Reactive hyperemia and oxygen extraction in the feline small intestine.

Abstract

Arterial flow and O2 extraction were continuously measured from an in situ, denervated loop of cat ileum. Following release of arterial occlusion of varying time periods, O2 extraction decreased transiently, returning to control levels as the hyperemia subsided. The hyperemia may overcompensate in attempting to repay the O2 deficit; consequently, O2 extraction is depressed. In the pump-perfused preparation (constant flow), O2 extraction rose following the release of arterial occlusion, indicating a shift to O2 extraction as the mechanism for repaying the O2 deficit in the absence of hyperemia. Following venous occlusion, reactive hyperemia failed to develop in the majority of cats and, when present, was highly blunted. O2 extraction rose transiently suggesting that, as with constant flow, this is the mechanism of O2 debt repayment in the absence of hyperemia. With venous pressure elevation, a decrease in blood flow was coupled to an increase in O2 extraction that resulted in an overall increase in calculated O2 consumption; O2 extraction progressively increased for each level of venous pressure. Estimated O2 consumption following occlusion suggests a decrease in O2 demand during arterial occlusion and an increased demand during venous occlusion. During venous occlusion, the myogenic and metabolic control mechanisms would elicit opposite effects. The blunted hyperemic response observed may result from the net influence of both mechanisms acting in opposition, i.e., a myogenic influence modulated by a metabolic one.