Post-occlusive reactive hyperemia and skeletal muscle capillary hemodynamics.

Abstract

In female Sprague-Dawley rats (n=6), the spinotrapezius muscle was exteriorized for evaluation of capillary hemodynamics pre-occlusion, 5min of feed artery occlusion (Occ), and 5min of reperfusion (Post-Occ). There were no differences in mean arterial pressure (MAP) or capillary diameter (Dc) between pre-occlusion and post-occlusion (P>0.05). During 30s of PORH, capillary fRBC was increased (pre: 59±4 vs. 30s-post: 77±2 cells/s; P<0.05) and VRBC was not changed (pre: 300±24 vs. 30s post: 322±25μm/s; P>0.05). Capillary hematocrit (Hctcap) was unchanged across the pre- to post-occlusion conditions (P>0.05). Following occlusion, there was a 20-30% decrease in the number of capillaries supporting RBC flow at 30s and 300s-post occlusion (pre: 92±2%; 30s-post: 66±3%; 300s-post: 72±6%; both P<0.05). Short-term feed artery occlusion (i.e. 5min) resulted in a more heterogeneous capillary flow profile with the presence of capillary no-reflow, decreasing the percentage of capillaries supporting RBC flow. A complex interaction between myogenic and metabolic mechanisms at the arteriolar level may play a role in the capillary no-reflow with PORH. Measurements at the level of the conduit artery mask significant alterations in blood flow distribution in the microcirculation.