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By C. Baldar. National American University.

CHAPTER 18 Control Mechanisms in Circulatory Function 293 returns blood pressure toward the normal level 25 mg benadryl visa. If the fall in mean arterial pressure is very large 25mg benadryl for sale, increased sympathetic neural activity to veins is added to the above responses buy benadryl 25 mg lowest price, causing contraction of the venous smooth muscle and re- ducing venous compliance order 25 mg benadryl free shipping. Decreased venous compliance shifts blood toward the central blood volume benadryl 25mg mastercard, increasing right atrial pressure and, in turn, stroke volume. The baroreceptor reflex influences hormone levels in addition to vascular and cardiac muscle. The most important influ- ence is on the renin-angiotensin-aldosterone system (RAAS). A reduction in arterial pressure and baroreceptor firing results in increased sympathetic nerve activity to the kidneys, which causes the kidneys to release renin, activat- ing the RAAS. The activation of this system causes the kid- neys to save salt and water. Salt and water retention in- creases blood volume and, ultimately, causes blood pressure to rise. The details of the RAAS are discussed later in this chapter and in Chapter 24. The information on the firing rate of the baroreceptors Carotid sinus baroreceptor nerve firing rate FIGURE 18. With normal pothalamus where the release of arginine vasopressin conditions, a mean arterial pressure of 93 mm Hg is near the (AVP) by the posterior pituitary is controlled (see Chapter midrange of the firing rates for the nerves. Decreased firing rate of the baroreceptors results in in- sion causes the operating range to shift to the right, putting 93 creased AVP release, causing the kidney to save water. An increase in arterial pressure causes decreased AVP release and increased excre- tion of water by the kidneys. Pulse pressure also influences the firing rate of the but they occur more slowly (a timescale of many hours to baroreceptors. For a given mean arterial pressure, the firing days) than ANS effects (seconds to minutes). An important property of the defense of arterial pressure by the baroreceptor reflex re- baroreceptor reflex is that it adapts during a period of 1 to sults in maintenance of blood flow to two vital organs: the 2 days to the prevailing mean arterial pressure. If resistance vessels of the heart and brain mean arterial pressure is suddenly raised, baroreceptor fir- participated in the sympathetically mediated vasoconstric- ing increases. If arterial pressure is held at the higher level, tion found in skeletal muscle, skin, and the splanchnic re- baroreceptor firing declines during the next few seconds. This does Firing rate then continues to decline more slowly until it re- not happen. Con- The combination of (1) a minimal vasoconstrictor effect sequently, if the mean arterial pressure is maintained at an of sympathetic nerves on cerebral blood vessels, and (2) a elevated level, the tendency for the baroreceptors to initi- robust autoregulatory response keeps brain blood flow ate a decrease in cardiac output and SVR quickly disap- nearly normal despite modest decreases in arterial pressure pears. However, a large decrease in arterial rate of baroreceptor firing for a given mean arterial pressure pressure beyond the autoregulatory range causes brain mentioned above (see Fig. This is an example of re- blood flow to fall, accounting for loss of consciousness. A “resetting” of the reflex in the central Activation of sympathetic nerves to the heart causes - nervous system (CNS) occurs as well. Consequently, the 1 adrenergic receptor-mediated constriction of coronary ar- baroreceptor mechanism is the “first line of defense” in the terioles and -adrenergic receptor-mediated increases in maintenance of normal blood pressure; it makes the rapid 1 cardiac muscle metabolism (see Chapter 17). The net effect control of blood pressure needed with changes in posture is a marked increase in coronary blood flow, despite the in- or blood loss possible, but it does not provide for the long- creased sympathetic constrictor activity. Receptors That Sense Central Blood Volume Pressure Range for Baroreceptors. The effective range Cardiopulmonary baroreceptors are located in the cardiac of the carotid sinus baroreceptor mechanism is approxi- atria, at the junction of the great veins and atria, in the ven- 294 PART IV BLOOD AND CARDIOVASCULAR PHYSIOLOGY tricular myocardium, and in pulmonary vessels. These events fibers run in the vagus nerve to the NTS, with projections lead to increases in cardiac output, SVR, and mean arterial to supramedullary areas as well. An example of this reaction is the cold pressor re- the stretch) of the cardiopulmonary receptors by reducing sponse—the elevated blood pressure that normally occurs central blood volume results in increased sympathetic when an extremity is placed in ice water.

