Wang W, Brändle M, Zucker I H
Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha 68198-4575.
Hypertension. 1993 May;21(5):687-94. doi: 10.1161/01.hyp.21.5.687.
It has been shown that alcohol administration causes baroreceptor reflex inhibition. The site of action of alcohol could reside anywhere within the baroreceptor reflex arc. Therefore, the goal of this study was to determine the effects of acute administration of alcohol on carotid sinus baroreceptor discharge characteristics. In pentobarbital-anesthetized dogs, the carotid sinus was isolated and perfused. Single unit baroreceptor discharge was recorded from the carotid sinus nerve along with carotid sinus diameter using sonomicrometry. Carotid sinus pressure-baroreceptor discharge and carotid sinus pressure-diameter curves were constructed. Perfusion of the carotid sinus with alcohol (100 mmol/L) significantly decreased the pressure threshold from 91.1 +/- 2.8 to 86.4 +/- 2.9 mm Hg (p < 0.05) and increased the peak discharge rate from 45.8 +/- 3.4 to 52.8 +/- 3.6 spikes per second (p < 0.01). The same phenomenon was seen during perfusion of the carotid sinus with acetaldehyde (2.5 mmol/L) but was not seen during perfusion with acetate (2.5 mmol/L). During perfusion of the carotid sinus with alcohol, the carotid sinus pressure-carotid sinus diameter relation did not change. The baroreceptor sensitization induced by alcohol is not an endothelium-dependent mechanism, because endothelial denudation did not block this alcohol-induced effect. Measurement of the duration of postexcitatory depression of carotid sinus baroreceptors, which is related to Na+,K(+)-ATPase activity, showed that perfusion of the carotid sinus with alcohol or acetaldehyde significantly reduced the duration of postexcitatory depression, indicating that the alcohol- and acetaldehyde-induced effect on baroreceptor discharge is most likely mediated by an inhibition of Na+,K(+)-ATPase.(ABSTRACT TRUNCATED AT 250 WORDS)
业已表明，给予酒精会导致压力感受器反射抑制。酒精的作用位点可能存在于压力感受器反射弧内的任何位置。因此，本研究的目的是确定急性给予酒精对颈动脉窦压力感受器放电特性的影响。在戊巴比妥麻醉的犬中，分离并灌注颈动脉窦。使用超声测量法记录来自颈动脉窦神经的单个单位压力感受器放电以及颈动脉窦直径。构建了颈动脉窦压力-压力感受器放电和颈动脉窦压力-直径曲线。用酒精（100 mmol/L）灌注颈动脉窦可使压力阈值从91.1±2.8显著降至86.4±2.9 mmHg（p<0.05），并使峰值放电率从每秒45.8±3.4增加至52.8±3.6个脉冲（p<0.01）。在用乙醛（2.5 mmol/L）灌注颈动脉窦时也观察到了相同现象，但在用乙酸盐（2.5 mmol/L）灌注时未观察到。在用酒精灌注颈动脉窦期间，颈动脉窦压力-颈动脉窦直径关系未改变。酒精诱导的压力感受器敏化不是一种内皮依赖性机制，因为内皮剥脱并未阻断这种酒精诱导的效应。测量与Na +,K(+)-ATP酶活性相关的颈动脉窦压力感受器兴奋后抑制的持续时间表明，用酒精或乙醛灌注颈动脉窦可显著缩短兴奋后抑制的持续时间，这表明酒精和乙醛对压力感受器放电的诱导作用很可能是由对Na +,K(+)-ATP酶的抑制介导的。（摘要截短至250字）
