电刺激兔下丘脑背内侧核及室旁核诱发的缺血性心律失常

MYOCARDIAL ISCHEMIC ARRHYTHMIAS ELICITED BY ELECTRIC STIMULATION TO DORSOMEDIAL NUCLEUS AND PARAVENTRICULAR NUCLEUS OF HYPOTHALAMUS IN RABBITS

本实验在迷走神经切断和未切断的麻醉兔上观察比较了单独电刺激下丘脑室旁核(PVH)、下丘脑背内侧核(DMH)及合并刺激PVH与DMH所诱发的缺血性心电变化(ST偏移)、定性心律失常(室性早搏)及升压反应。结果提示:DMH是诱发缺血性心电变化的高反应区,PVH则是诱发室性心律失常、血压升高的高反应区,PVH与DMH合并刺激能使两者反应叠加。迷走神经完整组与迷走神经切断组的结果比较提示,迷走神经的存在使刺激DMH及PVH+DMH诱发的缺血性ST偏移减轻,表明迷走神经对心肌缺血有保护作用,但对诱发室性早搏及升压反应的影响不明显。

Experiments were performend on vagotomized as well as on vagus intact anaesthetized rab- bits, observation and comparison were made on ST-segment deflection, ventricular premature con- traction(VPC) and pressor response induced simple or simultaneous stimulation of dorsomedial hypothalamic nucleus (DMH) and paraventricular hypothalamic nucleus (PVH). The results suggest that DMH is one of the areas with high response in eliciting ischemic ECG-ST segment change, and PVH is one of the key areas involved in the production of VPC and pressor re- sponse. When PVH and DMH were stimulated simultaneously, the two above mentioned re- sponses were augmented cooperatively. As prominent myocardial ischemic arrhythmia can be provoked in vagotomized rabbits, comparison between the results in vagus intact rabbits and those in vagotomized rabbits indicates that the presence of vagus nerve can reduce ST-segment deflec- tion induced by DMH and PVH+DMH stimulation, suggesting vagus might possess a protective action on neurogenic myocardial ischemia, but no significant influence on VPC and pressor re- sponse induced by stimulation of hypothalamus.