摘要
目的 观察ATP敏感性钾 (KATP)通道开放剂对模拟缺血窦房结细胞活性的影响 ,并探讨其作用机制。方法 取培养 2d的窦房结细胞 ,以低渗 ( 85mosmol/L)台盼蓝染色及四唑盐 (MTT)比色观察窦房结细胞活性的变化。结果 模拟缺血 4h后 ,窦房结细胞脆性增加、活性降低 ;KATP通道开放剂Pinacidil和Diazoxide能显著降低模拟缺血窦房结细胞脆性 ,增加细胞的活性 ,但两组间无明显的统计学差异 ;KATP通道阻断剂 5 HD能逆转Pinacidil及Diazoxide的上述作用。结论 KATP通道开放剂Pinacidil和Diazoxide对缺血窦房结细胞具有显著的保护作用 ,但这种效果能为KATP通道阻断剂 5 HD阻断。本研究提示窦房结细胞线粒体内膜可能有KATP通道存在 ,它的开放可能是细胞获得保护的关键。
Objective To investigate the effects of different ATP sensitive potassium (K ATP ) channel openers on the activity of primary cultured sinoatrial node cells during simulated ischemia and evaluate the mechanism of protection. Methods Postassium channel openers, Pinacidil and Diazoxide, and block 5 HD was used respectively or combined with ischemia condition in the culture mediums of 2 day cultivation sinoatrial node cells. The hypotonic (85 mosmol/L) trypon blue staining method and MTT colorimetry were used to study the effects of different ATP sensitive potassium channel activators. Results Osmotic fragility was significantly increased, and D 490 values were decreased in ischemic cells. ATP sensitive potassium channel openers, Pinacidil and Diazoxide, significantly delayed the progressive increase in the fragility and elevated the activity of ischemic sinoatrial node cells, but there were no significant difference between the cells cultured in Pinacidil+Ischemia and Diaxodie+Ischemia mediums. 5 HD completely reversed the protective effects of Pinacidil and Diazoxide. Conclusion ATP sensitive potassium channel activators, Pinacidil and Diazoxide, can protect sinoatrial node cells during simulated ischemia, but the anti ischemic efficacy is blocked by 5 HD. The findings suggest that K ATP channels probably exist in the inner membrane of mitochondrium of sinoatrial node cells, whose opening may play an important role in protection of ischemic cells.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2001年第11期1303-1305,共3页
Journal of Third Military Medical University
基金
国家自然科学基金资助项目 ( 39770 32 4 )
