急性心肌梗塞的治疗效果有赖于再灌注期间缺血心肌功能的恢复。再灌注能加重缺血心肌的损伤。再灌注过程中,心肌细胞内Ca~(2+)积蓄将引起多种细胞内改变最终导致不可逆损伤。以往的研究表明,Ca~(2+)慢通道阻滞剂未能阻止再灌注时细胞内 Ca~(2+)积蓄,大量的 Ca~(2+)进入心肌细胞并非通过 Ca~(2+)慢 The therapeutic effect of acute myocardial infarction depends on the recovery of ischemic myocardial function during reperfusion. Reperfusion can increase the damage of ischemic myocardium. During reperfusion, Ca2 + accumulation in cardiomyocytes will lead to a variety of intracellular changes that eventually lead to irreversible damage. Previous studies have shown that Ca ~ (2 +) slow channel blockers can not prevent intracellular Ca ~ (2+) accumulation during reperfusion, while Ca ~ (2+) entry into cardiomyocytes is not via Ca ~ (2+ )SLOW