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.