Elevated Oxygen Tension Inhibits Flow-Induced Dilation of Skeletal Muscle Arterioles

Abstract

The purpose of this study was to determine if elevated oxygen tension affects flow-induced dilation of in situ skeletal muscle arterioles. Cremaster muscle preparations from Sprague-Dawley rats were superfused with physiological salt solution (PSS) and viewed via television microscopy. A video micrometer was used to measure changes in arteriolar diameter in response to the increase in flow produced by occlusion of a parallel branch from the parent arteriole. Erythrocyte velocity was measured with an optical Doppler velocimeter. The superfusate PO2 was altered by changing the oxygen concentration of the equilibration gas between 0 and 21% O2. Elevation of superfusate PO2 to 10% O2 and 21% O2 significantly decreased arteriolar diameter compared to the control diameter during 0% O2 superfusion. Increases in arteriolar diameter during parallel arteriolar occlusion were reduced as superfusate PO2 was elevated. However, elevated PO2 had no significant effect on erythrocyte velocity through the perfused daughter vessel, either prior to or during parallel occlusion. As a result, blood flow through the dilating vessel was reduced with elevated PO2. As a result of the reduced arteriolar diameter, wall shear rate in the perfused daughter vessel was increased with elevated PO2, both prior to and during parallel occlusion. These observations demonstrate that elevated PO2 can override flow-induced vasodilation in the skeletal muscle microcirculation, leading to the persistence of an elevated wall shear rate.