5／6肾切除致慢性肾衰诱发左室心衰大鼠模型的病理生理

目的研究5／6肾切除引起慢性肾衰诱发左室心衰大鼠模型的病理生理机制。方法雄性SD大鼠经“两次手术切除法”行5／6肾切除，6周后造成慢性肾衰，8周后诱发左室心衰。试剂盒法测定血清钙、磷、肌酐、尿素氮。Bradford法测定24h尿蛋白量。左心室插管术测定心脏血流动力学指标心率（HR）、左室收缩压（LVSP）、左室舒张压（LVDP）、左室舒张末期压（LVEDP）及左室最大压力上升速度（dp／dtmax）和下降速度（-dp／dtmax）。称重法测定心脏重量参数。病理切片HE染色观测心肌病理情况。结果与假手术组相比，除血清钙水平外，病理组大鼠各项指标均比假手术组明显升高，表明慢性肾衰造模成功。与假手术组大鼠比较，病理组大鼠LVSP下降，LVDP和LVEDP均上升。病理组心脏重量参数均比假手术组升高。提示左室舒张和收缩（主要是舒张）功能损伤，发生左室心衰和左室心肌肥厚重构。结论5／6肾切除慢性肾衰诱发的大鼠左室心衰，病理生理学特点是左室舒张和收缩（主要是舒张）功能衰竭，和左室心肌肥厚重构。

Heart Failure Model Induced by Renal Failure in 5/6 Nephrectomized Rats

Objective The aim of this study is to establish a heart failure model renal failure through 5/6 nephrectomy in rat for the mechanism study of heart failure caused by renal disease. Methods Male SD rats were randomly divided into two groups, the model group and the sham group. Renal failure （ model group） was induced by 5/6 nephrectomy. After 6 weeks, the renal failure was induced effectively, and after 8weeks the heart failure emerged. The serum was obtained through rhanter to determine the serum calcium, phosphonium, creatinine, urea nitrogen and urine protein, detected by the Bradford method, as parameters evaluating the severity of renal failure. Heart rate （ HR）, left ventricular systolic pressure （ LVSP）, left ventricular diastolic pressure （LVDP）, left ventricular end-diastolic pressure （LVEDP）, and dp/dtmax was detected by left ventricular cannulating. Body weight （BW） , heart weight （ HW ） and left ventricular weight （ VW ） was measured through weighing method. Results Compared with the sham group, BW, LVSP, dp/dtmax were decreased. LVW, LVDP, LV- EDP,-dp/dtmax were markedly in 5/6 nephrectomized rats. Conclusion The pathophysiology characteristics of the Heart failure induced by renal failure in 5/6 nephrectomized rats are remodeling and the insufficiency of the diastolic（ the main point）and systolic function of the left ventricular.