一氧化氮途径在大鼠肝移植缺血再灌注损伤中的作用

本实验应用三袖套法大鼠原位肝移植模型,探讨一氧化氮途径在大鼠原位肝移植缺血再灌注损伤中对移植肝的功能作用及可能机制。加强一氧化氮途径能显著延长受体的存活率,改善肝功能及抑制肿瘤坏死因子（Ｔｈ卜ａ）的合成与表达;而抑制ＮＯ合成则能明显降低术后受体存活率、加剧肝功能恶化,上调ＴＮＦ－ａ及Ⅰ型细胞间粘附分子（ＩＣＡＭ－１）的表达。提示：ＮＯ途径很可能是肝移植缺血再灌注损伤的关键因素。

Role of nitric oxide pathway during ischemia/reperfusion injury in the rat liver transplantation

To investigate functional effects and probable mechanisms of nitric oxide synthesizing pathway on the grafted liver during ischemia-reperfusion injury(l/RI) in the rat orthotopic liver transplantation(OLT) by three-cuff method with minor modification. By administrating L-arginine to Supplement NO pathway, a high survival of recipient was obviously prolongeted, the hepatic function was strikingly amelirated, synthesis and expression of TNF-a were inhibited. In contast, the grafted liver fLinction and recipient survival were inferior in all cases where NO production was inhibited. NOS inhibitor up-regLllated the expression of TNF-a and ICAM-1 .Furthermore, histopathology revealed a more severe tissues and a more severe inflammatory response of the recipient after inhibitor of nitric oxide. Nitric oxide pathway during ischemia-reperfusion injury in liver transplantation may be critical determinent of successful organ transplantation.