心肌缺血再灌注损伤时细胞核膜钙泵功能的改变  

Changes of myocardial nuclear membrane Ca^(2+)-ATPase function in ischemia/reperfusion injury

作　　者：付爱玲[1] 何华美[1] 张乐之[1] 

机构地区：[1]第三军医大学药理学教研室

出　　处：《中国病理生理杂志》2003年第11期1453-1455,共3页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助课题 (No .30 10 0 0 70 )

摘　　要：目的 :研究心肌缺血再灌注损伤时心肌细胞核膜钙泵 (Ca2 + -ATPase)功能的改变。方法 :采用大鼠心肌缺血再灌注模型 ,密度梯度离心分离纯化细胞核 ,定磷法测定Ca -ATPase活性 ,[45Ca2 + ]直接测定核钙摄取。结果 :缺血再灌注损伤动物血浆MDA和FFA显著高于正常大鼠 (P <0 0 1) ,再灌注心肌细胞核膜Ca -ATPase在[Ca2 + ]i 较低时 ,酶活力低于正常细胞 ,而在 [Ca2 + ]i 较高浓度 5 0 μmol/L时酶活力高于正常细胞。对 [45Ca2 + ]摄取的变化与Ca-ATPase活性变化相似。结论 :心肌缺血再灌注损伤时核膜Ca2 + -ATPase功能发生了改变。AIM: The changes of myocardial nuclear membrane Ca 2+ -ATPase function was investigated in ischemia/reperfusion injury. METHODS: The model of myocardial ischemia/reperfusion injury was established in rats. Myocardial nuclei were purified with sucrose density centrifugation,the activity of Ca 2+ -ATPase was measured and calcium uptake was assayed with [ 45 Ca 2+ ] . RESULTS: Plasma levels of malondialdehyde (MDA) and free fatty acid (FFA) in myocardial ischemia/reperfusion injury increased significantly( P<0.01 vs control). Ca 2+ -ATPase activity and [ 45 Ca 2+ ] uptake was lower than normal at below 10 μmol/L, while higher at 50 μmol/L. CONCLUSION:These data indicate dysfunction of nuclear menbrane calcium pump and [ 45 Ca 2+ ] uptake function in myocardial ischemia/reperfusion injury.

关 键 词：心肌缺血再灌注损伤 Ca(2+)转运ATP酶 细胞核 病理生理过程 核膜钙泵 

分 类 号：R541.4[医药卫生—心血管疾病]