We've previously shown that supplemental oxygen (O2) reduces cardiac output and raises systemic vascular resistance in congestive heart failure (CHF) patients. In the present report we examined the effects of 100% O2 on forearm vascular resistance after 10 min of forearm circulatory arrest (FCA) in 8 normals (study 1). FCA is a potent vasodilator stimulus. Forearm flow (Q), (plethysmography; ml-min '-100 ml') and R (blood pressure + Q) were measured 5 sec after releasing FCA and every 15 sec for 3 min. O2 raised the minimum R (from 1.7 to 2.4, p<.02) and increased the rate of rise of R towards baseline. In study 2, we examined whether "peripheral abnormalities" as might be seen in CHF would enhance the O2 effect. The high sympathetic tone of CHF was simulated by lower body negative pressure (LBNP, -30 mmHg); the edema of CHF by forearm congestion (90 mmHg arm cuff inflation 5 min before initiating FCA). R was measured in 7 normals in a control state (A), with LBNP (B), with LBNP + forearm congestion (C), and when O2 was added to C (D). D increased minimum R and the rate of rise of R towards baseline (compared to the other 3 conditions). When the results of study 1 were compared to D in study 2, we noted that limb congestion and LBNP enhanced the O2 effect (R: interaction p<,0001, Q: interaction p<,0001). Thus O2 has a detrimental circulatory effect that may be important in CHF. Limb congestion and increased sympathetic tone enhance this effect.
|State||Published - 1996|