Cromakalim保护培养的心肌细胞耐受缺氧－复氧损伤

CROMAKALIM PROTE PROTECTS CULTURED CARDIOMYOCYTES FROM ANOXIA-REOXYGENATION DAMAGE

目的：探讨Ｋ＿（ＡＴＰ）通道开放剂Ｃｒｏｍａｋａｌｉｍ（ＣＲＫ）的直接细胞保护作用。方法：利用培养心肌细胞缺氧－复氧损伤模型观察ＣＲＫ的保护作用。结果：ＣＲＫ显著降低缺氧－复氧心肌细胞的ＬＤＨ漏出率及细胞内钙含量，而且呈浓度依赖性。上述作用可被选择Ｋ＿（ＡＴＰ）．通道阻滞剂Ｇｌｙｂｅｎｃｌａｍｉｄｅ（ＧＬＢ）所消除。结论：ＣＲＫ具有直接的心肌细胞保护作用，其机制表现为膜稳定作用及抑制细胞钙超载。

Objective:The aim of this experiment was to find out whether Cromakalim(CRK),a K_(ATP) channel opener,had direct protection of cardiomyocytes.Methods:On the model ofanoxia-reoxygena-tion damage in cultured cardiomyocytes,the effects of CRK on cardiOmyocytes were determined.Re-sults:CRK inhibited the leakage of intracellular LDH and intracellular calcium content in a dose-depen-dent manner. These effects were abolished by K_(ATP) specific blocker Glybenclamide(GLB)(1 umol/L)..onclusion:The results suggest that CRK is possessed of direct cytoprotection property by opening K_(ATP)channel.The mechanisms may include membrane stabilization and inhibition of calcium overload of car-diomyocytes.