Armour J A, Randall W C
Can J Physiol Pharmacol. 1985 Sep;63(9):1122-32. doi: 10.1139/y85-184.
Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.
电刺激犬的迷走交感神经复合体或心肺神经,无论全身动脉压有无改变,均可引发多种负性变时性和变力性心脏反应。在这种刺激停止后的即刻,可能会出现“反跳”性心动过速、心脏一个或多个区域的变力性增强超过对照值,和(或)全身动脉压升高。普萘洛尔或同侧慢性交感神经切除术可消除这些“反跳”现象。有人提出,犬心血管系统的“迷走神经”刺激后“反跳”主要是迷走交感神经复合体或心肺神经中存在的交感神经元件被激活的结果。