Reactive hyperemia and oxygen extraction in the feline small intestine.

Arterial flow and oxygen extraction were continuously measured from an in situ, denervated loop of cat ileum. Following release of arterial occlusion of varying time periods, oxygen extraction decreased transiently, returning to control levels as the hyperemia subsided. These results suggest that the hyperemia overcompensates in attempting to repay the oxygen deficit and, consequently, oxygen extraction is depressed. In the pump-perfused preparation (constant flow), oxygen extraction rose following the release of arterial occlusion indicating a shift to oxygen extraction as the mechanism for repaying the oxygen 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. In addition, oxygen extraction rose transiently suggesting that, as with constant flow, this is the mechanism of oxygen debt repayment in the absence of hyperemia. With venous pressure elevation, a decrease in blood flow was coupled to an increase in oxygen extraction that resulted in an overall increase in calculated oxygen consumption; oxygen extraction progressively increased for each level of venous pressure. Estimated oxygen consumption following occlusion suggests a decrease in oxygen demand during arterial occlusion and an increased demand during venous occlusion. However, during venous occlusion, the myogenic and metabolic control mechanisms would elicit opposite effects. Based on the results obtained following venous occlusion, we suggest that the blunted hyperemic response observed results from the net influence of both mechanisms acting in opposition, that is, a myogenic influence modulated by a metabolic one.