Flow is locally controlled in certain vascular beds by a process termed "autoregulation"36 (Fig. 6.5). By definition, autoregulation is the ability of an organ to maintain a relatively constant blood flow in the presence of changes in arterial perfusion pressure. The kidneys, brain, and heart are organs that exhibit autoregulation, whereas the skin and lungs are organs with minimal ability for autoregulation.
A schematic diagram of the changes in blood flow to an organ over a wide range of perfusion pressures in the presence or absence of autoregulation is shown in Fig. 6.5. In the absence of autoregulation, pressure-flow relationships are linear, and increases in driving pressure lead to direct increases in perfusion. An autoregulatory curve is characterised by a large range of pressures during which flow remains relatively constant. vasodilation is achieved at lower perfusion pressures by relaxation of smooth muscle, and vascular smooth muscle constriction occurs at higher perfusion pressures to maintain constant flow. The ability to autoregulate assumes that a set point of basal vasomotor tone allows for this dilatation or constriction to occur. Flow varies directly with pressure when the limits of autoregulation are exceeded. In regional beds that are maximally vasodilated, for example by a drug such as dipyridamole, the process of autoregulation is eliminated and flow is directly dependent on driving pressure (Fig. 6.5).37 Autoregulation of blood flow is affected to only a small extent by neural and humoral influences. Experimental investigations have demonstrated that the ability to autoregulate flow is largely an intrinsic property and even occurs in denervated tissues. As a result of this, autoregulation is considered to be a local phenomenon affected primarily by the active tone of arterioles.
Two major theories have been advanced to explain the mechanism of autoregulation.36 The first of these is the myogenic theory which suggests that elevations in perfusion pressure lead to stretch and increases in tension of vascular smooth muscle cells. The distension of the smooth muscle directly causes vasoconstriction to maintain flow constant despite an increased driving pressure. Conversely, at low perfusion pressures, there is less muscle tension, vascular smooth muscle cells relax, and blood flow is maintained despite the decrease in pressure. Therefore, the degree of tension smooth muscle is exposed to is the stimulus for regulation, and subsequent constriction/dilatation serves as the mediator of this mechanism. Autoregulation is advantageous to vital organs such as the brain, heart, and kidneys because blood flow is optimised even during periods of hypo- and hypertension. It has also been proposed that the myogenic mechanism protects capillaries from excessively high blood pressures which could cause these fragile vessels to rupture.
The metabolic theory of autoregulation is based on the state of oxygenation in the surrounding tissues. A reduction in perfusion pressure leads to a decrease in blood flow and tissue PO2 with concomitant increases in tissue PCO2 and other metabolites related to normal cellular activity (for example, lactic acid, adenosine, K+, and H+). The reduced PO2, increased PCO2, and vasodilator substances directly cause arteriolar relaxation, and blood flow increases. High perfusion pressures supply ample O2, remove CO2, and wash out vasodilators leading to vasoconstriction and decreases in tissue blood flow. Regardless of the validity of either the myogenic or the metabolic theory, both are based on the premise that autoregulation of tissue flow is a negative feedback mechanism, maintaining constancy of arterial flow during large changes in perfusion pressure.
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