急性缺血再灌流肾损伤的机理研究

STUDY ON THE MECHANISM OF ACUTE RENAL ISCHEMIC REPERFUSION INJURY IN RABBITS

目的：探讨急性缺血再灌流（IR）肾损伤的机理。方法：18只日本大耳白兔随机分为对照组、IR组。采用左肾切除，右肾动静脉夹闭1h再灌流3h致肾损伤模型。结果：IR组血和肾组织中丙二醛（MDA）及肾组织中WBC滞留数、肾小管计分和Na＋、Ca2＋浓度较对照组显著升高（P＜0．05）。血和肾组织SOD活力，肾组织NO含量显著降低（P＜0．05）。IR组有明显的组织学损伤改变。结论：氧自由基生成增多、NO减少和WBC滞留导致的无复流现象及Na＋、Ca2＋超载等因素参与了IR肾损伤。

Objective: To further investigate the mechanism of acute renal ischemic reperfusion injury(IRI). Methods: Japanese white rabbits were randomly divided into control and ischemic/reperfusion (IR) group. the renal ischemic reperfusion (IR) model was established by occlusion of right renal artery and vein for an hour and reperfusion for three hours after left nephrectomy. Results: MDA content in renal tissue and serum, concentration of Na+ and Ca2+, the number of WBC adhesion and scores of tubules in renal tissue in IR group were significantly higher than that in control group (P < 0.05), and the SOD activity in renal tissue and serum and NO content in renal tissue in IR group were obviously lower (P < 0.05). Furthermore, there was negative correlation between SOD and MDA in serum in IR group. In addition, renal histomorphological damage in either light or electronic microscope in IR group were evidently more serious than that in control group. Conclusion: It is shown that increase of oxygen free redicals (OFR), .decrease of NO content, WBC adhesion and recruitment and Na+. Ca2+ overload might be the causes of renal IRI.