刺激兔下丘脑室旁核诱发的心律失常与增压反应

在60只局麻与肌松剂制动的家兔,观察到用0.1—0.4mA,50Hz,1ms 的方波电刺激下丘脑室旁核(PV)能诱发频发性心律失常(包括室性与室上性期前收缩)及显著的动脉血压升高。与同侧的下丘脑外侧区(LHA)及腹内侧核(VMH)相比,刺激PV诱发期前收缩的次数更为频繁,增压反应幅度较大,且所需阈值亦较低。较低强度刺激LHA 在部分兔能引起血压下降与心率减慢,而PV 则一致地诱发增压反应。电刺激腓深神经能抑制刺激PV诱发的期前收缩,但在中脑中央灰质微量注射吗啡或电解毁损只能完全阻断刺激VMH诱发的期前收缩,而不能完全阻断PV诱发的期前收缩。这些结果提示,PV是下丘脑中诱发心律失常与血压增高的高反应区之一,并且可能具有不同于LHA或VMH的神经机制或下行神经通路。

THE ARRHYTHMIAS AND PRESSOR RESPONSE INDUCED BY STIMULATION OF THE PARAVENTRICULAR NUCLEUS OF THE HYPOTHALAMUS IN RABBITS

In 60 rabbits under local anesthesia and immobilization, extrasystoles andelevation of arterial blood pressure could be provoked by stimulation of the para-ventricular nucleus of the hypothalamus (PV) with 0. 1-0.4 mA, 50 Hz and1ms duration square wave current. The arrhythmias and accompanying pressorresponse were more pronounced during stimulation of PV than those produced bystimulation of the lateral hypothalamic area (LHA) and ventromedial hypothalamicnucleus (VMH). Stimulation of LHA with lower intensity induced a decreasein blood pressure and heart rate in some rabbits, but stimulation of PV alwaysprovoked elevation of blood pressure. Electrical stimulation of unilateral deepperoneal nerve could inhibit the arrhythmias induced by stimulation of PV. Micro-injection of morphine or electrolytic lesion of the central gray matter in mid-braincompletely abolished the arrhythmias induced by stimulation of VMH, but couldnot completely abolish those induced by PV stimulation. The results suggest thatPV is one of the areas in the hypothalamus of which stimulation induced severearrhythmias and marked pressor response. The mechanisms or descending neuralpathways of the arrhythmias induced by stimulation of PV may be different fromthose produced by stimulation of LHA and VMH.