Kryzhanovskiĭ G N, Pivovarov Iu I
Biull Eksp Biol Med. 1982 May;93(5):26-9.
It was shown in experiments on random-bred rats that the creation of the generator of pathologically enhanced excitation (GPEE) in the anterior amygdaline nucleus causes abnormalities of cardiac rhythm (bradysystole). These effects are realized via the vagus nerves. Discharges of the epileptic activity in the GPEE correlate with breaks of electric activity in the vagus (the central terminal) and cardiac complex loss. Coagulation of the GPEE area in the amygdala and brain cooling which entails the disappearance of GPEE activity lead to the recovery of normal cardiac rhythm. The data obtained are discussed from the standpoint of the general concepts of the role of the central hyperactive determinant structures in the pathology of visceral function regulation.
在对随机繁殖大鼠的实验中发现，在前杏仁核中创建病理性增强兴奋发生器（GPEE）会导致心律异常（心动过缓）。这些效应是通过迷走神经实现的。GPEE中的癫痫活动放电与迷走神经（中枢末梢）电活动的中断和心脏复合波的消失相关。杏仁核中GPEE区域的凝固以及导致GPEE活动消失的脑冷却会导致正常心律的恢复。从中枢过度活跃决定因素结构在内脏功能调节病理学中的作用的一般概念的角度讨论了所获得的数据。
