Metabolic hyperemia in canine gut

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Abstract
Blood flow through a trunk of the superior mesenteric artery (MBF) supplying a long ileal segment, arteriovenous oxygen content difference [(A-V)O2], the fraction of radiolabeled microspheres distributed to the mucosal-submucosal compartment of the gut wall (FBF) and the clearance of 86Rb were measured in anesthetized dogs. Oxygen uptake (VO2) and permeability-surface (PS) product were calculated. Perfusion of the gut lumen with an isomotic solution of glucose in saline increased MBF 9%, (A-V)O2 15% and VO2 26%. Perfusion of the lumen with isosmotic L-alanine in saline produced similar changes. Perfusion of the lumen with hyperosmotic mannitol in saline increased MBF 18%, VO2 10% and FBF 17%, but decreased (A-V)O2 8%. Intra-arterial infusion of prostacyclin and glucagon also increased MBF, VO2 and FBF while decreasing (A-V)O2. PS product was increased 18% by isosmotic glucose in saline, 11% by hyperosmotic mannitol in saline and 16% by intra-arterial infusion of glucagon. Active cotransport of glucose or L-alanine with Na in the gut apparently prompts a metabolic hyperemia in which most of the augmented blood flow passes through newly opened capillaries, thereby enhancing oxygen extraction. By contrast, intra-arterial vasodilator drugs and hyperosmotic mannitol solutions in the gut lumen prompt hyperemic responses in which much of the augmented blood flow fails to perfuse such capillaries.