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目的:采用Langendorff离体心脏灌注模型,研究异氟烷预处理对离体大鼠心肌缺血再灌注损伤的影响。方法:24只SD大鼠随机分为4组,每组6只,分别为缺血再灌注损伤组(IR组)、异氟烷预处理1组(IsoP 1组)、异氟烷预处理2组(IsoP 2组)和异氟烷预处理3组(IsoP 3组)。监测复灌后心功能恢复情况、冠脉流出液中磷酸肌酸激酶(CK)、乳酸脱氨酶(LDH)的释放量和心肌存活面积的变化。结果:复灌期间3组IsoP心脏各对应时间点的LVEDP均显著低于对照组(P<0.05~<0.01);再灌注30 min时IsoP各组LVDP的恢复均高于IR组(P<0.05),IsoP3组±dp／dtmax在再灌注30 min时的恢复百分比均高于IR组(P<0.05),IsoP1组+dp／dt max高于IR组(P<0.05);复灌后异氟烷预处理组各时间点的CK、LDH释放量均低于IR组(P<0.01);IsoP2组、IsoP1组和IsoP3组心肌存活面积百分比均高于IR组(P<0.01);预处理各组之间比较无显著性差异(P>0.05)。结论:IsoP对大鼠离体缺血再灌注心肌有保护作用,可以显著减轻心肌细胞的损伤,改善心功能,增加心肌存活面积。
OBJECTIVE: To study the effects of isoflurane preconditioning on myocardial ischemia-reperfusion injury in isolated rat hearts using Langendorff’s in vitro perfusion model. Methods: Twenty-four Sprague-Dawley rats were randomly divided into 4 groups (6 rats in each group): Ischemia reperfusion injury group (IR group), Isoflurane preconditioning group (IsoP 1 group), Isoflurane preconditioning group Group (IsoP 2 group) and isoflurane pretreatment group 3 (IsoP 3 group). The recovery of cardiac function after cardiopulmonary resuscitation was monitored. The release of phosphorylated creatine kinase (CK) and lactate deaminase (LDH) and the area of myocardial viability in coronary effluent were measured. Results: The LVEDP in each group at different time points during the reperfusion period was significantly lower than that in the control group (P <0.05 ~ <0.01). The LVDP recovery in each group was higher than that in the IR group at 30 min after reperfusion (P <0.05). The percentage of ± dp / dtmax of IsoP3 group at 30 min after reperfusion was higher than that of IR group (P <0.05) and IsoP1 + dp / dt max group was higher than that of IR group The release of CK and LDH in the alkane pretreatment group was lower than that in the IR group at each time point (P <0.01). The percentages of myocardial viability in the IsoP2, IsoP1 and IsoP3 groups were higher than those in the IR group (P <0.01) There was no significant difference between groups (P> 0.05). CONCLUSION: IsoP has a protective effect on myocardial ischemia-reperfusion injury in rats, which can significantly reduce the damage of myocardial cells, improve cardiac function and increase the area of myocardial viability.