Gill Bradley C, Moore Courtenay, Damaser Margot S
Cleveland Clinic Lerner College of Medicine, Department of Biomedical Engineering, Case Western Reserve University, 10900 Euclid Ave, Cleveland, OH 44195, USA.
Expert Rev Obstet Gynecol. 2010 Sep 1;5(5):567-580. doi: 10.1586/eog.10.48.
Postpartum stress urinary incontinence (SUI) is associated with chronic SUI in later life, which is 240% more likely to occur in women who deliver vaginally than those who did not. The etiology of SUI is multifactoral and has been associated with defects in both neuromuscular and structural components of continence. Specifically, clinical studies have demonstrated that pudendal nerve damage occurs during vaginal delivery, supporting the concept that neuromuscular damage to the continence mechanism can result in postpartum SUI. Urethral hypermobility and the loss of pelvic floor support, such as that involved in pelvic organ prolapse, have also been associated with SUI. Animal models provide an opportunity to investigate these injuries, individually and in combination, enabling researchers to gain further insight into their relative contributions to the development of SUI and the effectiveness of potential therapies for it. This article discusses the use of animal models of postpartum SUI in addition to the broad insights into treatment efficacy they provide.
产后压力性尿失禁(SUI)与晚年慢性SUI有关,经阴道分娩的女性发生慢性SUI的可能性比未经历阴道分娩的女性高240%。SUI的病因是多因素的,与控尿的神经肌肉和结构成分缺陷均有关。具体而言,临床研究表明,经阴道分娩时会发生阴部神经损伤,这支持了控尿机制的神经肌肉损伤可导致产后SUI的观点。尿道活动过度以及盆底支持结构丧失,如盆腔器官脱垂所涉及的情况,也与SUI有关。动物模型为单独或联合研究这些损伤提供了机会,使研究人员能够进一步深入了解它们对SUI发生发展的相对作用以及潜在治疗方法的有效性。本文除了讨论产后SUI动物模型的应用外,还阐述了其在治疗效果方面提供的广泛见解。