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目的评价糖尿病大鼠离体心脏缺血／再灌注后心脏功能的改变。方法链佐星(60mg／kg)诱导的糖尿病大鼠16只(D组),年龄匹配的健康雄性SD大鼠10只(C组),戊巴比妥钠(60mg／kg)麻醉后快速取出心脏,接上主动脉插管置于Langendorg装置上,Krebs-Henseleit缓冲液逆行灌注。平衡灌注20min,待心率(HR)及冠脉流量平稳后夹闭灌注道,进行全心缺血30min,复灌40min。持续监测心肌心电活动、左心室压峰值(LVPSP)、左室舒张末压(LVEDP)和左室压力最大上升／下降速率(±dp／dtmax),计算左室发展压(LVDP=LVPSP-LVEDP),用LVDP×HR(RDPP)表示左室作功。结果与C组相比,基础状态下,D组大鼠心脏HR减慢,LVDP、RDPP和±dp／dtmax降低,LVEDP升高(P<0.05或0.01);再灌注后HR、LVDP、RDPP、冠脉流出液、±dp／dtmax等心功能指标恢复百分率升高,肌酸激酶活性降低(P<0.05或0.01);心脏缺血-停搏时间延长。结论糖尿病心脏基础心功能损伤严重,但对缺血／再灌注的耐受性增强。
Objective To evaluate the changes of cardiac function in isolated rat hearts after ischemia / reperfusion. Methods Sixteen diabetic rats induced by streptozocin (60mg / kg), 10 healthy male SD rats (group C) and pentobarbital sodium (60mg / kg) were anesthetized and quickly removed Heart, aortic cannula placed on Langendorg device, Krebs-Henseleit buffer retrograde perfusion. Balance perfusion 20min, to be heart rate (HR) and coronary flow closed after clamping perfusion, the whole heart ischemia 30min, reperfusion 40min. The left ventricular pressure (LVPSP), left ventricular end-diastolic pressure (LVEDP) and left ventricular pressure (± dp / dtmax) were monitored continuously to measure the left ventricular pressure (LVDP = LVPSP-LVEDP ), LVDP × HR (RDPP) for left ventricular work. Results Compared with group C, the heart HR, the LVDP, RDPP and ± dp / dtmax were decreased and the LVEDP was increased (P <0.05 or 0.01). The HR, LVDP, Coronary effluent, ± dp / dtmax and other cardiac function indicators increased the percentage of recovery, decreased creatine kinase activity (P <0.05 or 0.01); heart ischemia-arrest time prolonged. Conclusions The basic cardiac function of diabetic heart is severely damaged, but its tolerance to ischemia / reperfusion is enhanced.