BLOOD-FLOW TO THE CANINE DIAPHRAGM DURING HEMORRHAGIC-SHOCK

Abstract

Previous studies have shown impairment of diaphragm function during shock. It is possible that the mechanism for this is decreased diaphragm perfusion, which leads to decreased function because of limitation of oxygen transport. In order to examine the degree to which oxygen transport is limited during shock, we measured the changes in blood flow to an oxygen consumption of the diaphragm during controlled hemorrhage. Blood flow through the left phrenic artery (.ovrhdot.Qdi) was measured with an electromagnetic flow probe as systemic arterial pressure (Pa) was decreased. The Pa-.ovrhdot.Qdi relationship was found to be linear with slope of approximately 0.145 ml/torr/min, and extrapolated pressure at zero flow of approximately 40 torr in normal control subjects. Inspiratory loading and infusion of isoproterenol led to a parallel shift in the Pa-.ovrhdot.Qdi curve such that there was a decrease in the extrapolated pressure at zero flow to 9 to 13 torr. Infusion of dopamine led to a parallel shift of the Pa-.ovrhdot.Qdi curve such that there was an increase in the extrapolated pressure at zero flow from approximately 34 to approximately 45 torr. In the normal control subjects, there was a decrease in oxygen consumption associated with the decrease in .ovrhdot.Qdi, but this was not true for either loading or isoproterenol. We conclude that during hypotension, blood flow to the diaphragm decreases. However, the diaphragm retains the ability to increase its blood flow in response to metabolic or pharmacologic stimuli. This is done primarily by a parallel shift in the pressure-flow relationship, which may represent a change in the critical closing pressure of the phrenic vasculature.