Hotter G, Closa D, Pi F, Prats N, Fernandez-Cruz L, Bulbena O, Gelpí E, Roselló-Catafau J
Molecular Pathology Unit, Centro de Investigación y Desarrollo, CSIC, Barcelona, Spain.
Transplantation. 1995 Feb 15;59(3):417-21.
The role of eicosanoid metabolism and its relationship with nitric oxide production in the ischemia-reperfusion associated with pancreas transplantation in the rat is explored in this study. Twenty-six male Sprague-Dawley rats were randomized into 3 groups, as follows: group 1, control animals not surgically manipulated; group 2, pancreas transplantation, after 12 hr of organ preservation in University of Wisconsin solution; group 3, same as group 2 but with administration of NG-nitro-L-arginine methyl ester (a nitric oxide synthase inhibitor) (10 mg/kg) before organ revascularization. The results show posttransplantation increases in edema and in 6-keto-prostaglandin F1 alpha (x1.9), thromboxane B2 (x4), and prostaglandin E2 (x5) levels in pancreatic tissue. Nitric oxide synthase inhibition reversed the increases in edema and eicosanoid production, which suggests that eicosanoid generation in the recipient rat would be mediated, in part, through a nitric oxide-dependent mechanism.
本研究探讨了类花生酸代谢在大鼠胰腺移植相关缺血再灌注中的作用及其与一氧化氮生成的关系。26只雄性Sprague-Dawley大鼠被随机分为3组,如下:第1组,未进行手术操作的对照动物;第2组,在威斯康星大学溶液中保存12小时后进行胰腺移植;第3组,与第2组相同,但在器官再灌注前给予NG-硝基-L-精氨酸甲酯(一种一氧化氮合酶抑制剂)(10mg/kg)。结果显示,移植后胰腺组织中的水肿以及6-酮-前列腺素F1α(增加1.9倍)、血栓素B2(增加4倍)和前列腺素E2(增加5倍)水平升高。一氧化氮合酶抑制逆转了水肿和类花生酸生成的增加,这表明受体大鼠中类花生酸的生成部分将通过一氧化氮依赖性机制介导。