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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。
In this study, acute myocardial ischemia caused by left ventricular branch of coronary heart in ligation of the right coronary artery. The results showed that not only ischemic myocardium obvious electrophysiological changes in the non-ischemic area also electrophysiological changes, the latter mainly for a wide range of non-ischemic area effective refractory period (ERP) showed a mild general extension, and Ischemic margins together form a refractory period and transitional bands. This electrophysiological disorder tends to induce the development of defibrinated arrhythmias. Increasing the concentration of several phenolics in circulating blood does not mimic the electrophysiological changes in the non-ischemic area. Irritation and peripheral nerve repair Rui can prolong the ERP in the case of natural heart rhythm, but it can not prolong ERP in the case of fixed heart rhythm. Tip electrophysiological changes in non-ischemic area is not due to myocardial ischemia caused by increased sympathetic or vagal tone, and may have other reasons.