Van Thiel D H, Sakr M, Zetti G, McClain C
Department of Surgery, University of Pittsburgh School of Medicine, Pennsylvania 15213.
Ren Fail. 1992;14(3):285-8. doi: 10.3109/08860229209106630.
The effect of FK 506 pretreatment on renal ischemia and reperfusion (I/R) injury was investigated. Adult male rats were assigned to one of two groups (20 animals each). Group 1 (controls) received 0.5 mL saline while group 2 received FK 506 (0.3 mg/kg) intravenously 24 h prior to the induction of renal ischemia. After a 60-min period of ischemia of the right kidney, a left nephrectomy was performed. Blood for BUN, creatinine, and tumor necrosis factor (TNF) was obtained prior to ischemia and on days 1, 2, 3, 5, 7, and 10. All surviving animals were sacrificed at day 10. FK 506 pretreatment reduced the serum levels of BUN (p less than .02), creatinine (p less than .02) and TNF (p less than .05) as compared to that seen in controls. Based upon these data, it appears that: (a) renal ischemia induces the release of TNF; (b) FK 506 pretreatment inhibits TNF production; and (c) FK 506 reduces renal injury association with I/R.
研究了FK 506预处理对肾缺血再灌注（I/R）损伤的影响。成年雄性大鼠被分为两组（每组20只动物）。第1组（对照组）接受0.5 mL生理盐水，而第2组在诱导肾缺血前24小时静脉注射FK 506（0.3 mg/kg）。右肾缺血60分钟后，进行左肾切除术。在缺血前以及第1、2、3、5、7和10天采集血液检测血尿素氮、肌酐和肿瘤坏死因子（TNF）。所有存活的动物在第10天处死。与对照组相比，FK 506预处理降低了血尿素氮（p<0.02）、肌酐（p<0.02）和TNF（p<0.05）的血清水平。基于这些数据，似乎：（a）肾缺血诱导TNF释放；（b）FK 506预处理抑制TNF产生；（c）FK 506减轻与I/R相关的肾损伤。
