关于女性尿失禁病理生理学的思考与假设。

U Ulmsten
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引用次数: 0

摘要

有人提出,尿道近端和膀胱颈的打开和关闭是由一系列周围结构调节的,其中最重要的是耻骨尿道-膀胱韧带,尿道下阴道壁,“吊床”,耻骨尾骨肌,提肛板和结缔组织,它们像胶水一样将这些结构相互连接起来。在这些结构之一中不适当的功能在某种程度上可以通过在另一个结构中改进的功能来补偿,从而保持控制。然而,尿道的支撑功能明显恶化——通常由耻骨尿道/耻骨膀胱韧带、耻骨尾骨肌肉和阴部下阴道壁维持——将导致明显的应激性尿失禁。这些结构的严重缺陷通常不能通过盆腔肌肉的锻炼来补偿。这是真的,特别是,如果结缔组织的功能也有缺陷,而结缔组织将泌尿生殖器结构“粘合”在一起。在这种情况下,必须考虑进行外科手术以减轻患者的症状。到目前为止所说的绝不能排除认识到内部尿道结构对维持尿失禁的作用的重要性,特别是尿道肌肉、结缔组织和血管化的质量。在一些具体的混合性尿失禁病例中,可以推测急迫症状是否可能由解剖功能障碍引起,导致尿道近端和膀胱颈在轻微的压力刺激下保持不自主地打开或迅速打开。如果是这样,膀胱颈和尿道近端的扩张可能会激活位于这里的拉伸感受器,从而引起不受抑制的逼尿肌收缩。雌激素受体存在于许多与保持失禁有关的结构中,这可能解释了绝经后患者,特别是未接受激素替代治疗的患者,泌尿生殖道功能障碍患病率增加的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Some reflections and hypotheses on the pathophysiology of female urinary incontinence.

It is proposed that opening and closure of the proximal urethra and bladder neck are regulated by a battery of surrounding structures, the most important being the pubourethral-vesical ligaments, the suburethral vaginal wall, 'the hammock', the pubococcygeus muscles, the levator plate and the connective tissue which like glue connects these structures to each other. Inappropriate function in one of these structures can, to some extent, be compensated for by an improved function in another hereby maintaining continence. However, a significantly deteriorated function in the support of urethra--normally maintained by the pubourethral/pubovesical ligaments, the pubococcygeus muscles and suburethral vaginal wall--will result in pronounced stress incontinence. Severe defects in these structures can generally not be compensated for by exercises of the pelvic muscles. This is true, in particular, if there is also a defect function in the connective tissue which 'glues' the urogenital structures to each other. Under such circumstances surgical procedures have to be considered to alleviate the patients symptoms. What is said so far must not exclude the importance of recognizing the role of the internal urethral structures to maintain continence, in particular the quality of urethral muscles, connective tissue and vascularization. In some specific cases of mixed incontinence it can be speculated whether the urge symptom can be caused by an anatomical dysfunction causing the proximal urethra and the bladder neck to remain involuntarily open or to open promptly at even minor pressure provocations. If so distension of the bladder neck and proximal urethra may activate stretch receptors located here which will induce uninhibited detrusor contractions. The presence of estrogen receptors in many of the structures involved in preserving continence may explain the increased prevalence of dysfunctions in the urogenital tract in postmenopausal patients, in particular in those not on hormone replacement therapy.

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