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膀胱过度活动症的肌源性基础。

A myogenic basis for the overactive bladder.

作者信息

Brading A F

机构信息

University Department of Pharmacology, Oxford, United Kingdom.

出版信息

Urology. 1997 Dec;50(6A Suppl):57-67; discussion 68-73. doi: 10.1016/s0090-4295(97)00591-8.

Abstract

OBJECTIVES

This article summarizes evidence supporting the conclusion that the spontaneous rises in pressure that occur in the overactive bladder, particularly in detrusor instability (DI), regardless of etiology, are myogenic.

METHODS

The evidence quoted has been obtained by several groups of investigators and includes electrophysiologic studies of detrusor myocytes, tension studies of strips of smooth muscle, in vivo experiments on animal models, and light and electron microscopic studies of the structure of the bladder wall.

RESULTS

The results of these studies demonstrate changes in the properties, structure, and innervation of the detrusor. These changes are consistent with the hypothesis that partial denervation of the detrusor may be responsible for altering the properties of the smooth muscle, leading to increased excitability and increased ability of activity to spread between cells, resulting in coordinated myogenic contractions of the whole detrusor.

CONCLUSIONS

It is suggested that alterations in the properties of the detrusor myocytes are a necessary prerequisite for the production of the unstable pressure rises seen in DI of any origin.

摘要

目的

本文总结了支持以下结论的证据,即膀胱过度活动症中出现的自发性压力升高,尤其是逼尿肌不稳定(DI),无论病因如何,均为肌源性。

方法

引用的证据由几组研究人员获得,包括对逼尿肌肌细胞的电生理研究、平滑肌条带的张力研究、动物模型的体内实验以及膀胱壁结构的光镜和电镜研究。

结果

这些研究结果表明了逼尿肌在特性、结构和神经支配方面的变化。这些变化与以下假设一致,即逼尿肌的部分去神经支配可能导致平滑肌特性改变,从而导致兴奋性增加以及活动在细胞间传播的能力增强,进而导致整个逼尿肌产生协调性肌源性收缩。

结论

提示逼尿肌肌细胞特性的改变是产生任何原因所致DI中不稳定压力升高的必要前提。

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