酵母膏联合氧嗪酸钾构建高尿酸血症模型大鼠继发的心血管病变

Development of secondary cardiovascular disease in hyperuricemia model rats induced by yeast extract combined with oteracil potassium

背景：高尿酸血症动物模型的构建是研究高尿酸血症与肾脏和心血管疾病相互关系的重要手段.目的：采用酵母膏和不同剂量的氧嗪酸钾建立高尿酸血症动物模型,寻找建模的最佳剂量.方法：以酵母膏（21 g/kg）或酵母膏联合不同剂量氧嗪酸钾（50~200 mg/kg）持续灌胃或腹腔注射28 d 建立高尿酸血症大鼠模型.结果与结论：酵母膏或酵母膏联合50~200 mg/kg 氧嗪酸钾持续灌胃或酵母膏联合50~100 mg/kg 氧嗪酸钾腹腔注射均能显著提高大鼠血清高尿酸水平,而对大鼠肾、心和动脉功能无明显影响.酵母膏联合200 mg/kg 氧嗪酸钾腹腔注射不仅使大鼠血清尿酸维持在高水平,也可引起大鼠肾脏、心脏及动脉形态和病理改变.说明酵母膏联合200 mg/kg 氧嗪酸钾腹腔注射是建立持续、稳定高尿酸血症动物模型的最佳配伍剂量,也是研究高尿酸血症引起继发性心血管病理损伤的良好模型.

BACKGROUND： The construction of hyperuricemia animal models is an important tool to study the relationship between hyperuricemia, renal disease and cardiovascular disease. OBJECTIVE： To establish hyperuricemia rat model using yeast extract combined with different doses of oteracil potassium and to explore the optimal dose for model establishment. METHODS： Rats were continuously treated with yeast extract or yeast extract combined with various doses of oteracil potassium by intragastric feeding or intraperitoneal injection for 28 days to establish rat hyperuricemia model. RESULTS AND CONCLUSION： Compared with the control group, there was significant increase in serum levels of uric acid in the groups of intragastric feeding with yeast extract alone, yeast extract combined with 50-200 mg/kg oteracil potassium or intraperitoneal injection with yeast extract combined with 50-100 mg/kg oteracil potassium; however, no remarkable effect on rat kidney, heart or artery was found. A continuously high level of serum uric acid and morphological and pathological changes in rat kidney, heart and arteries were detected when the dosage of oteracil potassium intraperitoneally injected combined with yeast extract was maximized to 200 mg/kg. These findings indicate that intraperitoneal injection of yeast extract combined with 200 mg/kg oteracil potassium is an optimal dosage for the construction of a persistent and stable hyperuricemia animal model; it is a favorable model for the study of pathological damages related to secondary cardiovascular diseases caused by hyperuricemia.