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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 establish a rat model of adriamycin-induced massive proteinuria by renal arteries to determine the relationship between hypoproteinemia and nephrotoxicity in patients with nephrotic syndrome. Methods Rats in experimental group (E1, E2, E3) were treated with adriamycin (5, 45, and 65 mg / kg) by renal artery respectively, and the renal artery and vein were tied for 8 min immediately after administration. Results A large amount of proteinuria occurred in rats of E2 group at about 15 days after treatment, showing no significant difference from the model group of classical nephropathy. In the E2 group, the glomerular foot process fusion was observed under the electron microscope. Conclusion Intraperitoneal injection of adriamycin 45mg / kg can induce a large amount of proteinuria in rats. Urine protein excretion in this model is the same as that of classical nephropathy model. However, other organs except kidneys are not exposed to doxorubicin .