Evans R G, Hayes I P, Ludbrook J
University of Melbourne Department of Surgery, Parkville, Victoria, Australia.
Eur J Pharmacol. 1992 Jun 5;216(2):265-72. doi: 10.1016/0014-2999(92)90369-f.
In conscious rabbits an inferior vena caval cuff was progressively inflated so cardiac output fell at a constant approximately 8% of its baseline value. There was a biphasic haemodynamic response, consisting of an initial compensatory phase during which there was progressive systemic vasoconstriction and tachycardia, followed by a decompensatory phase in which systemic vasoconstriction failed abruptly, blood pressure plummeted and heart rate declined. We tested the effects on the haemodynamic response of prior 4th ventricular, and in some cases intravenous, infusions of saline, yohimbine, clonidine, yohimbine plus clonidine, and bunazosin. From the results we conclude that a yohimbine-sensitive mechanism in the brainstem, possibly alpha 2-adrenoceptor-mediated, may be an essential element of the cardiac receptor-mediated decompensatory phase of acute central hypovolaemia, but does not contribute to the arterial baroreflex-mediated compensatory phase.
在清醒的兔子身上,逐渐给下腔静脉套囊充气,使心输出量以恒定的约为其基线值8%的幅度下降。存在双相血流动力学反应,包括初始的代偿期,在此期间会出现逐渐的全身血管收缩和心动过速,随后是失代偿期,在此期间全身血管收缩突然失效,血压骤降且心率下降。我们测试了先前向第四脑室以及在某些情况下静脉内输注生理盐水、育亨宾、可乐定、育亨宾加可乐定和布那唑嗪对血流动力学反应的影响。根据结果我们得出结论,脑干中一种对育亨宾敏感的机制,可能由α2 -肾上腺素能受体介导,可能是急性中枢性低血容量时心脏受体介导的失代偿期的一个关键要素,但对动脉压力反射介导的代偿期没有作用。