer" function of the blood hemoglobin system*.
#### **Factors That Shift the Ox... | {
"Header 1": "Reversible Combination of O<sub>2</sub> With Hemoglobin",
"token_count": 835,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The normal BPG in the blood always keeps the O<sub>2</sub>-hemoglobin dissociation curve shifted slightly to the right. In hypoxic conditions that last longer than a few hours,
the quantity of BPG in the blood increases considerably, thus shifting the $O_2$ -hemoglobin dissociation curve even farther to the right. T... | {
"Header 1": "Effect of BPG to Cause Rightward Shift of the Oxygen-Hemoglobin Dissociation Curve",
"token_count": 422,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
Effect of Intracellular Po<sub>2</sub> on Oxygen Usage Rate.
As explained in Chapter 3, when adenosine triphosphate (ATP) is used in the cells to provide energy, it is converted into ADP. The increasing concentration of ADP increases metabolic usage of $O_2$ as it combines with the various cell nutrients, releasing... | {
"Header 1": "Only a minute level of O<sub>2</sub> pressure is required in the cells for normal intracellular chemical reactions to take place. The reason for this phenomenon is that the respiratory enzyme systems of the cell, discussed in Chapter 68, have been configured so that when the cellular Po<sub>2</sub> is ... |
To begin the process of $CO_2$ transport, $CO_2$ diffuses out of the tissue cells in the dissolved molecular $CO_2$ form. On entering the tissue capillaries, the $CO_2$ initiates a host of almost instantaneous physical and chemical reactions, shown in **Figure 41-13**, which are essential for $CO_2$ transport... | {
"Header 1": "Only a minute level of O<sub>2</sub> pressure is required in the cells for normal intracellular chemical reactions to take place. The reason for this phenomenon is that the respiratory enzyme systems of the cell, discussed in Chapter 68, have been configured so that when the cellular Po<sub>2</sub> is ... |
Carbonic Anhydrase Catalyzes the Reaction of CO<sub>2</sub> With Water in Red Blood Cells. The dissolved CO<sub>2</sub> in the blood reacts with water to form *carbonic acid*. This reaction would occur much too slowly to be of importance were it not for the fact that there is an enzyme called *carbonic anhydrase* insid... | {
"Header 1": "Only a minute level of O<sub>2</sub> pressure is required in the cells for normal intracellular chemical reactions to take place. The reason for this phenomenon is that the respiratory enzyme systems of the cell, discussed in Chapter 68, have been configured so that when the cellular Po<sub>2</sub> is ... |
Earlier in the chapter, we noted that an increase in $CO_2$ in the blood causes $O_2$ to be displaced from the hemoglobin (the Bohr effect), which is an important factor in increasing $O_2$ transport. The reverse is also true—binding of $O_2$ with hemoglobin tends to displace $CO_2$ from the blood. This effec... | {
"Header 1": "When Oxygen Binds With Hemoglobin, CO<sub>2</sub> Is Released (the Haldane Effect) to Increase CO<sub>2</sub> Transport",
"token_count": 1873,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The nervous system normally adjusts the rate of alveolar ventilation to meet the demands of the body almost exactly so that the oxygen partial pressure (Po2) and carbon dioxide partial pressure (Pco2) in the arterial blood are hardly altered, even during heavy exercise and most other types of respiratory stress. This c... | {
"Header 1": "**Regulation of Respiration**",
"token_count": 2023,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
Oxygen, in contrast, does not have a major *direct* effect on the respiratory center of the brain in controlling respiration. Instead, it acts almost entirely on peripheral *chemoreceptors* located in the *carotid* and *aortic bodies*, and these chemoreceptors in turn transmit appropriate nervous signals to the respira... | {
"Header 1": "**Regulation of Respiration**",
"token_count": 2044,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
**Decreased Arterial Oxygen Stimulates the Chemoreceptors.** When the oxygen concentration in the arterial blood falls below normal, the chemoreceptors become strongly stimulated. This effect is demonstrated in **Figure 42-5**, which shows the effect of different levels of *arterial* Po<sub>2</sub> on the rate of ner... | {
"Header 1": "**Regulation of Respiration**",
"token_count": 720,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
**Figure 42-7** shows the effect of low arterial $PO_2$ on alveolar ventilation when the $PCO_2$ and $H^+$ concentrations are
**Figure 42-7.** The *lower red curve* demonstrates the effect of different levels of arterial Po2 on alveolar ventilation, showing a 6-fold increase in ve... | {
"Header 1": "Effect of Low Arterial Po<sub>2</sub> to Stimulate Alveolar Ventilation When Arterial CO<sub>2</sub> and H<sup>+</sup> Concentrations Remain Normal",
"token_count": 2002,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
The upper curve of **[Figure 42-11](#page-514-0)** also shows that if during exercise the arterial Pco2 does change from its normal value of 40 mm Hg, it has an extra stimulatory effect on ventilation at a Pco2 value greater than 40 mm Hg and a depressant effect at a Pco2 value less than 40 mm Hg.
**Neurogenic Contro... | {
"Header 1": "Effect of Low Arterial Po<sub>2</sub> to Stimulate Alveolar Ventilation When Arterial CO<sub>2</sub> and H<sup>+</sup> Concentrations Remain Normal",
"token_count": 2036,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
These periods of apnea result in significant decreases in Po2 and increases in Pco2, which greatly stimulate respiration. This stimulation, in turn, causes sudden attempts to breathe, which result in loud snorts and gasps followed by snoring and repeated episodes of apnea. The periods of apnea and labored breathing are... | {
"Header 1": "Effect of Low Arterial Po<sub>2</sub> to Stimulate Alveolar Ventilation When Arterial CO<sub>2</sub> and H<sup>+</sup> Concentrations Remain Normal",
"token_count": 1648,
"source_pdf": "datasets/websources/biochem/1671268744mpp.pdf"
} |
In the previous few chapters, we discussed several methods for studying respiratory abnormalities, including measuring vital capacity, tidal air, functional residual capacity, dead space, physiologic shunt, and physiological dead space. This array of measurements is only part of the armamentarium of the clinical pulmon... | {
"Header 1": "Effect of Low Arterial Po<sub>2</sub> to Stimulate Alveolar Ventilation When Arterial CO<sub>2</sub> and H<sup>+</sup> Concentrations Remain Normal",
"Header 2": "USEFUL METHODS FOR STUDYING RESPIRATORY ABNORMALITIES",
"token_count": 2020,
"source_pdf": "datasets/websources/biochem/1671268744mpp.... |
Such a recording is shown in **[Figure 43-3](#page-519-0)***A* for a person with normal lungs and in **[Figure 43-3](#page-519-0)***B* for a person with partial airway obstruction. In performing the FVC maneuver, the person first inspires maximally to the TLC and then exhales into the spirometer with maximum expiratory... | {
"Header 1": "Effect of Low Arterial Po<sub>2</sub> to Stimulate Alveolar Ventilation When Arterial CO<sub>2</sub> and H<sup>+</sup> Concentrations Remain Normal",
"Header 2": "USEFUL METHODS FOR STUDYING RESPIRATORY ABNORMALITIES",
"token_count": 1374,
"source_pdf": "datasets/websources/biochem/1671268744mpp.... |
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