Peralta C, Closa D, Hotter G, Gelpí E, Prats N, Roselló-Catafau J
Department of Medical Bioanalysis, Consejo Superior de Investigaciones Científicas, Barcelona, Spain.
Biochem Biophys Res Commun. 1996 Dec 4;229(1):264-70. doi: 10.1006/bbrc.1996.1790.
The concerted involvement of both NO and endothelin in the protective effect of preconditioning against hepatic ischemia-reperfusion induced injury has been evaluated in this study. Thus hepatic ischemia-reperfusion or preconditioning plus ischemia-reperfusion was induced in rats and the effect of nitric oxide administration or inhibition with addition of the endothelin antagonist Bosentan was evaluated. Results show that the increases in plasma GPT release after ischemia-reperfusion were prevented after preconditioning. Inhibition of nitric oxide abolished the effect of preconditioning, addition of the endothelin antagonist abolished the injurious effect of NO inhibition. Also, increased synthesis of endothelin has been detected after ischemia-reperfusion, and addition of NO or preconditioning prevented this increase, suggesting that increases of NO inhibit endothelin synthesis. Altogether this indicates that hepatic preconditioning is mediated by the inhibitory action of nitric oxide on endothelin levels.
本研究评估了一氧化氮（NO）和内皮素在预处理对肝缺血再灌注诱导损伤的保护作用中的协同参与情况。因此，在大鼠中诱导肝缺血再灌注或预处理加缺血再灌注，并评估给予一氧化氮或添加内皮素拮抗剂波生坦进行抑制的效果。结果显示，预处理后可防止缺血再灌注后血浆谷丙转氨酶（GPT）释放增加。抑制一氧化氮消除了预处理的效果，添加内皮素拮抗剂消除了一氧化氮抑制的损伤作用。此外，在缺血再灌注后检测到内皮素合成增加，添加一氧化氮或进行预处理可防止这种增加，表明一氧化氮的增加抑制了内皮素合成。总之，这表明肝脏预处理是由一氧化氮对内皮素水平的抑制作用介导的。
Zotero 插件