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DIAG 2725 Control of Special Circulations

DIAG 2725 Control of Special Circulations - TABLE 4—7...

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Unformatted text preview: TABLE 4—7. CHAPTER 4 [itamnscuni Plummet l51 Control of Special Circulations Circulation 1 Local Metabolic Control l Vasoactive Metabolites Sympathetic Control ‘ Mechanical Effects ___ l -M _ Coronary Most important Hypoxia i Least important Mechanical compression mechanism Adenosine l mechanism 1 during systole Cerebral Most important C02 Least important increases in intracraniai mechanism li‘ mechanism pressure decrease cerebral blood flow Skeletal muscle Most important Lactate Most important Muscular activity mechanism during Ki mechanism at rcsl compresses blood vessels exercise Adenosine (or. receptors, vasoconstriction; [$2 l receptors, vasodilation) 1 Skin Least important — Most important _. mechanism mechanism for temperature regulation (or; receptors, vasoconstriction) -_M . .7 1 Pulmonary Most importnai Hypoxia vasoconstricts ‘ Least important Lung inflation mechanism mechanism F» M Renal Most important —— Least important ——~ mechanism (myogenic; mechanism tubuloglomerular feedback) WM compression causes a brief period of occlusion and reduction of blood flow. When the period of occlu— sion is over (Le, systole is over), reactive hyperemia occurs to increase blood flow and 02 delivery and to repay the 02 debt that was incurred during the compression Cerebral Circulation The cerebral circulation is controlled almost en— tirely by local metabolites and exhibits autoregula— iion and active and reactive hyperemia. The most important local vasodilator in the cerebral circula— tion is C02 (or H"), An increase in cerebral FCOZ (producing an increase in H* concentration and a decrease in pH) causes vasodilation of the cerebral arterioles, which results in an increase in blood flow to assist in removal of the excess C02. It is interesting that many circulating vasoactive substances do nor affect the cerebral circulation be— cause their large molecular size prevents them from crossing the blood-brain barrier. Pulmonary Circulation The regulation of pulmonary circulation is dis— cussed fully in Chapter 5, Briefly, the pulmonary circulation is controlled by local metabolites, pri— marily by 02. The effect of 02 on pulmonary arterio— lar resistance is the exact opposite of its effect in other vascular beds: In the pulmonary circulation, hypoxia causes vasoconstriction. This seemingly counterintuitive effect of 02 also is explained in Chapter 5. Briefly, regions of hypoxia in the lung cause local vasoconstriction, which effectively shunts blood away from poorly ventilated areas where the blood flow would be “wasted” and toward well—ventilated areas where gas exchange can occur. Renul Circulation The regulation of renal blood flow is discussed in detail in Chapter 6. Briefly, renal blood flow is tightly autoregulated so that flow remains constant even when renal perfusion pressure changes. Renal autoregulation is independent of sympathetic in— nervation, and it is retained even when the kidney is denervated (eg, in a transplanted kidney). Auto— regulation is presumed to result from a combination of the myogenic properties of the renal arterioles and iubuloglomerular feedback (see Chapter 6). Skeletal Muscle Circulation Blood flow to skeletal muscle is controlled both by local metabolites and by sympathetic innerva- tion of its vascular smooth muscle. incidentally, the degree of vasoconstriction of skeletal muscle arterie oles is a major determinant of TPR because the mass of skeletal muscle is so large, compared with that of other organs. 0 At rest, blood flow to skeletal muscle is regu— lated primarily by its sympathetic innervation Vascular smooth muscle in the arterioles of skeletal muscle is densely innervated by sympa— thetic nerve fibers. Some fibers are vasocon— stricting (or1 receptors), and others are vasodi— lating ([32 receptors and muscarinic receptors). Thus, activation of on receptors causes vasocon— ...
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