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Unfortunately benadryl 25mg discount, there is no such ideal indicator 25 mg benadryl with amex, so the exact volume of the If the plasma [Na ] is 140 mmol/L purchase 25 mg benadryl with amex, blood glucose is 100 ECF cannot be measured generic benadryl 25 mg fast delivery. The equation indicates that Na and its accompany- termined from the volume of distribution of these ions: ra- ing anions (mainly Cl and HCO3 ) normally account for dioactive Na benadryl 25 mg without a prescription, radioactive Cl , radioactive sulfate, thio- more than 95% of the plasma osmolality. In some special 2– cyanate (SCN ), and thiosulfate (S2O3 ); radioactive circumstances (e. However, ity calculated from the above equation may be much lower ions are not completely impermeant; they slowly enter the than the true, measured osmolality as a result of the presence cell compartment, so measurements tend to lead to an over- of unmeasured osmotically active solutes (e. Measurements with inert sugars The concentrations of various electrolytes in plasma, in- (such as mannitol, sucrose, and inulin) tend to lead to an terstitial fluid, and ICF are summarized in Table 24. The underestimate of ECF volume because they are excluded ICF values are based on determinations made in skeletal from some of the extracellular water—for example, the wa- muscle cells. These cells account for about two thirds of the ter in dense connective tissue and cartilage. Concentrations are expressed niques are required when using these sugars because they in terms of milliequivalents per liter or per kg H2O. For fusible anions (such as Cl ) are higher in interstitial fluid 2 2 singly charged (univalent) ions, such as Na , K , Cl , or than in plasma. For doubly charged (di- extent (about 40% and 30%, respectively) by plasma pro- 2 2 2– valent) ions, such as Ca , Mg , or SO4 , 1 mmol is equal teins, and it is only the unbound ions that can diffuse 2 to 2 mEq. Some electrolytes, such as proteins, are polyva- through capillary walls. The usefulness of ex- Mg concentrations are higher than in interstitial fluid. The cells have a higher K , Mg , and protein concentration than in the surrounding intersti- 3 cations 3 anions (4) 2 tial fluid. The intracellular Na , Ca , Cl , and HCO3 If we know the total concentration (mEq/L) of all cations levels are lower than outside the cell. The anions in skele- in a solution and know only some of the anions, we can eas- tal muscle cells labeled “Others” are mainly organic phos- ily calculate the concentration of the remaining anions. Na is the major cation in plasma, and Cl and [Na ] are a consequence of plasma membrane Na /K - HCO3 are the major anions. The plasma proteins (mainly ATPase activity; this enzyme extrudes Na from the cell serum albumin) bear net negative charges at physiological and takes up K. The electrolytes are actually dissolved in the plasma in skeletal muscle cells are primarily a consequence of the water, so the second column in Table 24. The water content of plasma is vors the outward movement of these small, negatively 2 usually about 93%; about 7% of plasma volume is occupied charged ions. The intracellular [Mg ] is high; most is not 2 by solutes, mainly the plasma proteins. Intracellular [Ca ] is 2 tration in plasma to concentration in plasma water, we di- low; as discussed in Chapter 1, the cytosolic [Ca ] in rest- 7 vided the plasma concentration by the plasma water con- ing cells is about 10 M (0. Therefore, 142 mEq Na /L Ca is sequestered in organelles, such as the sarcoplasmic plasma becomes 153 mEq/L H2O or 153 mEq/kg H2O reticulum in skeletal muscle. It contains all of the small electrolytes in es- Intracellular and Extracellular Fluids Are sentially the same concentration as in plasma, but little pro- Normally in Osmotic Equilibrium tein. The proteins are largely confined to the plasma Despite the different compositions of ICF and ECF, the to- because of their large molecular size. Differences in small tal solute concentration (osmolality) of these two fluid ion concentrations between plasma and interstitial fluid compartments is normally the same. ICF and ECF are in os- (compare Columns 2 and 3) occur because of the different motic equilibrium because of the high water permeability protein concentrations in these two compartments. Two of cell membranes, which does not permit an osmolality factors are involved. If the osmolality changes in one cause the plasma proteins are negatively charged, they compartment, water moves to restore a new osmotic equi- cause a redistribution of small ions, so that the concentra- librium (see Chapter 2). But the lat- added to an original total body water volume of 42 L, the ter depends on the amount of solute present and the osmo- new total body water volume is 44 L. This fact follows from the definition of the term con- so the new osmolality at equilibrium is (7,980 3,990 centration: concentration amount/volume; hence, volume mOsm)/44 kg 272 mOsm/kg H2O. The main osmotically active ICF at equilibrium, calculated by solving the equation, 272 solute in cells is K ; therefore, a loss of cell K will cause mOsm/kg H2O volume 7,980 mOsm, is 29. From these cal- motically active solute in the ECF is Na ; therefore, a gain culations, we conclude that two thirds of the added water or loss of Na from the body will cause the ECF volume to ends up in the cell compartment and one third stays in the swell or shrink, respectively.

