Pubo-urethral ligament injury causes long-term stress urinary incontinence in female rats: an animal model of the integral theory.

PURPOSE

We examined the long-term effects of pubo-urethral ligament deficiency as a potential model of stress urinary incontinence compared to an established model of stress urinary incontinence.

MATERIALS AND METHODS

A total of 21 female Sprague-Dawley rats were randomly assigned to 1 of 3 groups, including pubo-urethral ligament transection, sham pubo-urethral ligament transection and bilateral pudendal nerve transection. Leak point pressure was measured 28 days later via an implanted suprapubic catheter. After leak point pressure measurement all animals were sacrificed. The pubic arch and pelvic organs were harvested for histological examination. The Wilcoxon rank sum test was used to evaluate differences in leak point pressure among the experimental groups.

RESULTS

At 28 days after pubo-urethral ligament transection mean +/- SD leak point pressure was significantly decreased when comparing pubo-urethral ligament transection and pudendal nerve transection to sham treatment (15.75 +/- 6.46 and 15.10 +/- 4.98 cm H(2)O, respectively, vs 42.56 +/- 11.58, p <0.001). No difference was noted when comparing pubo-urethral ligament transection to pudendal nerve transection (p = 0.76), indicating the long-term durability of pubo-urethral ligament transection on inducing stress urinary incontinence in the female rat. Histological examination of en bloc suprapubic areas demonstrated an absent pubo-urethral ligament in the pubo-urethral ligament transection group, and an intact pubo-urethral ligament in the sham treated and pudendal nerve transection groups.

CONCLUSIONS

Our results show that pubo-urethral ligament deficiency in the female rat induces long-term stress urinary incontinence that is comparable to that in the established stress urinary incontinence model via pudendal nerve transection. Our novel rat model could be used to investigate mechanisms of stress urinary incontinence in females, including the role of urethral hypermobility and potential therapeutic interventions for stress urinary incontinence.