de Jongh Rik, Dambros Miriam, Haenen Guido R M M, den Hartog Gertjan J M, Bast Aalt, van Kerrebroeck Philip E V, van Koeveringe Gommert A
Department of Urology, University Hospital Maastricht, Maastricht, The Netherlands.
Neurourol Urodyn. 2009;28(5):461-7. doi: 10.1002/nau.20677.
Reactive nitrogen and oxygen species (RNOS) likely play a role in the development of bladder dysfunction related to bladder outlet obstruction. Antioxidants protect against these free radicals. The aim of our study was to investigate the effect of bladder outlet obstruction on the endogenous antioxidant status of the bladder and to correlate this to bladder structure and function.
In 16 guinea pigs either a partial outlet obstruction or a sham operation was induced. The contractile responses of detrusor strips to electrical field stimulation (EFS), acetylcholine, potassium, and ATP were monitored 4 weeks after the operation. The nerve density in bladder tissue was determined by using the non-specific nerve marker PGP 9.5. Separate antioxidants and the total antioxidant status were assessed using the trolox equivalent antioxidant capacity (TEAC) test.
Contractile responses of detrusor strips to EFS were for the greater part based on neurogenic stimulation. The nerve-mediated responses in strips from obstructed bladders were lower compared to the sham group. Obstructed bladders showed a patchy denervation and the nerve density was significantly lower compared to the sham group. The total antioxidant capacity, the glutathione and the glutathione reductase (GR) levels significantly decreased in obstructed bladders compared to the sham group.
This study demonstrates that the antioxidant status of guinea pig bladders exposed to outlet obstruction decreased which might be associated with the observed reduction in nerve density. The results strengthen the hypothesis that oxidative stress is involved in the pathophysiology of bladder dysfunction related to obstructed bladders. Neurourol. Urodynam. 28:461-467, 2009. (c) 2008 Wiley-Liss, Inc.
活性氮和氧物种（RNOS）可能在与膀胱出口梗阻相关的膀胱功能障碍发展中起作用。抗氧化剂可抵御这些自由基。我们研究的目的是调查膀胱出口梗阻对膀胱内源性抗氧化状态的影响，并将其与膀胱结构和功能相关联。
对16只豚鼠进行部分出口梗阻或假手术。术后4周监测逼尿肌条对电场刺激（EFS）、乙酰胆碱、钾和三磷酸腺苷（ATP）的收缩反应。使用非特异性神经标志物PGP 9.5测定膀胱组织中的神经密度。使用特洛克斯等效抗氧化能力（TEAC）试验评估单独的抗氧化剂和总抗氧化状态。
逼尿肌条对EFS的收缩反应大部分基于神经源性刺激。与假手术组相比，梗阻膀胱条中的神经介导反应较低。梗阻膀胱显示出散在性去神经支配，且神经密度明显低于假手术组。与假手术组相比，梗阻膀胱中的总抗氧化能力、谷胱甘肽和谷胱甘肽还原酶（GR）水平显著降低。
本研究表明，暴露于出口梗阻的豚鼠膀胱的抗氧化状态降低，这可能与观察到的神经密度降低有关。结果强化了氧化应激参与与梗阻膀胱相关的膀胱功能障碍病理生理学的假说。《神经泌尿学与尿动力学》28:461 - 467，2009年。（c）2008威利 - 利斯公司。
