摘要
目的 建立双肾动脉给阿霉素致大量蛋白尿大鼠模型 ,以确定肾病综合征时低蛋白高脂血症与大量蛋白尿的关系。方法 实验 (E1、E2 、E3 )组大鼠经双肾动脉分别给阿霉素 (按肾组织重计 ) 2 5、45、6 5mg/kg ,给药后立即系扎双肾动静脉 8min。结果 E2 组大鼠于处理后 15d左右出现大量蛋白尿 ,与经典肾病模型组比较 ,无显著性差异。E2 组肾脏电镜下见肾小球足突融合。结论 经双肾动脉给阿霉素 45mg/kg ,可诱导大鼠产生大量蛋白尿 ;该模型尿蛋白排泄量与经典肾病模型相同 ,但除双肾以外的其他脏器均不暴露于阿霉素。
Objective To further study the relationship between hypoalbuminemia and hyperlipidemia in rats with nephrotic syndrome.?Methods A new rat model of massive proteinuria induced by bilateral renal artery perfusion with adriamycin was established. The kidneys in rat groups E 1, E 2 and E 3 were perfused by bilateral renal arteries in 1 min with 25, 45 or 65 mg of adriamycin per kilogram of kidney weight respectively, and then the 2 pairs of renal vessels were clamped for 8 min.?Results The rats in group E 3 all died.The increased urine protein excretion in group E 1[(135±2.97)mg/d] was not high enough. Expected heavy proteinuria was observed in group E 2, with no significant difference in the level of urine protein found between group E 2 and group C 4 (the classical model group) [(425.3±11.87)mg/d vs (441.93±16.83)mg/d, P > 0.05 ].Electron microscopy of kidneys in group E 2 revealed a fusion of podocytic foot processes. ?Conclusion The model of rat with massive proteinuria can be induced with 45 mg of adriamycin per kilogram of kidney weight by bilateral renal artery perfusion. The new rat model is special for its quantity of proteinuria is similar to that of the classical model and the organs other than the kidneys are not exposed to adriamycin.
出处
《徐州医学院学报》
CAS
1999年第5期356-358,共3页
Acta Academiae Medicinae Xuzhou
基金
江苏省自然科学基金!BK9715 5
