兔急性心肌缺血时心肌非缺血区的电生理学变化

Electrophysiological Changes in the Non-ischemic Zone during Acute Myocardial Ischemia in Rabbits

本研究通过结扎家免在位心脏冠状动脉左室支造成急性心肌缺血。结果显示不仅缺血区心肌有明显的电生理变化，在非缺血区亦有电生理变化，后者主要表现为广泛的非缺血区域有效不应期（ERP）呈普遍轻度延长，与缺血边缘带共同形成一个不应期离散和跃变带。这种电生理紊乱易于诱发折反性心律失常的产生。升高循环血中几条酚胺浓度并不能模拟非缺血区的电生理变化。刺激连走神经外周瑞虽可使自然心律情况下的ERP延长，但却不能使固定心律情况下的ERP延长。提示非缺血区的电生理学变化并非由于心肌缺血时交感或迷走神经张力增高所致，而可能有其它原因。

The acute myocardial ischemis was achieved by ligating the lef ventricufar branch of coronary artery of insitu rabbit heart. In this model,we found that the effective refractory period (ERP)in the non-ischemic zone (NZ)prolonged,and the ERP in the peripheral ischemic zone(PZ)shortened significantly.Thereby a great ERP jump exists betwixt NZ and PZ. This ERP jump is in favourable,of the occurrance of re-entry arrhythmias. The intrarenous drip of epinephrine (0.1mg/kg) couldn't mimic the ERP changes in NZ. The efferent vagostimulation could prolong the ERP at natural heart rate,but couldn' t at fixed heart rate. The results suggest that the increasing in sympathetic or paraspopathetic tone is not responsible for the prolongation of ERP in NZ during acute myocardial ischemia.