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S2 These proteins are disrupted in the group of genetic dis- eases collectively called muscular dystrophy 25 mg benadryl with mastercard, and their lack or malfunction leads to muscle degeneration and weakness and death (see Clinical Focus Box 8 generic 25 mg benadryl. Polymyositis is an inflammatory disorder that produces Myosin filament damage to several or many muscles (Clinical Focus Box 8 buy discount benadryl 25mg. The progressive muscle weakness in polymyositis usu- ally develops more rapidly than in muscular dystrophy cheap benadryl 25mg. New York: Springer-Verlag benadryl 25mg low price, tween the surface membrane and contractile filaments. In several forms of mus- these diseases is Duchenne’s muscular dystrophy cular dystrophy, both laminin and dystrophin are lacking (DMD) (also called pseudohypertrophic MD), which is an or defective. X-linked hereditary disease affecting mostly male children A disease as common and devastating as DMD has long (1 of 3,500 live male births). The recent identifica- gressive muscular weakness during the growing years, be- tion of three animals—dog, cat, and mouse—in which ge- coming apparent by age 4. A characteristic enlargement of netically similar conditions occur promises to offer signifi- the affected muscles, especially the calf muscles, is due to cant new opportunities for study. The manifestation of the a gradual degeneration and necrosis of muscle fibers and defect is different in each of the three animals (and also dif- their replacement by fibrous and fatty tissue. The mdx most sufferers are no longer ambulatory, and death usu- mouse, although it lacks dystrophin, does not suffer the ally occurs by the late teens or early twenties. Re- rious defects are in skeletal muscle, but smooth and car- search is underway to identify dystrophin-related proteins diac muscle are affected as well, and many patients suffer that may help compensate for the major defect. A related (and cause of their rapid growth, are ideal for studying the nor- rarer) disease, Becker’s muscular dystrophy (BMD), mal expression and function of dystrophin. Progress has has similar symptoms but is less severe; BMD patients of- been made in transplanting normal muscle cells into mdx ten survive into adulthood. Some six other rarer forms of mice, where they have expressed the dystrophin protein. A Using the genetic technique of chromosome mapping gene expressing a truncated form of dystrophin, called (using linkage analysis and positional cloning), re- utrophin, has been inserted into mice using transgenic searchers have localized the gene responsible for both methods and has corrected the myopathy. DMD and BMD to the p21 region of the X chromosome, The mdx dog, which suffers a more severe and human- and the gene itself has been cloned. It is a large gene of like form of the disease, offers an opportunity to test new some 2. About shows prominent muscle fiber hypertrophy, a poorly un- one third of DMD cases are due to new mutations and the derstood phenomenon in the human disease. Taking ad- other two thirds to sex-linked transmission of the defective vantage of the differences among these models promises gene. The BMD gene is a less severely damaged allele of to shed light on many missing aspects of our understand- the DMD gene. The product of the DMD gene is dystrophin, a large pro- tein that is absent in the muscles of DMD patients. The function of dy- References strophin in normal muscle appears to be that of a Burkin DJ, Kaufman SJ. The alpha7beta1 integrin in mus- cytoskeletal component associated with the inside surface cle development and disease. The childhood muscular dystrophies: most important of these is laminin 2, a protein associated Making order out of chaos. A skeletal muscle fiber is surrounded on its outer sur- gitudinal elements terminate in a system of terminal cister- face by an electrically excitable cell membrane supported nae (or lateral sacs). These contain a protein, calsequestrin, by an external meshwork of fine fibrous material. Together that weakly binds calcium, and most of the stored calcium these layers form the cell’s surface coat, the sarcolemma. Although they traverse other set of membranes called the sarcoplasmic reticulum the muscle fiber, T tubules do not open into its interior. The SR many types of muscles, T tubules extend into the muscle is specially adapted for the uptake, storage, and release of fiber at the level of the Z line, while in others they penetrate calcium ions, which are critical in controlling the processes in the region of the junction between the A and I bands. Within each sarcomere, the association of a T tubule and the two terminal cisternae at its SR consists of two distinct portions. The longitudinal ele- sides is called a triad, a structure important in linking mem- ment forms a system of hollow sheets and tubes that are brane action potentials to muscle contraction. Children (about 20% of cases) and electrical activity of the affected muscle, as measured by adults may both be affected.

