摘要
目的 :探讨心肌梗塞致心力衰竭大鼠模型不同时期尿液水通道蛋白 - 2 (AQP2 )浓度的改变及其与低钠血症的关系。方法 :应用左冠状动脉结扎复制慢性心力衰竭大鼠模型 ,对该模型术后不同时期的大鼠应用Western蛋白印迹测定尿液AQP2浓度并测定 2 4h尿量、血钠、尿渗量等指标。结果 :在左冠状动脉结扎术后心力衰竭大鼠模型 ,尿液AQP2浓度变化有两个峰 ,一是在术后 3d ,二是在术后第 9周 ;不同时期心力衰竭组的血钠 ,尿渗量与对照组比较均存在显著差异。术后第 9周心肌梗塞心衰组尿液AQP2光密度值 (36 5 %± 10 3% )明显高于心肌梗塞心功能代偿组 (179%± 81% )及对照组 (99%± 48% ) (P <0 0 1)。结论 :左冠状动脉结扎术后不同时期心衰大鼠尿液AQP2变化的规律反映了AQP2基因在心力衰竭进程中表达明显增高 ,肾脏AQP2基因表达增高是心力衰竭伴低钠血症的重要发病原因。
AIM: To study urinary concentration of aquaporin-2 water channel protein(AQP2) at different stages of chronic heart failure(CHF) rats and its relation to hyponatremia. METHODS: Male Sprague-Dawley rats(200~250 g) underwent either a left coronary artery ligation (a model of CHF) or a sham-operation. At different stage after surgery, urinary AQP2 concentration was measured by Western blot. 24-hours urine volume, serum sodium and urine osmolality were measured at the same time. RESULTS: There were two peaks of urinary excretion of AQP2 in severe heart failure rats model: one was the third day after operation, the other was the 9th week. Serum sodium and urine osmolality were significantly different in CHF rats as compared with sham-operated rats. Seven weeks after surgery, urinary AQP2 concentration was increased significantly insevere CHF rats compared with the mild ones and the control ones(365%±103% vs 179%±81% and 99%±48%, P< 0.01).CONCLUSION: The variation of urinary AQP2 excretion at different stages after ligation showed that the expression of AQP2 gene was increased obviously in CHF rats, and its expression level was higher as the heart failure became more severe.This is the important reason of heart failure with hyponatremia.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2000年第8期690-693,共4页
Chinese Journal of Pathophysiology
基金
广东省自然科学基金资助! (No .970 35 5 )