摘要
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。
Some isolated rabbit hearts were perfused for 90min,no significant changes were found in creatine phosphokinase(CPK),coronary flow and coronary vascular resistance,and ventricular arrhythmias did not occur.Compared with the unperfused group,the change of myocardial water content after perfusion of 90 min was insignificant.These results indicated that the perfusion model was stable.After 15 min's myocardial ischemia and 5 min's reperfusion,the malondialdehyde(MDA) and CPK content in plasma began to increase.When perfused for 30 and 60 min,MDA and CPK increased significantly.With the prolongation of reperfusion time,the coronary flow decreased and coronary vascular resistance increased gradually.The water content in myocardium was higher in the ischemic rabbits reperfused for 60 min than in the unischemic group.During reperfusion,the incidence of ventricular arrhythmias was also higher than in the unischemic group.The results indicated that obviously,lipid peroxidation had happened and induced a series of pathologic damage.This model,therefore,can satisfactorily show that damage caused by myocardial ischemic-reperfusion induces pathologic changes.
关键词
心肌缺血
再灌注损伤
动物模型
疾病模型
isolated heart
myocardial reperfusion injury
coronary circulation
vascular resistance
creatine phosphokinase
arrhythmia
malondialdehyde
