A model of the mesenteric circulation.

Abstract

A model of the mesenteric microcirculation is proposed that explains three observed variations in the hyperemic response of the small intestine to different dilator stimuli. The model assumes a two-component circulation in which one component delivers more than enough blood flow and oxygen to meet the metabolic demands of the resting tissue served by this "flow-independent component." The second portion, known as the "flow-limited component" delivers an insufficient blood supply for tissue needs and, therefore, restricts the metabolism of the parenchyma it serves. The three types of reported hyperemic responses are a) hyperemia induced by certain drugs, such as nifedipine and acetylcholine, in which case only the flow-limited component is dilated and one observes an increase in blood flow to the gut without any increase in intestinal oxygen consumption; b) hyperemia induced by stimulating active cotransport of nutrients from the intestinal lumen, in which case the tissue served by the flow-independent component increases its metabolism and oxygen demand, resulting in an increase in oxygen consumption that exceeds proportionately the increase in blood flow; and c) hyperemia induced by other vasodilator drugs, such as adenosine, in which case both vascular components are dilated and both blood flow and oxygen uptake are increased, but the increase in blood flow is proportionately greater than the increase in oxygen consumption.