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Pubo-urethral ligament transection causes stress urinary incontinence in the female rat: a novel animal model of stress urinary incontinence.

Kefer JC, Liu G, Daneshgari F

Glickman Urological Institute, Lerner Research Institute, The Cleveland Clinic, Cleveland, Ohio, USA.

PURPOSE: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Published 14 January 2008 in J Urol, 179(2): 775-8.
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