Intrinsic regulation of intestinal oxygenation in the anesthetized dog

Abstract

To help prevent imbalances between cellular O2 supply and demand, intrinsic modulation of intestinal blood flow and O2 extraction is linked to the metabolic requirements of the gut parenchyma. Flow and O2 extraction responses to changes in intestinal O2 demand, perfusion pressure and venous outflow pressure were examined. At low initial arteriovenous O2 difference [(a-v)O2 .ltoreq. 5 vol%], augmentation of O2 extraction is the primary mechanism utilized by the intestine to accelerate tissue O2 supply following feeding or infusion of dinitrophenol. Functional hyperemia played an important role when the initial (a-v)O2 or O2 uptake were high. In the fasted state, autoregulatory vasodilation allows intestinal flow to recover 40-50% following a small reduction of perfusion pressure: tissue O2 uptake remains unaltered because O2 extraction rises to the appropriate level. For larger reductions in perfusion pressure the intensity of flow autoregulation is diminished and elevated O2 extraction is the primary mechanism used to maintain adequate intestinal oxygenation. In the fed state, intestinal flow actually rises when perfusion pressure is lowered to 80-90% of normal. This superregulation of intestinal flow is not due to an enhanced myogenic sensitivity; instillation of food into the gut lumen diminished or abolished the vasoconstrictor response to venous hypertension.