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Modification by Beta-Adrenergic Blockade of the Circulatory Responses to Acute Hypoxia in Man

机译:通过β-肾上腺素能阻断对人急性缺氧循环反应的修饰。

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摘要

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.
机译:在17名健康男性中,β-肾上腺素能阻滞显着降低了与吸入7.5%氧气相关的心动过速和心输出量升高,持续7至10分钟。低氧血症并未增加6名受试者的肾上腺素或去甲肾上腺素的血浆浓度。此外,前臂中α和β受体的阻滞不会改变由缺氧引起的前臂中的血管舒张,提供了药理学证据,表明所用程度和持续时间的缺氧与人体内循环儿茶酚胺浓度的升高无关。 β-肾上腺素能受体的刺激,可能是心脏交感神经的刺激,导致人急性缺氧时心输出量和心率增加。缺氧期间前臂血管舒张的机制仍不确定。

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