兔下丘脑室旁核刺激引起的肾交感神经传出活动的抑制

本实验用家兔,氯醛糖及尿酯混合静脉麻醉,制动,人工呼吸,颈部分离出三对神经——迷走、窦及主动脉神经,以备实验中切断。记录股动脉压、肾交感神经传出性放电活动(RSED)及其频率幅度直方图。借助脑立体定向仪刺激下丘脑室旁核,当刺激较强时,在交感神经放电短暂增加之后,可引起血压升高及RSED抑制。这一抑制过程可分为两个时相:血压不变期间的初期抑制时相及与血压升高同时并存的后期抑制时相。实验发现RSED总抑制时程及后期抑制时程均与血压变动具有正相关关系,而初期抑制时程与血压变动无相关关系。切断压力感受性神经前后,虽初期抑制时程的均值无显著差异,但在切断压力感受性神经后,总抑制时程及后期抑制时程的均值大大缩短。当用较弱刺激施于室旁核时,可不引起血压变化,但仍能引起RSED抑制。这个抑制亦可因切断压力感受神经而显著缩短。上述实验结果表明:(1) 在中枢内存在着一个室旁核-肾交感传出系统的抑制机制;(2) 初期抑制来源于中枢性抑制机制,而后期抑制时相主要来源于压力感受性反射,但亦有中枢抑制机制的参与;(3) RSED的中枢抑制可能并不是兴奋后压抑,而是自室旁核至脊髓交感节前神经元的主动性抑制。

INHIBITION OF RENAL SYMPATHETIC EFFERENT ACTIVITIES INDUCED BY STIMULATION OF THE PARAVENTRICULAR NUCLEUS OF THE HYPOTHALAMUS(PVH) IN RABBITS

Experiments were performed on rabbits anesthetized with chloralose-urethane mixture, paralyzed with gallamine triethiodide, and ventilated artificially. Bilateral vagi, aortic and carotid sinus nerves were severed. Renal sympathetic efferent discharge (RSED) and its histogram were recorded, while the blood pressure (BP) of the femoral artery was monitored.When PVH was strongly stimulated, a transient increase of RSED was observed, which was followed by an inhibition of RSED. The inhibition of RSED was divided into two phases: the initial inhibitory phase without change in BP and the late inhibitory phase with an increase of BP. It was found that both the duration of total inhibition and the late, but not initial, inhibitory phase were positively correlated with the alterations of BP. When PVH was weakly stimulated, no change in BP was observed, but the inhibition of RSED still appeared. The inhibition duration was shortened remarkably following cutting of baroreceptor nerves. In some experiments, the RSED inhibition was not accompanied by a definite excitatory response. The present results indicate that 1) an inhibitory mechanism of PVH-renal sympathetic efferent system is present in the central nervous system; 2) the initial inhibitory phase of RSED originates from central mechanisms, while the late inhibitory phase is associated with the baroreceptor reflex and a direct action of the central nervous system; 3) the inhibition of RSED seems not to be a post-excitation depression, but an active inhibition exerted by the PVH on the spinal sympathetic preganglionic neurons.