钙离子在心肌缺血预适应中的作用

The role of Ca^(2+) in the myocardial ischemic preconditioning

目的观察钙离子变化对心肌缺血预适应内源性保护机制的影响。方法将50只雄性SD大鼠随机分为五组,缺血对照(IC)组;缺血预适应(IP)组;缺血预适应+维拉帕米(IP+Vera)组;钙通道激动剂(Bay8644)组;L-型钙通道阻滞剂(维拉帕米,Verapamil)组。实验中观察缺血前及再灌后左心功能,检测乳酸脱氢酶(LDH)、三磷酸腺苷(ATP)等含量并辅以心肌超微结构观测。结果与IC组相比,IP组、Bay8644组各项指标均提示心功能恢复好转(P<0.05),且IP组与Bay8644组相比较,各项指标差异无统计学意义(P>0.05);在IP组中加入维拉帕米后,各项指标均提示心肌损伤明显加重(P<0.05)。结论(1)心肌缺血预适应可诱导出心肌内源性保护作用。(2)钙通道拮抗剂可通过减少钙离子内流而阻断心肌缺血预适应的心肌保护作用。(3)增加钙离子内流可模拟IP的心肌保护作用。

Objective To investigate the role of Ca^2＋ in the mechanism of ischemic preconditioning effects, Methods Fifty Sprague-Dawley male rats were divided into 5 groups randomly： IC group, ischemic control, IP group, ischemia followed by reperfusion; IP ＋ Verapamil group, Bay k8644 group, Verapamil group. Results Siginifleant heart functional recovery was observed in IP group as campared with that in IC group（P 〈 0.05）. Administration of verapamll completely abolished the IP-induced cardiac protection. Administration of Bay k8644 could mimic cardiac protection against ischemia-reperfusion injury. Conclusion IP can induce myocardial protective effects against ischemia-reperfusion injury. Transient Ca^2＋ influx elicits strong protection against ischemia-reperfusion injury viaprotein kinase C signaling pathway.