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一种模拟分娩创伤诱导压力性尿失禁的小鼠模型。

A mouse model of simulated birth trauma induced stress urinary incontinence.

作者信息

Lin Yi-Hao, Liu Guiming, Daneshgari Firouz

机构信息

Glickman Urological Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.

出版信息

Neurourol Urodyn. 2008;27(4):353-8. doi: 10.1002/nau.20509.

DOI:10.1002/nau.20509
PMID:17849481
Abstract

AIMS

To facilitate future applications of transgenic or knockout technologies in studies of simulated birth trauma induced stress urinary incontinence (SUI), we aimed to create a mouse model of SUI and explore the possible pathogenesis of this condition.

METHODS

Thirty female C57BL/6 mice were randomly distributed into five groups. Four groups underwent vaginal distention (VD) for 1 hr, using a modified 6-Fr. Foley catheter with a balloon dilated to 0.3, 0.2, or 0.1 ml or sham distention. Four days after VD, all mice underwent leak-point pressure (LPP) measurement via an implanted suprapubic tube (SPT). The normal control group only had SPT placement and LPP measurement. After sacrifice, the urethras of the mice were harvested for routine histological examination and nerve staining.

RESULTS

LPPs were significantly lower in groups after VD with 0.3- or 0.2-ml balloon than in control and sham distention groups (10.29 +/- 6.70, 14.65 +/- 6.51, 37.78 +/- 5.10, and 30.30 +/- 5.30 cm H(2)O, respectively). There were no significant differences in LPP between control and sham groups. Histology showed no significant differences in urethral striated muscle among the five groups. The density of immunoreactive neurofilaments in the urethra decreased after VD with 0.3- or 0.2-ml balloon.

CONCLUSION

As a model of birth trauma, VD can induce SUI in female mice, the severity of which is related to intravaginal balloon size. Partial urethral denervation plays a plausible role in the pathogenesis of SUI. This novel mouse model could be used for further mechanistic studies of female SUI.

摘要

目的

为促进转基因或基因敲除技术在模拟分娩创伤所致压力性尿失禁(SUI)研究中的未来应用,我们旨在创建SUI小鼠模型并探究该病症的可能发病机制。

方法

30只雌性C57BL/6小鼠随机分为五组。四组使用改良的6F Foley导管进行1小时的阴道扩张(VD),球囊分别扩张至0.3、0.2或0.1毫升或假扩张。VD后4天,所有小鼠通过植入的耻骨上导管(SPT)进行漏点压力(LPP)测量。正常对照组仅进行SPT放置和LPP测量。处死后,采集小鼠尿道进行常规组织学检查和神经染色。

结果

0.3毫升或0.2毫升球囊VD组的LPP显著低于对照组和假扩张组(分别为10.29±6.70、14.65±6.51、37.78±5.10和30.30±5.30厘米水柱)。对照组和假扩张组之间的LPP无显著差异。组织学显示五组尿道横纹肌无显著差异。0.3毫升或0.2毫升球囊VD后尿道免疫反应性神经丝密度降低。

结论

作为分娩创伤模型,VD可诱导雌性小鼠发生SUI,其严重程度与阴道内球囊大小有关。部分尿道去神经支配在SUI发病机制中可能起作用。这种新型小鼠模型可用于女性SUI的进一步机制研究。

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