摘要
在离体大鼠心脏灌流模型上,缺血(旷置)30分钟后恢复灌流,导致心脏发生典型的再灌注损伤,表现为严重心律失常,心功能低下,心肌组织蛋白和细胞内酶漏出,细胞内钙和钠超负荷,K^+/Na^+比值降低,心肌脂质过氧化产物增加等。缺血心脏再灌注的同时,应用MnSO_4作为Na^+—Ca^(2+)交换抑制剂,明显抑制了再灌注损伤的发生。反之再灌注时应用Na^+-K^+ ATP酶抑制剂哇巴因,则使再灌注损伤更加严重,结果提示Na^+—Ca^(2+)交换机制在再灌注损伤中具有重要的发病学意义。
On the Langendorff's perfusion model, after stoppage of perfusion for 30 min and reperfused for 1.5min, the isolated rat hearts demonstrated severe myocardial damage: severe arrhythmia, loss of contractile force, leakage of intracellular protein and enzymes, decrease of myocardial K^4 and ratio of intracellular K^+/Na^+ increase of myocardial Ca^(2+), Na^+ and formation of lipid peroxidation products. Mn^(2+) as a inhibitor of Na^+/Ca^(2+) exchange, signifi cantly prevented the reperfusion damage when given at the beginning of reper fusion. On the contrary, ouabain, inhibitor of Na/K ATPase, made the reperfusion damage even severer.This paper suggests that Na^+/Ca^(2+) exchange mechanism plays an important role in the pathogenesis of reperfusion damage.
基金
国家"七.五"攻关资助项目
