七氟烷预处理对成年及幼年大鼠心肌缺血/再灌注损伤保护作用的对比研究

摘要

Aim To observe and contrast the cardioprotective effect of sevoflurane preconditioning on isolated adult and young rat hearts with ischemia reperfusion injury and explore its possible mechanism. Methods 36 adult male SD rats were randomly divided into 3 groups ( 12 each ): control group ( Shaml ).ischemia-reperfusion group ( I/R1 ). sevoflurane preconditioning group ( S1 ); 36 young male SD rats were randomly divided into 3 groups ( 12 each ): control group ( Sham2 ) , ischemia-reperfusion group ( I/R2 ) . sevoflurane preconditioning group ( S2 ). All hearts were linked to the Langendorff apparatus. Left ventricular end-diastolic pressure ( LVEDP ), Left ventricular developed pressure ( LVDP ), + dp/dtmax, Heart rate ( HR ) were recorded at the end of equilibration and 15 min of reperfusion. Cardiocyte apoptotic index and myocardial infarct size were measured with TUNEL and TTC staining method at 15 min and 60 min of reperfusion respectively. After 15 min of reperfusion , phosphoAkt and total Akt were determined by Western blot analysis. Results No differences in baseline hemodynamics were observed among the groups ( P ＞ 0. 05 ).Compared with group I/R1 ,group Sl resulted in a significantly improved functional recovery, had a significant increase in HR . LVDP, + dp/dtmax , a decrease in LVEDP and a significant decrease in IS( P＜ 0. 05 ) .Compared with group I/R2 , group S2 resulted in a significantly improved functional recovery, had a significant increase in HR, LVDP, + dp/dtmax , a decrease in LVEDP and a significant decrease in IS ( P ＜ 0. 05 ).Meanwhile, group S also markedly increased the expression of p-Akt compared with group I/R. Conclusiori IMAC sevoflurane preconditioning may effectively protect the hearts against ischemia-reperfusion injury in the adult and young isolated rat hearts by activating PI3 K/Akt signal pathway.%目的 观察比较七氟烷预处理对成年及幼年大鼠心肌缺血/再灌注损伤保护作用及可能机制.方法 36 只成年♂ SD 大鼠随机分为3组:对照组(sham 1组),缺血/再灌注组(I/R 1组),七氟烷预处理组(S 1组);36只幼年♂ SD大鼠随机分为3组:对照组(sham 2组),缺血/再灌注组(I/R 2组),七氟烷预处理组(S 2组).采用 Langendorff 离体大鼠心肌灌注模型.对照组,自然灌流120 min;缺血/再灌注组,平衡灌注30 min,缺血30 min,复灌60 min;七氟烷组,平衡灌注15 min,含七氟烷的K-H 液10 min,洗出5 min,缺血30 min,再灌注60 min.记录各组心脏在平衡末及复灌15 min的左室舒张末压(LVEDP)、左室发展压(LVDP)、左室压力升高或降低最大速率(±dp/dtmax)、心率(HR).复灌15 min时,TUNEL法检测凋亡细胞,免疫印迹法(Western blot)半定量检测p-Akt和总Akt的含量;复灌末TTC法计算心肌梗死面积百分比.结果 平衡灌注末各组间心功能指标(基础值)差异未见统计学意义(P>0.05).灌注结束时,S 1组较I/R 1组以及S 2组较I/R 2组心功能明显改善,心肌梗死面积减少和凋亡指数降低(P<0.05),同时p-Akt表达水平升高(P<0.05).结论 1 MAC的七氟烷预处理可能通过增强 Akt的磷酸化来减轻成年及幼年大鼠的心肌缺血/再灌注损伤.