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离体兔心循环式血液灌注９０ｍｉｎ，随着灌注时间延长，心肌肌酸磷酸激酶释放量、冠脉流量及冠脉阻力均无明显变化；灌注过程中无室性心律失常发生；灌注９０ｍｉｎ的心肌含水量与非灌注组比较，无显著差异，说明该模型的稳定性较好。心肌缺血１５ｍｉｎ后，再灌注５ｍｉｎ时，血中丙二醛含量和肌酸磷酸激酶释放量有所增加；随着再灌注时间延长，冠脉流量逐渐减少，冠脉阻力进行性增高；再灌注期间室性心律失常的发生率明显高于非缺血组；再灌注的心肌含水量也明显而于非缺血组。可见，此种缺血再灌注离体兔心模型，能较好地反映心肌缺血再灌注损伤引起的病理生理变化。
Cardiac circulation blood perfusion 90min, with prolonged perfusion, myocardial creatine phosphokinase release, coronary flow and coronary resistance were no significant changes; no ventricular arrhythmia during perfusion; myocardial perfusion 90min There was no significant difference between the water content and the non-perfusion group, indicating that the stability of the model is better. Myocardial ischemia 15min, reperfusion 5min, the blood MDA and creatine phosphokinase release increased; as the reperfusion time, coronary flow decreased, coronary resistance increased; reperfusion Ventricular arrhythmia during the incidence was significantly higher than the non-ischemic group; reperfusion myocardial water content was significantly in the non-ischemic group. Can be seen that such an ischemia-reperfusion rabbit heart model can better reflect the myocardial ischemia-reperfusion injury caused by the pathophysiological changes.