Decreased supply-dependent oxygen consumption in the skeletal muscle of the spontaneously hypertensive rat during acute hypoxia

The purpose of this study was to correlate microvascular oxygen delivery (DO2) and consumption (VO2) in the skeletal muscle of spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats (WKY) with hemodynamics during acute hypoxia. We expected greater abnormalities in central and microvascular hemodynamics during hypoxic induced shock in the SHR compared with the WKY due to microvascular rarefaction. The inspired oxygen fraction (FiO(2)) was lowered from 0.21 to 0.15, 0.1, 0.08, and 0.05 in anesthetized, mechanically ventilated rats. Lactate and base deficit values were similar for both groups at 0.21 and 0.15 FiO(2), but higher in SHR at lower FiO(2). Baseline aortic blood flow (SHR, 56.2 +/- 4.0 mL min(-1); WKY, 61.8 +/- 5.3 mL min(-1)) and systemic DO2 (SHR, 9.02 +/- 0.82 mL min(-1); WKY, 9.32 +/- 0.54 mL min(-1)) increased similarly when FiO(2) was lowered to 0.15. Further reductions in FiO(2) caused lower aortic flow and systemic DO2 in the SHR than WKY at 0.08 and 0.05 FiO(2). Spinotrapezius blood flow increased from baseline (SHR, 24.8 +/- 1.8 nL s(-1); WKY, 22.7 +/- 2.1 nL s(-1)) in both groups when FiO(2) was reduced to 0.15; further reductions in FiO(2) decreased blood flow in both groups, with lower values in the SHR group at 0.1 and 0.08 FiO(2). The SHR group demonstrated higher venous oxygen saturation at low values of FiO(2) compared with WKY. This reduced oxygen extraction in SHR resulted in a lower supply-dependent VO2 at low values of spinotrapezius DO2, perhaps attributed to arteriolar thickening and rarefaction seen in chronic hypertension.