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在离体大鼠心脏灌流模型上,无钠灌流10分钟后再恢复钠的灌流,导致心脏发生与钙反常相似的病理表现和组织损伤,严重心律紊乱,心功能低下,心脏挛缩,组织蛋白和细胞内酶漏出,心肌钙和钠超负荷,K~+/Na~+比值降低,心肌脂质过氧化产物增加,组织超微结构损伤。无钠灌流同时无钙灌流,心肌的损伤明显减轻,本文对Na~+/Ca~(2+)交换机制在再灌注损伤中的发病学意义进行了探讨。
In the isolated rat cardiac perfusion model, sodium perfusion was resumed 10 minutes after sodium-free perfusion, resulting in abnormal cardiac pathology and tissue damage similar to calcium, severe cardiac rhythm disturbances, cardiac dysfunction, cardiac contracture, tissue protein and Intracellular enzyme leakage, cardiac calcium and sodium overload, K ~ + / Na ~ + ratio decreased, myocardial lipid peroxidation products increased tissue ultrastructure damage. Sodium-free perfusion and calcium-free perfusion, myocardial injury was significantly reduced in this paper Na ~ + / Ca ~ (2+) exchange mechanism in the pathogenesis of reperfusion injury were discussed.