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

作　　者：贾三庆[1] 刘秀华[1] 胡大一[1] 汪丽蕙[1] 唐朝枢[1] 

机构地区：[1]北京医科大学第一医院心内科,北京医科大学心血管基础所

出　　处：《北京医科大学学报》1996年第5期350-352,共3页Journal of Peking University(Health Sciences)

摘　　要：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.

关 键 词：心肌缺氧 CROMAKALIM 

分 类 号：R541.405[医药卫生—心血管疾病]