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通过在膀胱颈周围放置金属环建立的膀胱活动低下新小鼠模型。

New mouse model of underactive bladder developed by placement of a metal ring around the bladder neck.

作者信息

Eljamal Kareman, Kajioka Shunichi, Maki Tomoko, Ushijima Miho, Kawagoe Kentaro, Lee Ken, Sasaguri Toshiyuki

机构信息

Department of Clinical Pharmacology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Department of Urology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

出版信息

Low Urin Tract Symptoms. 2021 Apr;13(2):299-307. doi: 10.1111/luts.12359. Epub 2020 Oct 21.

Abstract

OBJECTIVE

To develop a new mouse model of underactive bladder (UAB) caused by chronic bladder outlet obstruction (BOO).

METHODS

BOO was created in 6-week-old male C57BL/6 mice using surgery to loosely place a silver jump ring around the bladder neck of each mouse. Micturition behavior (assessed with a metabolic cage) and cystometry were used to evaluate bladder function at 8 and 16 weeks after BOO. Following completion of the functional studies, the bladders of the mice were excised, weighed, and subjected to histological analysis.

RESULTS

Micturition behavior analysis showed that mice subjected to BOO for 16 weeks had a lower frequency of micturition (7.3 ± 1.1 vs 12.5 ± 3.0 times/d, P < .05) and volume per void (106.0 ± 0.1 vs 133.9 ± 3.2 μL, P < .05) than mice subjected to BOO for 8 weeks. Cystometry revealed that mice subjected to BOO for 16 weeks had lower baseline pressure (8.4 ± 0.6 vs 14.0 ± 0.7 cmH O, P < .01) and micturition pressure (13.9 ± 1.1 vs 42.8 ± 1.7 cmH O, P < .05) than mice subjected to BOO for 8 weeks. BOO caused progressive increases in bladder mass and collagen deposition over time.

CONCLUSIONS

We successfully established a novel mouse model of UAB using surgery to place a silver jump ring loosely on the bladder neck. BOO initially induced bladder overactivity but subsequently resulted in UAB due to deterioration of detrusor smooth muscle contractility and progressive deposition of collagen in the bladder wall.

摘要

目的

建立一种由慢性膀胱出口梗阻(BOO)引起的膀胱过度活动症(UAB)的新小鼠模型。

方法

对6周龄雄性C57BL/6小鼠进行手术,在每只小鼠膀胱颈部松散地放置一个银质跳环,制造BOO模型。在BOO术后8周和16周,使用代谢笼评估排尿行为,并进行膀胱测压以评估膀胱功能。功能研究完成后,切除小鼠的膀胱,称重并进行组织学分析。

结果

排尿行为分析显示,与接受BOO 8周的小鼠相比,接受BOO 16周的小鼠排尿频率更低(7.3±1.1次/天 vs 12.5±3.0次/天,P<0.05),每次排尿量更少(106.0±0.1 μL vs 133.9±3.2 μL,P<0.05)。膀胱测压显示,与接受BOO 8周的小鼠相比,接受BOO 16周的小鼠基线压力更低(8.4±0.6 cmH₂O vs 14.0±0.7 cmH₂O,P<0.01),排尿压力更低(13.9±1.1 cmH₂O vs 42.8±1.7 cmH₂O,P<0.05)。随着时间的推移,BOO导致膀胱质量和胶原沉积逐渐增加。

结论

我们通过手术在膀胱颈部松散放置银质跳环,成功建立了一种新的UAB小鼠模型。BOO最初诱发膀胱过度活动,但随后由于逼尿肌平滑肌收缩力下降和膀胱壁胶原的逐渐沉积而导致UAB。

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