就多种药物或措施改善心肌缺血/再灌注损伤的关键环节或信息通路进行了探讨.以大鼠心肌为材料,选取腺苷A1受体激动剂R-苯异丙基腺苷(R-PIA)为保护剂,分别或同时加入ATP敏感性钾通道阻滞剂格列苯脲、蛋白激酶C(PKC)抑制剂等,观察对氧自由基、一氧化氮、ATP酶和一氧化氮合酶基因等的影响,并与缺血预处理组比较,结果显示:R-PIA和缺血预处理后均有较好的保护作用,这些作用依赖钾通道的开放与蛋白激酶C(PKC)的激活;虽然钾通道的开放部分依赖PKC的激活,但ATP敏感性钾通道可能是居于下游的、比PKC更关键的因素.
The key process and information gateway of ischemia/reperfusion injure after improved by drugs and way were researched. Langendorff installation and cardiac muscle of Wistar rats were used. The excitant of adenosine A1 recepor R-PIA was selected as protecting medicine; ATP sensitive potassium channel retarder glybenclamide and PKC inhibitor stauroprine were used simultaneously or separately. The changes of oxygen free radical, nitric oxide, ATPase and inducible nitric oxide synthetase gene were observed, which were compared with ischemia pretreatment at that time. The results showed that R-PIA and ischemia preconditioning had preferable protection and these effects depend on the opening of potassium channel and the activing of PKC. The opening of potassium channel depends on partly the activing of PKC, but opening of potassium channel may be a key factor even more than PKC at downriver position.
柏华,卢景雰,颜振瀛,古力努尔,张敏. R-PIA保护心肌影响钾通道和一氧化氮的研究[J].生物化学与生物物理进展,2000,27(4):403-406
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