Nutrient stimulation of mesenteric blood flow - implications for older critically ill patients

Figure 1 Factors involved in the regulation of postprandial blood pressure. (1) ingestion of a meal, with a greater carbohydrate load results in a greater postprandial hypotensive response; (2) Meal-induced gastric distension from the meal triggers stretch receptors in the stomach wall, increasing sympathetic nerve outflow; (3) gastric content is emptied into the small intestine, and, in response to the nutrient in the small intestine; (4, 5) gastrointestinal peptides are secreted from the small intestine (e.g., GLP-1 and GLP-2, glucagon-like peptide-1 and 2; GIP, glucose insulinotropic polypeptide); (6) gastrointestinal peptides stimulate mesenteric vessel dilation; (7) this results in reduced circulating blood volume and the reduction in blood pressure is detected by baroreceptors; (8a) the “gastrovascular” and baroreceptor reflexes stimulate sympathetic activity to increase heart rate (HR), stroke volume (SV) and thus cardiac output (CO) to maintain postprandial blood pressure; (8b) skeletal vasculature constricts to decrease peripheral blood flow. ¹These factors are affected by age and have been identified as potential pathophysiological mechanisms of postprandial hypotension. Figure drawn by Ms. T. Nguyen. GIP: Glucose-dependent insulinotropic peptide; GLP: Glucagon-like peptide.