Song Qi-Xiang, Balog Brian M, Kerns James, Lin Dan Li, Sun Yinghao, Damaser Margot S, Jiang Hai-Hong
Department of Biomedical Engineering, The Cleveland Clinic, Cleveland, Ohio; Department of Urology, Changhai Hospital, The Second Military Medical University, Shanghai, People's Republic of China; Advanced Platform Technology Rehabilitation R&D Center of Excellence, Louis Stokes Cleveland Veterans Affairs Medical Center, Cleveland, Ohio.
Neurourol Urodyn. 2015 Apr;34(4):381-6. doi: 10.1002/nau.22561. Epub 2014 Feb 5.
Pudendal nerve and external urethral sphincter (EUS) injury during vaginal delivery are risk factors for stress urinary incontinence (SUI). Although most patients with short-term postpartum SUI regain continence within 1 year, they have a higher predisposition to develop recurrent SUI years later, suggesting a possible mechanistic relationship. In contrast, animal models generally recover spontaneously and have not been studied much in the long term. The aim of this study was to investigate the long-term effects of simulated childbirth injury in rats.
Thirty-four Sprague-Dawley female rats underwent sham injury or pudendal nerve crush and vaginal distension (PNC + VD), a simulated childbirth injury. Nine weeks later, leak point pressure (LPP) and EUS electromyography (EMG) were recorded simultaneously. The pudendal nerve was harvested for histological analysis. EUS neuromuscular junctions (NMJs) and their innervation were qualitatively assessed using immunofluorescence. A t-test was used to compare quantitative outcomes between groups, with P < 0.05 indicating a significant difference.
There was no significant difference in LPP or EUS EMG amplitude or firing rate between the two groups. Nonetheless after PNC + VD, NMJs in the EUS were diffuse and were innervated by tortuous and multiple axons, demonstrating that reinnervation of the EUS was still in progress.
Although continence function recovered 9 weeks after simulated childbirth injury, innervation of EUS was not complete at this time point, suggestive of persistent neurogenic deficiency which when compounded by the effects of aging may lead to a delayed recurrence of SUI in this animal model with increased age.
阴道分娩时阴部神经和尿道外括约肌(EUS)损伤是压力性尿失禁(SUI)的危险因素。尽管大多数产后短期SUI患者在1年内恢复控尿能力,但数年后他们复发SUI的倾向更高,提示可能存在机制上的关联。相比之下,动物模型通常能自发恢复,且长期研究较少。本研究的目的是调查大鼠模拟分娩损伤的长期影响。
34只Sprague-Dawley雌性大鼠接受假损伤或阴部神经挤压及阴道扩张(PNC + VD),即模拟分娩损伤。9周后,同时记录漏点压力(LPP)和EUS肌电图(EMG)。采集阴部神经进行组织学分析。使用免疫荧光定性评估EUS神经肌肉接头(NMJ)及其神经支配。采用t检验比较两组之间的定量结果,P < 0.05表示差异有统计学意义。
两组之间的LPP、EUS EMG振幅或放电频率无显著差异。尽管如此,在PNC + VD后,EUS中的NMJ分散,由扭曲且多支的轴突支配,表明EUS的再支配仍在进行中。
尽管模拟分娩损伤9周后控尿功能恢复,但此时EUS的神经支配尚未完成,提示存在持续性神经源性缺陷,随着年龄增长,这种缺陷可能导致该动物模型中SUI延迟复发。