While local venous outflow was measured in anesthetized dogs, various constituents of intestinal chyme were placed in the jejunal lumen to identify those responsible for postprandial intestinal hyperemia. Digested food and its supernatant increased local blood flow, whereas its precipitate, undigested food, and pancreatic enzymes did not. In the jejunum bile alone had no effect, but it markedly enhanced the hyperemic effect of digested food. Bile in the ileal lumen, however, increased local blood flow. At physiological postprandial concentrations in the jejunum, glucose, and micellar solutions of oleic acid and monoolein increased flow, but taurocholate and 16 common dietary amino acids did not. The hyperemic effect of lipids required the presence of taurocholate. Of the 16 amino acids, only Glu and Asp increased flow at 10 times the physiological concentrations (28 and 20 mM, respectively). The study indicates that the constituents of chyme responsible for postprandial intestinal hyperemia are the hydrolytic products of food, especially those of carbohydrates and fats and that bile plays an important role in the hyperemia.
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.
The relative contribution of dietary fat, protein, carbohydrate, and ethanol to postprandial intestinal hyperemia was assessed by comparing the vascular and metabolic effects of luminal placement of various solutions prepared from standard high -fat, high-protein, and high-carbohydrate test diets, corn oil, and ethanol in the jejunum of anesthetized dogs. The high-fat diet (45% fat, 18% protein, 29% carbohydrate) produced the greatest hyperemia (+30.4% of control), followed by high-protein (22% fat, 64% protein, 4% carbohydrate) (+24.1%) and high-carbohydrate (8% fat, 18% protein, 68% carbohydrate) (+18.2%) diets. When the fat content of the high-carbohydrate diet was raised to equal that of the high-protein diet, the two diets produced the same degree of hyperemia. All three diets produced a significantly greater hyperemia than the solutions containing the same amount of fat. All these dietary solutions increased intestinal oxygen consumption. Ethanol, however, increased blood flow without altering oxygen consumption. Thus, on weight basis, fat produces the greatest hyperemia, but the contribution of protein and carbohydrate to postprandial intestinal hyperemia cannot be considered as insignificant. The hyperemia results from a synergistic effect of all three dietary components.
Vascular effects of raising local arterial concentration of pentagastrin (2-1,500ng/ml), secretin (0.2-150mU/ml), and cholecystokinin (0.2-150mU/ml) in the duodenum, jejunum, heart, kidney, forelimb, spleen, and the skin and muscle of the forelimb were studied in 54 anesthetized dogs. Secretin produced similar vasodilation in all organs. The minimal increment in local blood secretin concentration for vasodilation ("concentration requirement") was between 7 and 32 mU/ml. Pentagastrin produced vasodilation only in the duodenum and jejunum and the concentration requirement was between 25 and 50 ng/ml. Cholecystokinin did not affect vascular resistance of the forelimb, skin, or muscle. In the heart, kidney, and spleen, cholecystokinin produced vasodilation but the concentration requirement was above 21-33 mU/ml. In contrast, vasodilation in the duodenum and jejunum appeared when cholecystokinin concentration was increased by only 2.5 mU/ml. Furthermore, almost all its vasodilating effect occurred below an increment of 10 mU/ml. Comparison of our data with the reported cardiovascular adjustments and blood concentration of gastrointestinal hormones following a meal suggests that cholecystokinin may contribute to postprandial intestinal hyperemia.
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