Enhanced adenosine triphosphate release from the Urothelium of patients with painful bladder syndrome: A possible pathophysiological explanation
Enhanced adenosine triphosphate release from the Urothelium of patients with painful bladder syndrome: A possible pathophysiological explanation
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DOI：
10.1016/j.juro.2007.05.116
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发表时间：
2007-10-01
影响因子：
6.6
通讯作者：
Chess-Williams, Russell
中科院分区：
文献类型：
--
作者：
Kumar, Vivek;Chapple, Christopher R.;Chess-Williams, Russell
目的：我们建立了三磷酸腺苷的释放水平的膀胱疼痛综合征患者的尿路刺激和比较，从正常的人blader.Materials和方法：活检的尿路刺激疼痛膀胱综合征患者进行拉伸的130%和150%的原始长度，和10 Hz的电刺激。荧光素酶测定用于定量三磷酸腺苷释放。神经毒素河豚毒素被用来阻止腺苷三磷酸释放的神经源。结果：有一个显着更大的释放腺苷三磷酸后，从疼痛与控制膀胱的尿道机械拉伸。无论是以绝对值表示（平均值+/- SE 3，791.4 +/- 667.9 vs 77.6 +/- 16.2 pM gm（-1）组织）还是以相对于基线的增加表示（282.2% +/- 24.8% vs 175.4% +/- 21.7%），疼痛膀胱与对照膀胱中三磷酸腺苷释放的增加均具有统计学显著性。同样，电场刺激膀胱后，疼痛膀胱与对照膀胱的三磷酸腺苷也有明显的释放（1，348.6 +/- 278.2 vs 61.7 +/- 10.1 pM gm（-1）组织，p < 0.005），代表278% +/- 41.5%对137.9% +/- 4.4%的基线增加（p < 0.005）。腺苷三磷酸释放的来源是nonneuronal在89%的疼痛膀胱和84%的control bladders.Conclusions：有一个显着增加的水平，腺苷三磷酸释放从尿路疼痛的膀胱相比，从正常的膀胱，这表明在这种情况下，腺苷三磷酸的一个重要的潜在的功能作用。
Purpose: We established the level of adenosine triphosphate release by the urothelium in patients with painful bladder syndrome and compared it with that from the normal human bladder.Materials and Methods: Biopsies of urothelium from patients with painful bladder syndrome were subjected to stretch by 130% and 150% of the original length, and 10 Hz electric stimulation. A luciferase assay was used to quantify adenosine triphosphate release. The neurotoxin tetrodotoxin was used to block the neuronal source of adenosine triphosphate release.Results: There was a significantly greater release of adenosine triphosphate following mechanical stretch of the urothelium from painful vs control bladders. The increase in adenosine triphosphate release in painful vs control bladders was statistically significant whether expressed in absolute values (mean +/- SE 3,791.4 +/- 667.9 vs 77.6 +/- 16.2 pM gm(-1) tissue) or as an increase over baseline (282.2% +/- 24.8% vs 175.4% +/- 21.7%). Similarly there was a significant release of adenosine triphosphate following electrical field stimulation of the urothelium from painful vs control bladders (1,348.6 +/- 278.2 vs 61.7 +/- 10.1 pM gm(-1) tissue, p < 0.005), representing a 278% +/- 41.5% vs 137.9% +/- 4.4% increase above baseline (p < 0.005). The source of adenosine triphosphate release was nonneuronal in 89% of painful bladders and in 84% of control bladders.Conclusions: There is a significantly increased level of adenosine triphosphate release from the urothelium of painful bladders in comparison to that from normal bladders, suggesting an important potential functional role for adenosine triphosphate in this condition.