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If the magnitude of the vector is decreased purchase benadryl 25 mg with mastercard, them that is less than that between A and B and greater than the voltage decreases order benadryl 25mg with amex. This is also true of other combina- tions of points cheap benadryl 25 mg free shipping, such as A and C benadryl 25mg for sale, B and D purchase 25 mg benadryl amex, and D and F. Voltage differences exist in all cases and are determined by the relative influences of the positive and negative ends of edges of a dish of salt solution in which the dipole can be the dipole. What the electrodes instead of the electrode being changed rela- would happen if the dipole were to change its orientation tive to the dipole. In each posi- tion, the dipole sets up current fields similar to those shown in Figure 13. The voltage measured depends on how the electrodes are positioned relative to those currents. These imaginary ex- periments illustrate two characteristics of a dipole that de- termine the voltage measured at distant points in a volume conductor: direction of the dipole relative to the measuring points and magnitude (voltage) of the dipole; this is an- other way of saying that a dipole is a vector. Portions of the ECG Are Associated With Electrical Activity in Specific Cardiac Regions We can use this analysis of a dipole in a volume conductor to rationalize the waveforms of the ECG. Of course, the ac- tual case of the heart located in the chest is not as simple as the dipole in the tub of salt solution for two main reasons. First, excitation of the heart does not create one dipole; in- FIGURE 13. We will focus current flows from the positive to the negative poles (See text with the net dipole emerging as an average of all the indi- for details. Second, the body is not a homogeneous vol- 226 PART IV BLOOD AND CARDIOVASCULAR PHYSIOLOGY ume conductor. The most significant problem is that the Consider the voltage changes produced by a two-di- lungs are full of air, not salt solution. Despite these prob- mensional model in which the body serves as a volume con- lems, the model is useful in an initial understanding of the ductor and the heart generates a collection of changing generation of the ECG. An electrocardiographic recorder (a At rest, myocardial cells have a negative charge inside voltmeter) is connected between points A and B (lead I, see and a positive charge outside the cell membrane. By convention, when point A is positive relative to depolarize, the depolarized cells become negative on the point B, the ECG is deflected upward, and when B is posi- outside, whereas the cells in the region ahead of the de- tive relative to A, downward deflection results. The lengths of the arrows are proportional to cause all cells are negative on the outside. When the cells the magnitude (voltage) of the net dipole, which is related in a given region depolarize during normal excitation, to the mass of myocardium generating the net dipole. The depolar- colored arrows show the magnitude of the dipole compo- ized portion constitutes the negative side, and the yet-to- nent that is parallel to the line between points A and B (the be-depolarized portion constitutes the positive side of the recorder electrodes); this component determines the volt- dipole. The tub of salt solution is analogous to the rest of age that will be recorded. With electrodes located at various points around the The P Wave and Atrial Depolarization. The net dipole generated by this excitation has a magnitude proportional to the mass of the atrial mus- cle involved and a direction indicated by the solid arrow. The head of the arrow points toward the positive end of the dipole, where the atrial muscle is not yet depolarized. The negative end of the dipole is located at the tail of the arrow, where depolarization has already occurred. Point A is, therefore, positive relative to point B, and there will be an upward deflection of the ECG as determined by the mag- nitude and direction of the dipole. Once the atria are com- pletely depolarized, no voltage difference exists between A and B, and the voltage recording returns to 0. The voltage change associated with atrial excitation appears on the ECG as the P wave. Af- ter the P wave, the ECG returns to the baseline present be- k fore the P wave. The ECG is said to be isoelectric when there is no deflection from the baseline established before the P wave.

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