van de Borne P, Mark A L, Montano N, Mion D, Somers V K
Department of Internal Medicine, University of Iowa, Iowa City 52242, USA.
Hypertension. 1997 Jun;29(6):1278-83. doi: 10.1161/01.hyp.29.6.1278.
Alcohol intake has been shown to worsen obstructive sleep apnea and increase nocturnal hypoxemia. The mechanisms of this action are unclear. Animal studies suggest that a reduction in chemoreflex sensitivity may be implicated. Using a double-blind, randomized, vehicle-controlled design, we tested the hypothesis that oral alcohol intake depresses chemoreflex sensitivity in humans. We examined the effects of oral alcohol intake (1.0 g/kg body wt) on blood pressure, heart rate, heart rate variability, muscle sympathetic nerve activity, forearm vascular resistance, and minute ventilation in 16 normal male subjects. Peripheral and central chemoreflex sensitivity were measured in response to hypoxia (n = 10) and hypercapnia (n = 6), respectively. Plasma alcohol increased from 0 to 23.2 +/- 1.5 mmol/L (107 +/- 7 mg/dL) at 60 minutes and 20.2 +/- 1 mmol/L (93 +/- 4 mg/dL) at 85 minutes after alcohol intake (P < .0001). Alcohol induced an increase in heart rate from 59 +/- 2 to 66 +/- 2 beats per minute (P < .01) and increased the ratio of low- to high-frequency variability of heart rate (P < .05). Although alcohol increased sympathetic nerve activity by up to 239 +/- 22% of baseline values (P < .01), forearm vascular resistance after alcohol was lower than that after vehicle (P < .05). Blood pressure did not increase compared with the vehicle session. Oxygen saturation during hypoxia after alcohol was 4 +/- 1% lower than it was during hypoxia after vehicle (P < .05) although arterial blood PO2 was unchanged. Alcohol did not affect the cardiovascular, sympathetic, or ventilatory responses to either hypoxia or hypercapnia. Acute increases in plasma alcohol increase heart rate and sympathetic nerve activity; blood pressure is not increased, probably because of vasodilator effects of alcohol. Alcohol does not alter chemoreflex responses to hypoxia or hypercapnia; thus, alterations in chemoreflex sensitivity are unlikely to explain the effects of alcohol on sleep apnea. Alcohol may reduce the affinity of hemoglobin for oxygen.
饮酒已被证明会加重阻塞性睡眠呼吸暂停并增加夜间低氧血症。这种作用的机制尚不清楚。动物研究表明，化学反射敏感性降低可能与之有关。我们采用双盲、随机、溶剂对照设计，检验了口服酒精会降低人体化学反射敏感性这一假设。我们研究了口服酒精（1.0克/千克体重）对16名正常男性受试者的血压、心率、心率变异性、肌肉交感神经活动、前臂血管阻力和分钟通气量的影响。分别针对低氧（n = 10）和高碳酸血症（n = 6）测量外周和中枢化学反射敏感性。饮酒后60分钟时血浆酒精浓度从0升至23.2±1.5毫摩尔/升（107±7毫克/分升），85分钟时升至20.2±1毫摩尔/升（93±4毫克/分升）（P <.0001）。酒精使心率从每分钟59±2次增加到66±2次（P <.01），并增加了心率低频与高频变异性的比值（P <.05）。尽管酒精使交感神经活动增加至基线值的239±22%（P <.01），但饮酒后的前臂血管阻力低于服用溶剂后的（P <.05）。与服用溶剂的时段相比，血压没有升高。尽管动脉血氧分压未变，但饮酒后低氧期间的氧饱和度比服用溶剂后低氧期间低4±1%（P <.05）。酒精对低氧或高碳酸血症的心血管、交感神经或通气反应没有影响。血浆酒精的急性升高会增加心率和交感神经活动；血压未升高，可能是因为酒精的血管舒张作用。酒精不会改变对低氧或高碳酸血症的化学反射反应；因此，化学反射敏感性的改变不太可能解释酒精对睡眠呼吸暂停的影响。酒精可能会降低血红蛋白对氧的亲和力。
