Richardson D W, Kontos H A, Raper A J, Patterson J L
J Clin Invest. 1967 Jan;46(1):77-85. doi: 10.1172/JCI105513.
In 17 healthy men, beta-adrenergic blockade reduced significantly the tachycardia and the elevation of cardiac output associated with inhalation of 7.5% oxygen for 7 to 10 minutes. Hypoxia did not increase plasma concentrations of epinephrine or norepinephrine in six subjects. Furthermore, blockade of alpha and beta receptors in the forearm did not modify the vasodilation in the forearm induced by hypoxia, providing pharmacologic evidence that hypoxia of the degree and duration used was not associated with an increase in the concentrations of circulating catecholamines in man. Part of the increase in cardiac output and heart rate during acute hypoxia in man is produced by stimulation of beta-adrenergic receptors, probably by cardiac sympathetic nerves. The mechanism of the vasodilation in the forearm during hypoxia remains uncertain.
在17名健康男性中,β-肾上腺素能阻滞显著降低了因吸入7.5%氧气7至10分钟所引起的心动过速和心输出量升高。在6名受试者中,低氧并未增加血浆肾上腺素或去甲肾上腺素浓度。此外,前臂α和β受体的阻滞并未改变低氧引起的前臂血管舒张,这提供了药理学证据,表明所用程度和持续时间的低氧与人体循环儿茶酚胺浓度升高无关。人体急性低氧期间心输出量和心率增加的部分原因可能是心脏交感神经刺激β-肾上腺素能受体所致。低氧期间前臂血管舒张的机制仍不确定。