摘要
采用左肾动脉夹闭６０分钟再灌注致缺血性肾衰模型，观察再灌注后肾脏皮质、外髓、内髓中ＮＯ（ＮＯ稳定代谢产物）的动态变化；再灌注后加用ＮＯ底物（Ｌ－精氨酸）或ＮＯ生成抑制剂（Ｌ－ＮＮＡ）对肾脏ＮＯ生成及肾功能的影响。结果表明：再灌注后肾组织ＮＯ含量显著下降，再灌注２４小时无明显恢复。使用Ｌ－ＮＮＡ可进一步减少ＮＯ２生成，加重肾功能损害；Ｌ－精氨酸对肾脏ＮＯ２生成和肾功能均无显著改善。结果提示：再灌注后ＮＯ的生成减少，ＮＯ的生成抑制源于肾脏ＮＯ生成能力的损害，ＮＯ的减少可加重肾功能损害。
Acute renal failure models were established by occlusion of the left renal artery followed by reperfusion. Changes of NO(the stable metabolites of NO)in renal cortex,outer and inner medulla,and the effects of L-NNA and L-arginine on NO levels and on the renal function were studied. NO levels in kidney were found to drop markedly after reperfusion and remained low at the 24th hour. L-NNA made the NO levels and the renal function decreased further while L-arginine had no benefit to NO levels and the renal function After acute ischemia and reperfusion,NO secretion in kidney was impaired,being not mediated though L-arginine deficiency.The decrease of NO in kidney might play a role on the impairment of renal function.
出处
《中华泌尿外科杂志》
CAS
CSCD
北大核心
1996年第6期349-352,共4页
Chinese Journal of Urology
