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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。
In the isolated rat heart perfusion model, perfusion was recovered 30 minutes after ischemia (exclusion), resulting in a typical reperfusion injury of the heart with severe arrhythmia, impaired cardiac function, myocardial tissue protein and intracellular enzyme leakage, Intracellular calcium and sodium overload, K ~ + / Na ~ + ratio decreased myocardial lipid peroxidation products increased. At the same time of ischemia reperfusion, MnSO_4 was used as a Na ~ + -Ca ~ (2+) exchange inhibitor, which significantly inhibited the reperfusion injury. On the other hand, the application of Na ~ + -K ~ + ATPase inhibitor ouabain during reperfusion resulted in more severe reperfusion injury, suggesting that Na ~ + -Ca ~ (2+) exchange mechanism is important in reperfusion injury The significance of the disease.