Influence of acute alcohol ingestion on sympathetic neural responses to orthostatic stress in humans
Influence of acute alcohol ingestion on sympathetic neural responses to orthostatic stress in humans
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DOI：
10.1152/ajpendo.00674.2010
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发表时间：
2011-05-01
影响因子：
5.1
通讯作者：
Larson, Robert A.
中科院分区：
文献类型：
--
作者：
Carter, Jason R.;Stream, Sarah F.;Larson, Robert A.
急性酒精摄入对人体立位应激交感神经反应的影响。Am J Physiol Endocrinol Metab 300：E771-E778，2011.首次发表于2011年2月15日; doi：10.1152/ajpendo.00674.2010.-据报道，急性饮酒可降低直立位挑战期间的平均动脉压（MAP），这一反应可能导致酒精介导的晕厥。肌肉交感神经活动（MSNA）增加，在直立应激，以帮助维持MAP，但酒精对MSNA反应在直立应激的影响尚未确定。我们假设酒精摄入会减弱动脉血压和MSNA对下体负压（LBNP）的反应。在进行性LBNP（-5、-10、-15、-20、-30和-40 mmHg; 3分钟/阶段）期间记录30名受试者（年龄24 ± 1岁）的MAP、MSNA和心率（HR）。在初始进行性LBNP（治疗前）后，受试者饮用酒精（0.8 g乙醇/kg体重; n = 15）或安慰剂（n = 15），并重复进行性LBNP（治疗后）。酒精增加静息心率（59 +/- 2至65 +/- 2次/分，P < 0.05），MSNA（13 +/- 3至19 +/- 4次爆发/分钟，P < 0.05），MSNA爆发潜伏期（1，313 +/- 16至1，350 +/- 17 ms，P < 0.05）与安慰剂相比（组x治疗相互作用，P <0.05）。在进行性LBNP期间，酒精后观察到MAP显著降低，但安慰剂后未观察到（组x时间x治疗，P < 0.05）。相比之下，MSNA和HR在所有LBNP方案中均增加，但试验或组间无差异。然而，酒精改变了MSNA爆发潜伏期反应进行性LBNP。总之，在进行性LBNP期间，MSNA缺乏对动脉血压较大下降的调整，加上交感神经爆发潜伏期反应的改变，表明酒精会减弱MSNA对直立性应激的反应。
Influence of acute alcohol ingestion on sympathetic neural responses to orthostatic stress in humans. Am J Physiol Endocrinol Metab 300: E771-E778, 2011. First published February 15, 2011; doi: 10.1152/ajpendo.00674.2010.-Acute alcohol consumption is reported to decrease mean arterial pressure (MAP) during orthostatic challenge, a response that may contribute to alcohol-mediated syncope. Muscle sympathetic nerve activity (MSNA) increases during orthostatic stress to help maintain MAP, yet the effects of alcohol on MSNA responses during orthostatic stress have not been determined. We hypothesized that alcohol ingestion would blunt arterial blood pressure and MSNA responses to lower body negative pressure (LBNP). MAP, MSNA, and heart rate (HR) were recorded during progressive LBNP (-5, -10, -15, -20, -30, and -40 mmHg; 3 min/stage) in 30 subjects (age 24 +/- 1 yr). After an initial progressive LBNP (pretreatment), subjects consumed either alcohol (0.8 g ethanol/kg body mass; n = 15) or placebo (n = 15), and progressive LBNP was repeated (posttreatment). Alcohol increased resting HR (59 +/- 2 to 65 +/- 2 beats/min, P < 0.05), MSNA (13 +/- 3 to 19 +/- 4 bursts/min, P < 0.05), and MSNA burst latency (1,313 +/- 16 to 1,350 +/- 17 ms, P < 0.05) compared with placebo (group x treatment interactions, P < 0.05). During progressive LBNP, a pronounced decrease in MAP was observed after alcohol but not placebo (group x time x treatment, P < 0.05). In contrast, MSNA and HR increased during all LBNP protocols, but there were no differences between trials or groups. However, alcohol altered MSNA burst latency response to progressive LBNP. In conclusion, the lack of MSNA adjustment to a larger drop in arterial blood pressure during progressive LBNP, coupled with altered sympathetic burst latency responses, suggests that alcohol blunts MSNA responses to orthostatic stress.