首页> 外文期刊>The Journal of Urology >Time dependent changes in diabetic cystopathy in rats include compensated and decompensated bladder function.
【24h】

Time dependent changes in diabetic cystopathy in rats include compensated and decompensated bladder function.

机译:大鼠糖尿病性膀胱病变的时间依赖性变化包括代偿性和代偿性膀胱功能。

获取原文
获取原文并翻译 | 示例
           

摘要

PURPOSE: Diabetic bladder dysfunction is among the most common and bothersome complications of diabetes mellitus. While bladder filling and voiding problems have been reported, the precise functional changes in diabetic bladders remain unclear. We investigated time dependent changes in bladder function in streptozotocin induced diabetic rats. MATERIALS AND METHODS: Cystometrograms and detrusor muscle contractility were examined in male age matched control and diabetic Sprague-Dawley rats (Harlan, Indianapolis, Indiana) 3, 6, 9, 12 and 20 weeks after diabetes induction with streptozotocin. RESULTS: Diabetes decreased average body weight and increased bladder weight, capacity and compliance. Peak detrusor leak pressure increased gradually from weeks 3 to 6 to 9 in diabetic rats (mean +/- SEM 47.3 +/- 2.5, 50.8 +/- 3.0 and 56.0 +/- 3.6 cm H(2)O) and in controls (36.9 +/- 1.4, 37.7 +/- 1.5 and 41.6 +/- 1.81 cm H(2)O, respectively). However, at 12 and 20 weeks diabetic rats deviated strongly from this trendwith peak detrusor leak pressure decreasing vs controls (41.6 +/- 2.8 and 37.3 +/- 0.9 vs 45.2 +/- 1.7 and 49.6 +/- 1.4 cm H(2)O, respectively) and post-void resting pressures increasing from 9-week levels vs controls (interactions p <0.0001). In contractility studies increased contractile force responses of diabetic animals to carbamylcholine chloride, potassium chloride, adenosine 5'-triphosphate and electric field stimulation peaked at 6 or 9 weeks but at 12 to 20 weeks they generally reverted toward those of controls (carbamylcholine chloride and electrical field stimulation interactions p = 0.0022 and 0.01, respectively). CONCLUSIONS: Diabetic bladders may undergo a transition from a compensated to a decompensated state and transition in the streptozotocin rat model may begin 9 to 12 weeks after induction.
机译:目的:糖尿病性膀胱功能障碍是糖尿病中最常见和最麻烦的并发症之一。尽管已经报道了膀胱充盈和排尿问题,但糖尿病膀胱的确切功能变化仍不清楚。我们调查了链脲佐菌素诱导的糖尿病大鼠膀胱功能的时间依赖性变化。材料与方法:在链脲佐菌素诱导糖尿病后第3、6、9、12和20周,对雄性年龄匹配的对照组和糖尿病Sprague-Dawley大鼠(Harlan,印第安纳波利斯,印第安纳州)检查了膀胱收缩压和逼尿肌收缩力。结果:糖尿病降低了平均体重,并增加了膀胱重量,容量和顺应性。糖尿病大鼠中逼尿肌的峰值渗漏压力从第3周逐渐增加到6至9至9(平均+/- SEM 47.3 +/- 2.5、50.8 +/- 3.0和56.0 +/- 3.6 cm H(2)O)和对照组(分别为36.9 +/- 1.4、37.7 +/- 1.5和41.6 +/- 1.81 cm H(2)O)。但是,在第12周和第20周时,糖尿病大鼠与对照组相比,逼尿肌漏气峰值峰值明显降低(41.6 +/- 2.8和37.3 +/- 0.9 vs 45.2 +/- 1.7和49.6 +/- 1.4 cm H(2)。分别为O)和无效后静息压力从9周水平相对于对照组增加(相互作用p <0.0001)。在收缩性研究中,糖尿病动物对氨基甲酰胆碱氯化物,氯化钾,5'-三磷酸腺苷的收缩力反应增强,并且电场刺激在6或9周达到峰值,但在12至20周时,它们通常恢复为对照(氨基甲酰胆碱和电场刺激相互作用p分别为0.0022和0.01)。结论:糖尿病膀胱可能经历了从代偿状态到失代偿状态的转变,而链脲佐菌素大鼠模型的转变可能在诱导后9至12周开始。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号