Zhang X, Abdel-Rahman A A, Wooles W R
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, North Carolina 27858-4354.
Hypertension. 1989 Sep;14(3):282-92. doi: 10.1161/01.hyp.14.3.282.
We investigated the acute hemodynamic effects of ethanol microinjection into brain areas known to influence cardiovascular function and reflexes. In chloralose-anesthetized rats, ethanol had no effect on baseline mean arterial pressure, heart rate, or sympathetic efferent discharge when microinjected into the nucleus tractus solitarius, the dorsal motor nucleus of the vagus, the rostral ventrolateral medulla, or the posterior hypothalamus. On the other hand, ethanol microinjection into the anterior hypothalamus caused a site-dependent pressor effect and an increase in sympathetic efferent discharge. Baroreceptor heart rate response but not sympathetic efferent discharge response was impaired by ethanol microinjection into the nucleus tractus solitarius, the dorsal motor nucleus of the vagus, and the rostral ventrolateral medulla, suggesting that ethanol involves one or more of these areas in its inhibitory effect on baroreceptor heart rate response and that ethanol has a selective action on baroreceptor reflex control of heart rate. The findings that 1) the effect was dose dependent and 2) injection of ethanol outside of, or an equal volume of cerebrospinal fluid into, the nucleus tractus solitarius had no effect on the response strongly suggest that the observed effect on baroreceptor heart rate response was ethanol mediated. Ethanol microinjection into the dorsal motor nucleus of the vagus impaired the heart rate response, thus raising the possibility that leakage of ethanol to that area from the nucleus tractus solitarius might have contributed to its effect. These findings show that ethanol has a pressor and sympathoexcitatory site of action within the anterior hypothalamus and that it selectively impairs baroreceptor heart rate response via a central site of action; the mechanisms by which ethanol produces these effects remain to be elucidated.
我们研究了向已知影响心血管功能和反射的脑区微量注射乙醇的急性血流动力学效应。在氯醛糖麻醉的大鼠中，当向孤束核、迷走神经背运动核、延髓头端腹外侧区或下丘脑后部微量注射乙醇时，乙醇对基线平均动脉压、心率或交感神经传出放电没有影响。另一方面，向前下丘脑微量注射乙醇会引起部位依赖性升压效应，并增加交感神经传出放电。向孤束核、迷走神经背运动核和延髓头端腹外侧区微量注射乙醇会损害压力感受器心率反应，但不会损害交感神经传出放电反应，这表明乙醇在其对压力感受器心率反应的抑制作用中涉及这些区域中的一个或多个，并且乙醇对压力感受器反射性心率控制具有选择性作用。以下发现：1）效应呈剂量依赖性；2）在孤束核外注射乙醇或向孤束核注射等量脑脊液对反应没有影响，强烈表明观察到的对压力感受器心率反应的效应是由乙醇介导的。向迷走神经背运动核微量注射乙醇会损害心率反应，因此增加了乙醇从孤束核泄漏到该区域可能导致其效应的可能性。这些发现表明，乙醇在前下丘脑内具有升压和交感兴奋作用位点，并且它通过中枢作用位点选择性地损害压力感受器心率反应；乙醇产生这些效应的机制仍有待阐明。
