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

Time dependent changes in diabetic cystopathy in rats include compensated and decompensated bladder function
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DOI:
10.1016/s0022-5347(06)00582-9
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发表时间:
2006-07-01
期刊:
影响因子:
6.6
通讯作者:
Imrey, Peter B.
Imrey, Peter B.
中科院分区:
医学1区
文献类型:
--
作者:
Daneshgari, Firouz;Liu, Guiming;Imrey, Peter B.

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目的:糖尿病膀胱功能障碍是糖尿病最常见、最棘手的并发症之一。虽然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。材料和方法:采用链脲佐菌素(STZ)诱导的糖尿病大鼠模型,观察膀胱收缩和逼尿肌收缩功能的变化(哈兰,印第安纳波利斯,印第安纳州)链脲佐菌素诱导糖尿病后3、6、9、12和20周。结果:糖尿病降低了平均体重,增加了膀胱重量、容量和顺应性。糖尿病大鼠的逼尿肌漏压峰值从第3周至第6周至第9周逐渐增加(平均值± SEM 47.3 ± 2.5、50.8 ± 3.0和56.0 ± 3.6 cm. H2O)和对照组(分别为36.9 +/- 1.4、37.7 +/- 1.5和41.6 +/- 1.81 cm H2O)。然而,在12周和20周,糖尿病大鼠强烈偏离这种趋势,与对照组相比,逼尿肌漏压峰值降低(41.6 +/- 2.8和37.3 +/- 0.9 vs 45.2 +/- 1.7和49.6 +/- 1.4 cm H2O,和排尿后静息压从9周水平增加(相互作用P < 0.0001)。在收缩力研究中,糖尿病动物对氯化氨甲酰胆碱、氯化钾、腺苷三磷酸和电场刺激的收缩力反应在6或9周时达到峰值,但在12至20周时,它们通常恢复到对照组的水平(氯化氨甲酰胆碱和电场刺激相互作用p分别= 0.0022和0.01)。糖尿病膀胱可能经历从代偿状态到失代偿状态的转变,并且在链脲佐菌素大鼠模型中的转变可能在诱导后开始9至12周开始。
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. H2O) and in controls (36.9 +/- 1.4, 37.7 +/- 1.5 and 41.6 +/- 1.81 cm H2O, respectively). However, at 12 and 20 weeks diabetic rats deviated strongly from this trend with 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 H2O, 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.