实验性自身免疫性脑脊髓炎小鼠的排尿功能障碍:多发性硬化症样疾病

Lucie Evena, Ourdia Boualia, Mathieu Roumiguiea, Olivier Cuvillierb, Bernard Malavauda, Xavier Gamea
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引用次数: 1

摘要

背景:多发性硬化症(MS)是影响年轻人的最常见的致残性神经系统疾病。下尿路功能障碍(LUTD)在MS过程中很常见,是对上尿路的器质性影响和生活质量受损的原因。实验性自身免疫性脑脊髓炎(EAE)是多发性硬化症的一种动物模型,其特征是小鼠的尾巴和后肢瘫痪进展为截瘫,但泌尿参数和排尿行为尚不清楚。我们的目的是研究健康小鼠和EAE小鼠的排尿行为,以确定EAE引起的变化。方法:膀胱功能研究包括排尿行为和膀胱充盈术。结果:EAE小鼠出现了严重的膀胱功能障碍,其特征是每次排尿量减少(138.8±20比213±17.5µL, P = 0.018),排空后残尿频率显著增加(30%比61%,P = 0.0496),排空后残尿量增加(260±15比197.5±12µL, P = 0.045)。膀胱测量分析显示,逼尿肌过度活动明显增加(69% vs. 1%, P < 0.0001)。结论:我们的研究,通过临床和膀胱检查表征了EAE小鼠的膀胱功能障碍,显示功能障碍与人类多发性硬化症中发现的神经性膀胱疾病相似,使该模型有望评估新化合物。世界肾脏病杂志,2016;5(1):4-10 doi: http://dx.doi.org/10.14740/wjnu245w
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Voiding Dysfunction in Mice With Experimental Autoimmune Encephalomyelitis: A Multiple Sclerosis-Like Disease
Background: Multiple sclerosis (MS) is the most common disabling neurological disorder affecting young adults. Lower urinary tract dysfunction (LUTD) is common during the course of MS and is responsible for an organic impact on the upper urinary tract and for impaired quality of life. Experimental autoimmune encephalomyelitis (EAE), an animal model of MS, is characterized in mice by paralysis of the tail and hind limbs progressing to paraplegia, but urinary parameters and voiding behavior are not well understood. We aimed to study micturition behavior of both healthy and EAE mice to determine changes induced by EAE. Methods: Bladder function study included micturition behavior and filling cystometry. Results: EAE mice developed profound bladder dysfunction characterized by a decrease in urine volume per micturition (138.8 ± 20 vs. 213 ± 17.5 µL, P = 0.018), significantly more frequent postvoid residual urine (30% vs. 61%, P = 0.0496), and increased postvoid residual volume (260 ± 15 vs. 197.5 ± 12 µL, P = 0.045). Cystometric analysis showed significantly more frequent detrusor overactivity (69% vs. 1%, P < 0.0001). Conclusions: Our study, characterizing bladder dysfunction in EAE mice by clinical and cystometric examination, showed that dysfunction was similar to neurological bladder disorders found in human multiple sclerosis and makes this model promising to assess new compounds. World J Nephrol Urol. 2016;5(1):4-10 doi: http://dx.doi.org/10.14740/wjnu245w
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