氯离子通道阻滞剂对心肌低氧复氧损伤的影响  

Role of chloride channel blockers in anoxia cardiac myocytes

作　　者：向小峰[1] 唐其柱[1] 胡佑伦[1] 史锡腾[1] 唐琳[1] 

机构地区：[1]武汉大学人民医院生物医学工程研究室,430060

出　　处：《中华心血管病杂志》2003年第6期448-451,共4页Chinese Journal of Cardiology

摘　　要：目的　研究氯离子流在心肌缺氧、缺氧再灌注、缺氧预处理中的病理生理作用。方法利用培养的心肌细胞 ,制作低氧复氧、缺氧预处理和低渗预处理模型 ,并使用氯离子通道阻滞剂SITS和Tamoxifen进行干预 ,最后检测细胞存活率及培养细胞上清液中乳酸脱氢酶 (LDH)、丙二醛 (MDA)和超氧化物歧化酶 (SOD)的活性变化。结果　使用氯离子通道阻滞剂后的低氧复氧组 ,其细胞存活率及上清液中LDH、MDA及SOD活性与对照组相比无明显差异 ;加入氯离子通道阻滞剂后再进行缺氧预处理、低渗预处理的各组 ,细胞存活率及LDH、MDA和SOD的活性与单纯低氧复氧组相比无显著性差异。结论　氯离子通道阻滞剂、缺氧预处理、低渗预处理对心肌缺氧损伤均具有保护作用 ,而缺氧预处理、低渗预处理的这一保护作用能被氯离子通道阻滞剂阻断。Objective To investigate the physiological and pathological role of Cl - currents during the course of anoxia, anoxia/reoxygenation, anoxia preconditioning and hypotonic preconditioning in the cultivated cardiac myocytes. Method Cultivated cardiac myocytes were treated with chloride channel blocker SITS and Tamoxifen respectively before they were under the conditions of anoxia/reoxygenation, anoxia preconditioning and hypotonic preconditioning, then the cell viability and contents of lactate dehydrogenase(LDH),malondialdehyde (MDA) and superoxide dismutase(SOD) in the supernatant were determined. Results LDH and MDA release in the SITS and Tamoxifen pretreatment group decreased while the cell viability and contents of SOD increased compared with the only anoxia/reoxygenation group ( P <0.01); the same changes can be found in the anoxia or hypotonic preconditioning group with SITS and Tamoxifen pretreatment. Conclusion Chloride channel blocker, anoxia preconditioning and hypotonic preconditioning could increase cardiac myocytes tolerance against anoxia. Chloride channel blocker also blocks the protection of anoxia preconditioning and hypotonic preconditioning.

关 键 词：氯离子通道阻滞剂 心肌缺氧 低氧 复氧损伤 

分 类 号：R541[医药卫生—心血管疾病]