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实验性膀胱出口梗阻后膀胱过度活动大鼠模型中 Cajal 间质细胞的分布及一氧化氮合酶的表达。

Distribution of interstitial cells of Cajal and expression of nitric oxide synthase after experimental bladder outlet obstruction in a rat model of bladder overactivity.

机构信息

Department of Urology, Chonnam National University Medical School, Gwangju, South Korea.

出版信息

Neurourol Urodyn. 2011 Nov;30(8):1639-45. doi: 10.1002/nau.21144. Epub 2011 Jul 20.

Abstract

AIMS

Recent studies have showed that interstitial cells (ICs) are widely distributed in the genitourinary tract and have suggested their involvement in spontaneous electrical activity and muscle contraction. Nitric oxide (NO) is thought to play a role in bladder overactivity related with bladder outlet obstruction (BOO). The purposes of this study were to investigate the effect of bladder overactivity induced by BOO on ICs and nitric oxide synthase (NOS) isoforms in rat urinary bladder.

METHODS

Female Sprague-Dawley rats (230-240  g, n = 40) were divided into two groups: control (group Con, n = 20) and partial BOO (group BOO, n = 20). After 4 weeks, urodynamic studies measuring contraction interval and contraction pressure were done. The cellular localization of cKit immunoreactive ICs and the expression of endothelial NOS (eNOS) and neuronal NOS (nNOS) were determined by Western blot and immunohistochemistry in the rat urinary bladder.

RESULTS

Filling cystometry studies demonstrated a reduced interval between voiding contractions and an increased voiding pressure in BOO bladders. The contraction interval time (2.9 ± 0.35  min) was significantly decreased in the BOO group compared to the control (6.1 ± 0.05; P < 0.05). The population of ICs was increased in the suburothelial and muscle layers in BOO bladders. ICs had a close contact with each other and neighboring nNOS expressing cells.

CONCLUSIONS

These results demonstrated an increased population of ICs in the BOO rat model and suggest that the functional change of ICs and NOS isoforms may contribute to the pathophysiology of bladder overactivity induced by BOO.

摘要

目的

最近的研究表明,间质细胞(ICs)广泛分布于泌尿生殖道,并提示其参与自发性电活动和肌肉收缩。一氧化氮(NO)被认为在与膀胱出口梗阻(BOO)相关的膀胱过度活动中发挥作用。本研究旨在探讨 BOO 引起的膀胱过度活动对大鼠膀胱 ICs 和一氧化氮合酶(NOS)同工型的影响。

方法

将 40 只雌性 Sprague-Dawley 大鼠(230-240g,n=40)分为两组:对照组(n=20)和部分 BOO 组(n=20)。4 周后,行尿动力学研究,测量收缩间期和收缩压。通过 Western blot 和免疫组化法测定大鼠膀胱中 cKit 免疫反应性 ICs 的细胞定位和内皮型 NOS(eNOS)和神经元型 NOS(nNOS)的表达。

结果

充盈膀胱测压研究表明,BOO 膀胱的排尿收缩间隔缩短,排尿压升高。与对照组相比,BOO 组的收缩间隔时间(2.9±0.35min)明显缩短(P<0.05)。BOO 膀胱的黏膜下和肌层中 IC 数量增加。ICs 彼此之间以及与邻近的 nNOS 表达细胞密切接触。

结论

这些结果表明,BOO 大鼠模型中 ICs 的数量增加,提示 ICs 和 NOS 同工型的功能变化可能有助于解释 BOO 引起的膀胱过度活动的病理生理机制。

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