Zhou Z Z, Wurster R D, Jones S B
Loyola University of Chicago, Stritch School of Medicine, Department of Physiology, Maywood, Illinois 60153.
J Auton Nerv Syst. 1992 Jun 1;39(1):1-12. doi: 10.1016/0165-1838(92)90245-c.
We examined the contributions of arterial baroreceptor reflexes in mediating sympathoadrenal activation during endotoxicosis. Conscious rats with chronic sinoaortic denervation (SAD) or sham-operation (SHAM) were subject to endotoxin treatment (5 mg/kg, i.v.). Hemodynamic responses, renal sympathetic nerve activity (RSNA) and plasma catecholamines were assessed at different times post endotoxin infusion. In both SAD and sham groups, intravenous endotoxin injection induced a rapid and significant sympathoadrenal activation, as indicated by a parallel elevation of RSNA and plasma catecholamines. Such activation peaked 15-30 min following endotoxin and was sustained throughout the 2-3 h protocol. The early response of the sympathoadrenal system to endotoxin is more profound in SAD rats compared to sham rats. We propose that the afferent neural input from arterial baroreceptors is not essential in mediating sympathoadrenal activation during sepsis. The elimination of feedback buffering mechanisms with SAD may account for the augmented sympathetic response seen in SAD animals.
我们研究了动脉压力感受器反射在内毒素血症介导交感肾上腺激活过程中的作用。对慢性去窦主动脉神经（SAD）或假手术（SHAM）的清醒大鼠进行内毒素治疗（5mg/kg，静脉注射）。在内毒素输注后的不同时间评估血流动力学反应、肾交感神经活动（RSNA）和血浆儿茶酚胺。在SAD组和假手术组中，静脉注射内毒素均诱导了快速且显著的交感肾上腺激活，表现为RSNA和血浆儿茶酚胺平行升高。这种激活在内毒素注射后15 - 30分钟达到峰值，并在整个2 - 3小时的实验过程中持续存在。与假手术大鼠相比，SAD大鼠交感肾上腺系统对内毒素的早期反应更为强烈。我们认为，在脓毒症期间，来自动脉压力感受器的传入神经输入对于介导交感肾上腺激活并非必不可少。SAD消除了反馈缓冲机制，这可能解释了在SAD动物中观察到的交感反应增强现象。
