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Division of Cardiology, The Milton S. Hershey Medical Center, The Pennsylvania State University, Hershey 17033; and Lebanon Veterans Affairs Medical Center, Lebanon, Pennsylvania 17042
Received 23 August 1996; accepted in final form 24 January 1997.
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 ml1;
P < 0.02; vascular resistance 1.7 ± 0.2 vs. 2.4 ± 0.4 mmHg · min · 100 ml · ml1;
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, O2
raised 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.
vascular resistance; lower body negative pressure; venous congestion
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