【摘要】 目的:研究Na+通道阻滞剂河豚毒素(Tetrodotoxin,TTX)停搏液对离体大鼠心肌α肌动蛋白(α-actin)的影响及其机制。方法:20只Wistar大鼠随机均分入St.Thomas-2停博组(STH-2组),TTX停博组(TTX组),建立离体心脏Langendorff和Neely灌注模型,搏动稳定后,灌注30min后停搏60min,再灌注60min,观察各组心脏停搏前后的心率(HR)、冠状动脉流量(CAF)、左心室收缩末期压力(LVESP)和压力变化速率(±dp/dt)的恢复率,采用免疫组化检测钙蛋白酶(Calpain),免疫组化和Westernblot检测α-actin的分布及量的变化。结果:恢复灌注后,TTX停搏组的各项心功能恢复率明显优于STH-2组(P<0.01,P<0.05),STH-2组的calpain分布紊乱,表达量明显增多(P<0.01);α-actin分布紊乱,表达量明显减少(P<0.01)。结论:以TTX阻断Na+通道为特点的心脏停搏液对大鼠心肌缺血-再灌注损伤(Myocardial ischemia/reperfusion injury,MIRI)时的α-actin及心功能的保护作用优于STH-2停搏液,其机制可能是直接或者间接的减少激活calpain引起的。更多还原

【Abstract】 Objective:To investigate the effects of cardioplegia with Na+ channel inhibitor tetrodotoxin(TTX)on myocardialα-actin of isolated rat hearts and its and mechanism. Methods:Langendorff and Neely perfusion models were steadily established,then the rat hearts(10 hearts in each group)were arrested by cardioplegia(St. Thomas No. 2 solution,STH-2) in group STH-2,and by cardioplegia(TTX)in group TTX respectively after perfusion for 30 minutes. These arrested hearts were remained for 60 minutes and then underwent reperfusion for 60 minutes.Pre-ischemia and post-ischemia hemodynamic parameters of the rat hearts(HR,CAF,LVESP and recovery rate of pressure change speed)were studied and changes of calpain was detected by immunohistochemistry and myocardialα-actin by Western blot and immunohistochemistry. Results:There was no differences between two groups before myocardial ischemia.But the recovery of myocardial hemodynamic parameters during reperfusoin in group TTX was better than that in group STH-2(P<0.01 or P<0.05).Distribution of calpain was disordered and the expression increased(P<0.01),and distribution of α-actin was disordered,but the expression decreased significantly(P<0.01)in group STH-2. Conclusion:The protective effects of cardioplegia with Na+ channel inhibitor TTX on myocardial α-actin and myocardial hemodynamic parameters were better than those in group STH-2 during myocardial ischemia/reperfusion injuries(MIRI)on isolated rat hearts. Mechanism of protection effects was caused probably by activating calpain directly or indirectly.更多还原