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机构地区:[1]第三军医大学西南医院全军烧伤研究所,创伤、烧伤与复合伤国家重点实验室,重庆400038
出 处:《第三军医大学学报》2007年第11期1017-1019,共3页Journal of Third Military Medical University
基 金:国家自然科学基金重点项目(30430680);国家杰出青年科学基金(30125040)~~
摘 要:目的利用外源性一氧化氮(nitric oxide,NO)供体S-亚硝基谷胱甘肽(S-nitrosoglutathione,GSNO)对比观察不同浓度NO对缺氧心肌细胞活力的影响。方法培养4—6d心肌细胞分为常氧组(N)、缺氧组(H)和缺氧+GSNO组(H+G);H+G组依照加入GSNO浓度的不同又分为3组:缺氧+GSNO30μmol/L组(H+G30)、缺氧+GSNO200μmol/L组(H+G200)、缺氧+GSNO4000μmol/L组(H+G4000)。分别观察其对缺氧(1%O2、5%CO2和94%N2)4h心肌细胞损害的影响。结果缺氧引起培养心肌细胞上清LDH活性增加,细胞存活率(MTY法)降低,H+G30组和H+G4000组损伤加重,H+G200组损伤减轻。结论一定浓度范围内的NO具有细胞保护效应。Objective To clarify the effect of NO on hypoxic myocardium in rats. Methods Myocardial cells from neonatal Wistar rats aged 1 -2 days cultured for 4 -6 days, then pretreated with GSNO (30, 200, 4 003 μmol/L) were exposed to normoxia (N) or hypoxia (H) ( 1% 02, 5% CO2 and 94% N2 ) for 4 h. The NO content and LDH in the supernatant were detected. Results NO of 1.43, 7.2 and 70 μmol/L were detected respectively in the supernatant of hypoxic myocardial cells treated by GSNO (30,200 and 4 000 μmol/L). Compared with normoxic group, LDH activity increased and myocardial cell activity decreased markedly in H + G30 and H + G4000 groups but less injury was observed in H + G200 group. Conclusion NO of certain concentration can markedly abate myocardial cell injury induced by hypoxia.
分 类 号:R322.11[医药卫生—人体解剖和组织胚胎学] R329.24[医药卫生—基础医学]
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