摘要
目的 :探讨泌尿系梗阻后肾脏功能的改变机制。方法 :2 0只大鼠随机分为实验组 (n =10 )及对照组 (n =10 )。实验组双侧输尿管梗阻 2 4h后解除梗阻 ,对照组手术同实验组 ,但不结扎。所有大鼠于术前 3d及术后 4d测量饮水量、食量、体重及尿量 ;术后 4d抽取动脉血化验 ,同时取出双侧肾脏 ;右肾全肾快速放入液氮冰冻备份 ,左肾分离出内髓 (IM)、外髓内带 (ISOM)、外髓外带加肾皮质 (OSOM +C) ,免疫杂交法检测 3型钠氢交换通道 (NHE3)、钠钾ATP酶 (Na -K -ATPase)和钠 -钾 - 2氯协同转运通道蛋白 (BSC - 1)。结果 :实验组输尿管梗阻 2 4h后引起肾脏水钠排泄异常 ,机体水电解质紊乱 ;肾脏不同部位NHE3、Na-K -ATPase及BSC - 1表达均较对照组降低 (P均<0 .0 1)。结论 :NHE3、Na-K -ATPase及BSC - 1水平降低可能是泌尿系梗阻后肾小管性钠回吸收障碍。
Aim: To explore the molecular mechanism of renal function defects after urinary obstruction. Methods: A total of 20 male Munich-Wister rats were randomly divided into bilateral ureteral obstruction (BUO) group and sham operated control (sham) group with 10 in each group. With the semiquantitative immunoboltting methods, the expression levels of type 3 Na +/H + exchanger (NHE3) ,Na-K-ATPase and type 1 bumetanide sensitive Na-K-2Cl cotransporter (BSC-1) were examined. The functional data were observed.Results: Consistent with polyuria and reduced urinary osmolality, the expressions of NHE3, Na-K-ATPase and BSC-1 of BUO group were lower than those of sham group. Conclusion: The downregulation of major renal sodium transporters after BUO may contribute to the impaired renal tubular sodium reabsorption, decreased urinary concentration, and postobstructive polyuria.
出处
《郑州大学学报（医学版）》
CAS
北大核心
2004年第6期947-950,共4页
Journal of Zhengzhou University(Medical Sciences)
基金
河南省杰出青年科学基金资助项目 0 2 12 0 0 0 110 0
河南省杰出人才创新基金资助项目 0 2 2 10 0 2 0 0 0
河南省高等学校创新人才培养工程项目2 0 0 2 -2 0 0 7
