Effects of supplemental oxygen on forearm vasodilation in humans

Abstract

Crawford, Paul, Peter A. Good, Eric Gutierrez, Joshua H. Feinberg, John P. Boehmer, David H. Silber, and Lawrence I. Sinoway.Effects of supplemental oxygen on forearm vasodilation in humans. J. Appl. Physiol. 82(5): 1601–1606, 1997.—Supplemental O2 reduces cardiac output and raises systemic vascular resistance in congestive heart failure. In this study, 100% O2 was given to normal subjects and peak forearm flow was measured. In experiment 1, 100% O2 reduced blood flow and increased resistance after 10 min of forearm ischemia (flow 56.7 ± 7.9 vs. 47.8 ± 6.7 ml ⋅ min−1 ⋅ 100 ml−1; P < 0.02; vascular resistance 1.7 ± 0.2 vs. 2.4 ± 0.4 mmHg ⋅ min ⋅ 100 ml ⋅ ml−1; P < 0.03). In experiment 2, lower body negative pressure (LBNP; −30 mmHg) and venous congestion (VC) simulated the high sympathetic tone and edema of congestive heart failure. Postischemic forearm flow and resistance were measured under four conditions: room air breathing (RA); LBNP+RA; RA+LBNP+VC; and 100% O2+LBNP+VC. LBNP and VC did not lower peak flow. However, O2raised minimal resistance (2.3 ± 0.4 RA; 2.8 ± 0.5 O2+LBNP+VC, P < 0.04). When O2 alone ( experiment 1) was compared with O2+LBNP+VC ( experiment 2), no effect of LBNP+VC on peak flow or minimum resistance was noted, although the return rate of flow and resistance toward baseline was increased. O2 reduces peak forearm flow even in the presence of LBNP and VC.