Possible mechanisms for the initiation and maintenance of postprandial intestinal hyperemia

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Abstract
Postprandial intestinal hyperemia is a locally mediated vascular response to the presence of nutrients in the lumen. In this review we discuss the role of various constituents of chyme in the development of the hyperemia and possible mechanisms of action. The luminal contents that produce the hyperemia are digested products of food; undigested food or pancreatic enzymes have no effect. Micellar fatty acids are the most potent vasodilators, whereas amino acids at physiological concentrations have little effect on intestinal blood flow. However, by-products of protein digestion are as potent as those of carbohydrates in increasing the blood flow. Bile increases ileal but does not alter jejunal blood flow. In addition, bile enhances the glucose-induced hyperemia and renders fatty and amino acids vasoactive. The mechanisms by which bile exerts its effect on the vasoactivity of these nutrients are poorly understood. The intestinal hyperemic response to the presence of nutrients in the lumen is mediated by a variety of regulatory pathways that vary with the nutrient. Factors involved include tissue metabolic rate, metabolites, nutrient absorption, tissue osmolality, tissue oxygen tension, intestinal peptides such as neurotensin and vasoactive intestinal polypeptide, and paracrine substances such as prostaglandins and histamine. It is likely that the hyperemia results from the complex interplay of all these factors on the intestinal vascular smooth muscle. Extrinsic and intrinsic nerves play a minor role in nutrient-induced hyperemia.

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