四氧嘧啶诱发兔糖尿病模型的胰岛素管理及糖尿病肾病模型建立

目的:探索四氧嘧啶诱发兔糖尿病的胰岛素管理、血糖变化规律及肾脏病理变化。方法:静脉注射四氧嘧啶100mg/kg建立兔糖尿病模型,监测血糖、体重变化,并给予胰岛素皮下注射;12周后监测尿白蛋白、肾重/体重值,肾脏组织PAS染色。结果:静脉注射四氧嘧啶24h内10%兔死于低血糖,至72h83.3%兔血糖大于16.0mmol/L,胰岛素用量逐渐减少,至12周63.3%兔血糖基本可控制于16.0￣25.0mmol/L。12周时病理显示糖尿病兔肾小球体积增大,系膜细胞增生,系膜基质增多,部分毛细血管管腔闭塞,肾小管上皮细胞颗粒样变性、空泡变性,管腔内见蛋白管型。结论:按100mg/kg静脉注射四氧嘧啶后兔死亡率低,可形成稳定的糖尿病模型,分阶段胰岛素管理,用量逐渐减少,12周时可形成典型糖尿病肾病模型。

Administration of insulin to the rabbit model with diabetes mellitus induced by alloxan and the formatin of diabetic nephropathy

Objective To study the insulin administration to the rabbit model with diabetes mellitus induced by alloxan, fluctuation pattern of blood glucouse and nephrotic pathological change. Method Alloxan was intravenously injected by 100mg/kg body weight to make male Japanese white rabbit model with diabetes mellitus. Blood glucouse and body weight were monitored and insulin was subcutaneously injected to control blood glucouse. Urine albumin and kidney weight/body weight ratio were detected, kidney tissue in PAS was observed at the end of 12 weeks. Results 10% rabbits died from low blood glucouse reaction within 24 hours after alloxan injection and blood glucouse of 83.3% rabbits had exceeded 16.0mmol/L after 72 hours. Insulin needs of rabbits with diabetes mellitus gradually decreased and blood glucouse of 63.3% rabbits fluctuated between 16.0～25.0mmol/L at the end of 12 weeks. Renal damages included enlargement of glomerular volume, mesangial cells proliferation, mesangial matrix accumulation, partial caillary cavity occlusion and tubular interstitial injury. Conclusion Rabbits intravenously injected 100mg/kg alloxan show low mortality, stable diabetes mellitus model, gradually decreasing insulin needs and formed typical diabetic nephropathy model at the end of 12 weeks.