Hyperemia, active

Active hyperemia. The increase in blood flow caused by enhanced tissue activity is referred to as active hyperemia. Assuming a constant blood pressure, then according to Ohm s law (Q = AP/R), the increase in blood flow is the result of a decrease in local vascular resistance. Tissue metabolism causes several local chemical changes that can mediate this metabolic vasodilation. These include ... 

Resistance in the arterioles of the working muscles is regulated locally. As discussed previously, active hyperemia results in production of several factors that cause metabolic vasodilation. Exercising muscles generate COz, H+ and K+ ions, heat, and adenosine. The vasodilator effect of these locally produced substances overrides the vasoconstrictor effect of the sympathetic system in the muscle. As a result, local vascular resistance is decreased. The combination of increased driving pressure and decreased local vascular resistance causes an increase in blood flow to the working muscles. 

Table V-l. Properties of Active Hyperemia and Congestion (Passive Hyperemia)...

Within physiological limits, blood flow depends upon secretion, and an increase in secretion causes an increase in blood flow by means of the mechanisms responsible for active hyperemia. 

A number of plants of the cucumber family yield these drastic drugs. They are of complex composition, each containing several active principles, resinous and alkaloidal. They produce continuous watery stools, with intense irritation and hyperemia (Sollmann, 1944). 

Pseudoephedrine is an orally active sympathomimetic amine exerting its decongestant action by acting directly on a-adrenergic receptors in the respiratory tract mucosa producing vasoconstriction resulting in shrinkage of swollen nasal mucous membranes, reduction of tissue hyperemia, edema, and nasal... 

Reactive hyperemia is the increased blood flow over normal values that is seen following a period of interruption of flow. Reactive hyperemia is attenuated by glibenclamide in both coronary and skeletal muscle vascular beds, suggesting a role of K xp channels in this phenomenon (Clayton et al., 1992). Activation of K xp channels under these conditions may occur through a buildup of vasodilator metabolites (e.g., adenosine) during the period of occlusion. 

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