期刊名稱: European Urology. 2010 Mar;57(3):506-12. (Impact Factor: 6.512)
論文題目: Recovery of Continence Function following Simulated Birth Trauma Involves Repair of Muscle and Nerves in the Urethra in the Female Mouse
論文作者: Yi-Hao, Lin et al. (
論文摘要:
Objectives – The natural history and the mechanisms behind the alteration of vaginal distension (VD) in a mouse model are not clear. We examined the temporal sequelae of VD and pudendal nerve transection (PNT) on leak-point pressure (LPP) and the muscular and nerve components of the urethra in mice.
Materials and Methods – Seventy-two virgin female C57BL/6 mice were equally distributed into three groups. The VD group underwent VD for 1 h. The PNT group received bilateral PNT. A control group underwent sham VD. Each group was divided into four subgroups of six mice for measurement of LPP at 0, 4, 10, and 20 d after VD or PNT. LPP was measured. Morphology and neurofilament-immunoreactive nerve of the urethra were assessed.
Results – LPP was decreased at 0, 4, and 10 d but not at 20 d after VD. Decreased LPP persisted to 20 d in the PNT group. The external urethral striated muscle appeared disrupted and/or wavy in two mice at 0 d, in three mice at 4 d, in one mouse at 10 d, and in one mouse in 20 d after VD. The density of neurofilament-immunoreactive nerve in the urethra was reduced at 4 and 10 d after VD, but not at 20 d, and at 4, 10, and 20 d after PNT compared with the corresponding values of the sham VD group. The limitation of this animal model is that the pelvic floor structure of the mouse is different from that of female humans. Therefore, results of this study should be carefully applied to human subjects.
Conclusions – VD causes reversible stress urinary incontinence in female mice. Recovery of continence function following VD is associated with repair of the external urethral sphincter and reinnervation of the urethra. This mouse model will be useful for mechanistic investigation and targeting of therapeutic intervention by taking advantage of genetic manipulation.
論文導讀: 本篇文章的目的在探討瞭解使用陰道擴張造成小鼠尿失禁動物模型的自然病史及可能的機轉，分別接受陰道擴張及會陰神經截斷的小鼠，我們使用漏尿點壓力(LPP)及尿道的肌肉及神經成份來分析並解釋。我們使用C57BL/6小鼠分成三組，第一組接受0.3毫升陰道擴張一小時，第二組接受兩側會陰神經截斷，第三組為對照組，每一組在手術後又分成 0, 4, 10, 20天四個不同時間點接受檢查及分析，第一組漏尿點壓力在 0, 4, 10天較低，第二組漏尿點壓力在 0, 4, 10, 20天皆較低，第一組尿道神經纖維密度在 4, 10天較低，第二組尿道神經纖維密度在 4, 10, 20天較低，以上結果發現陰道擴張造成小鼠尿失禁是可逆的，禁尿功能的恢復似乎與尿道神經纖維的密度有相關性，但動物模型的骨盆構造與人體畢竟不完全相同，想要用來解釋人類尿失禁的機轉必須要更謹慎。
