Supplemental O-2 reduces cardiac output and raises systemic vascular r
esistance in congestive heart failure. In this study, 100% O-2 was giv
en to normal subjects and peak forearm flow was measured. In experimen
t 1, 100% O-2 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).10
0 ml(-1); P < 0.02; vascular resistance 1.7 +/- 0.2 vs. 2.4 +/- 0.4 mm
Hg.min.100 ml.ml(-1); P < 0.03). In experiment 2, lower body negative
pressure (LBNP; -30 mmHg) and venous congestion (VC) simulated the hig
h 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% O-2+LBNP+VC. LBNP a
nd VC did not lower peak flow. However, O-2 raised minimal resistance
(2.3 +/- 0.4 RA; 2.8 +/- 0.5 O-2+LBNP+VC, P < 0.04). When O-2 alone (e
xperiment 1) was compared with O-2+LBNP+VC (experiment 2), no effect o
f LBNP+VC on peak flow or minimum resistance was noted, although the r
eturn rate of flow and resistance toward baseline was increased. O-2 r
educes peak forearm flow even in the presence of LBNP and VC.