缓冲神经在刺激兔下丘脑诱发室性期前收缩中的作用

1.静脉注射氰化钾(0.3mg/kg)可引起血压升高和室性心律失常,并能使刺激下丘脑诱发的室性期前收缩增多。去除双侧窦神经后,上述现象消失。2.刺激降压神经时,刺激下丘脑诱发的室性期前收缩显著减少。3.切断双侧缓冲神经后短时内,刺激下丘脑诱发的室性期前收缩极度增多,并且不易被躯体传入冲动所抑制。二小时后,这种室性期前收缩减少,且可为刺激腓深神经所抑制。4.电刺激延髓中线区不仅可以降低血压,而且能减弱刺激下丘脑诱发的升压反应、抑制刺激下丘脑诱发的室性期前收缩。损毁该区后,刺激腓深神经不再能抑制刺激下丘脑诱发的室性期前收缩。5.上述结果表明:化学感受性反射能易化刺激下丘脑诱发的室性期前收缩,而压力感受性反射可以抑制这种室性期前收缩,但躯体传入冲动对这种心律失常的抑制作用并不依赖于缓冲神经的存在,而有赖于延髓中线核群的完整性。

ACTION OF BUFFER NERVES ON THE VENTRICULAR EXTRASYSTOLES INDUCED BY HYPOTHALAMIC STIMULATION IN RABBITS

Experiments were carried out on 48 rabbits under light urethane-chloraloseand local anaesthesia.The blood pressure and EGG were recorded on the poly-graph.Intravenous injection of KCN(0.3 mg/kg)could induce ventricular extrasys-toles and facilitate the hypothalamic stimulation-induced ventricular extrasystoles(HVEs).This phenomenon was abolished after bilateral section of the carotidsinus nerves.HVEs could be diminished by stimulation of the depressor nerve,and increasedmarkedly accompanied with the rising of blood pressure after the buffer nerveswere cut.Two hours later when the blood pressure returned to the control level,these extrasystoles diminished and could be inhibited by deep peroneal nervestimulation.HVEs were also decreased by stimulation of an area at midline of themedulla oblongata 0-2 mm rostral to the obex.After destroying this area,theinhibitory effect of deep peroneal nerve stimulation on these extrasystoles wasabolished.It is concluded that HVEs can be facilitated by chemoreceptor excitationand inhibited by baroreceptor excitation.The inhibitory effect of deep somaticnerve stimulation on the HVEs does not depend upon the buffer nerves,but isrelated to the function of medial medulla oblongata.