Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine whether angiotensin converting enzyme inhibition could ameliorate renal ischemic injury. Both a chronic rat model and a rat isolated perfused kidney (IPK) model were used. Adult rats were subjected to 60 min of left hilar crossclamping and right nephrectomy. Captopril (1 mg/kg) was given intravenously 5-10 min prior to clamping (CAP-pre, n = 5), at reperfusion (CAP-post, n = 5), or 30 min after reperfusion (CAP-30 min post, n = 5). Other groups of rats received enalapril (0.8 mg/kg iv) in the same manner (ENAL-pre, n = 5; ENAL-post, n = 5; ENAL-30 min post, n = 4). Serum creatinine in the treated groups was compared to ischemic control (NS, n = 7) for 7 days. In the IPK experiments, kidneys were similarly treated with CAP or ENAL. Vascular resistance (VR) and oxygen consumption (O2 CON) were determined from pressure, flow, and oxygen tension data for 60 min after initial equilibration. In the chronic model, Day 2 serum creatinine was significantly lower in all treated groups vs ischemic control. By Day 7, serum creatinine remained significantly lower in all ENAL-treated groups and in the CAP-30 min post group, although other CAP-treated groups had appreciably, although not significantly, lower creatinines, too. Histologic examination of CAP-pre kidney revealed intact morphology compared to ischemic control where acute tubular necrosis was observed. In the IPK experiments, CAP- and ENAL-treated kidneys had VR values that were significantly lower than those of ischemic controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril amelioration of renal reperfusion injury. 804 Nov 45