Kefer John C, Liu Guiming, Daneshgari Firouz
Glickman Urological Institute, Lerner Research Institute, The Cleveland Clinic, Cleveland, Ohio, USA.
J Urol. 2008 Feb;179(2):775-8. doi: 10.1016/j.juro.2007.09.025. Epub 2007 Dec 20.
We hypothesized that transection of the pubo-urethral ligament in the female rat would cause stress urinary incontinence, as indicated by decreased leak point pressure. We created a novel model of pubo-urethral ligament deficiency in the rat and validated our model through comparison with an established model of stress urinary incontinence.
A total of 21 female age matched Sprague-Dawley rats (Harlan, Indianapolis, Indiana) were randomly assigned to 5 groups, including pubo-urethral ligament transection or sham pubo-urethral ligament transection with leak point pressure measured 4 days (groups 1 and 2) or 10 days (groups 3 and 4) postoperatively and bilateral pudendal nerve transection with leak point pressure measured 4 days postoperatively (group 5). Leak point pressure was measured in all groups via a suprapubic catheter. The Wilcoxon signed rank test was used to evaluate differences between the groups.
Leak point pressure was significantly decreased in the pubo-urethral ligament transection groups compared to that in the sham treated groups after 4 days (mean +/- SEM 16.3 cm +/-2.74 vs 36.6 +/- 8.39 cm H(2)O, p <0.00001), although it was no different from that in the pudendal nerve transection group (14.5 +/- 1.06 cm H(2)O, p <0.44). Ten days after surgery leak point pressure remained significantly lower in the pubo-urethral ligament transection groups compared to that in the sham treated groups (17.6 +/- 6.36 vs 31.2 +/- 5.14 cm H(2)O, p <0.00001), indicating the durability of pubo-urethral ligament transection for inducing stress urinary incontinence in female rats.
Our results demonstrate that deficiency of the pubo-urethral ligament in the female rat induces stress urinary incontinence comparable to that in a previously established model of pudendal nerve transection induced stress urinary incontinence. This novel rat model could be used to investigate the mechanisms of urethral hypermobility in female stress urinary incontinence or potential therapeutic interventions for stress urinary incontinence.
我们假设切断雌性大鼠的耻骨尿道韧带会导致压力性尿失禁，表现为漏点压力降低。我们创建了一种新型的大鼠耻骨尿道韧带缺损模型，并通过与已建立的压力性尿失禁模型进行比较来验证我们的模型。
总共21只年龄匹配的雌性Sprague-Dawley大鼠（Harlan，印第安纳波利斯，印第安纳州）被随机分为5组，包括耻骨尿道韧带切断组或假耻骨尿道韧带切断组，分别在术后4天（第1组和第2组）或10天（第3组和第4组）测量漏点压力，以及双侧阴部神经切断组，在术后4天测量漏点压力（第5组）。通过耻骨上导管测量所有组的漏点压力。采用Wilcoxon符号秩检验评估组间差异。
与假手术组相比，耻骨尿道韧带切断组在术后4天漏点压力显著降低（平均±标准误16.3 cm±2.74 vs 36.6±8.39 cm H₂O，p<0.00001），尽管与阴部神经切断组无差异（14.5±1.06 cm H₂O，p<0.44）。术后10天，耻骨尿道韧带切断组的漏点压力仍显著低于假手术组（17.6±6.36 vs 31.2±5.14 cm H₂O，p<0.00001），表明耻骨尿道韧带切断在诱导雌性大鼠压力性尿失禁方面具有持久性。
我们的结果表明，雌性大鼠耻骨尿道韧带缺损诱导的压力性尿失禁与先前建立的阴部神经切断诱导的压力性尿失禁模型相当。这种新型大鼠模型可用于研究女性压力性尿失禁中尿道活动过度的机制或压力性尿失禁的潜在治疗干预措施。
