离体大鼠心肌细胞钠超负荷与缺氧-复氧损伤  

ANOXIA-REOXYGENATION INJURY IN ISOLATED RAT MYOCYTES IS MODULATED BY CELL SODIUM DURING THE ANOXIA PERIOD

作　　者：李兆萍[1] 唐朝枢[1] 苏静怡[1] 

机构地区：[1]北京医科大学病理生理教研室

出　　处：《生理学报》1989年第3期304-307,共4页Acta Physiologica Sinica

基　　金：国家科委资助项目

摘　　要：本工作在离体成年大鼠心肌细胞缺氧-复氧模型上,观察到细胞无氧孵育时加入Na^+-K^+ATP酶抑制剂哇巴因,增加细胞内钠离子浓度,复氧孵育后造成了更严重的细胞损伤及钙超负荷,缺氧期末细胞内钠离子浓度与复氧后钙超负荷的程度呈显著正相关。复氧期给予Na^+-Ca^(2+)交换抑制剂Mn^(2+),明显减轻了细胞的缺氧-复氧损伤,Mn^(2+)还显著抑制了无钠孵育引起的细胞损伤。结果提示:缺氧期细胞内钠超负荷是复氧时细胞内钙超负荷发生的条件,Na^+-Ca^(2+)交换是Ca^(2+)进入细胞的重要途径。Using the model of anoxia-reoxygenation injury in isolated rat myocytes, we observed that incubation of myocytes with ouabain, inhibitor of Na^+-K^+ ATPase, during anoxia period significantly increased the cell sodium content. These myocytes demonstrated severe injury and intracellular calcium overload during reoxygenation period. The sodium content of myocytes at the end of anoxia period was positively correlated with the overload of intracellular calcium at reoxygenation (r=0.882, P<0.01). Mn^(2+), an inhibitor of Na^+-Ca^(2+) exchange, significantly attenuated the anoxia-reoxygenation injury when given during reoxygenation period. Mn^(2+) also inhibited the cell injury caused by incubation of myocytes with Na^+-free medium. These results suggest that anoxia-reoxygenation injury of rat myocytes is modulated by cell sodium during the anoxia period, and the Na^+-Ca^(2+) exchange mechanism plays an important role in influx of extracellular calcium during reoxygenation period.

关 键 词：缺氧损伤 哇巴因 钠 心肌细胞 

分 类 号：R541.02[医药卫生—心血管疾病]