AIMS: Pudendal nerve injury in the rat has been a useful animal model for studying stress urinary incontinence (SUI). However, the effect of pudendal nerve injury on activity of the external urethral sphincter (EUS) is relatively unexplored. The aims of this study were to examine voiding and the EUS electromyogram (EMG) in a durable SUI model in rats with bilateral or unilateral pudendal nerve transections. In addition, the effects of denervation on urethral anatomy were investigated. METHODS: A leak point pressure (LPP) test was first used to demonstrate that pudendal nerve transection induced SUI. Cystometry exhibited changes in voiding function and EUS-EMG measurements provided a quantitative evaluation of EUS activity during voiding. The morphological changes in sections through the mid-urethra were assessed with hematoxylin and eosin (H&E) staining. RESULTS: A significant decrease in average LPP was detected in rats 6 weeks after bilateral pudendal nerve transection (BPNT). Abnormal urodynamic measurements including a decrease in contraction amplitude and voided volume as well as an increase in contraction duration, and residual volume all indicated inefficient voiding. In addition EUS-EMG silent periods were reduced and the frequency of EUS-EMG bursting during voiding was increased. Atrophy of striated muscle in the EUS was also detected in rats with pudendal nerve transection(s). CONCLUSIONS: Our results indicate that pudendal nerve transection in rats decreases urethral outlet resistance and causes striated muscle atrophy in the EUS, EUS-EMG abnormalities and inefficient voiding. The results demonstrate that BPNT is a durable model for SUI.
AIMS: Pudendal nerve injury in the rat has been a useful animal model for studying stress urinary incontinence (SUI). However, the effect of pudendal nerve injury on activity of the external urethral sphincter (EUS) is relatively unexplored. The aims of this study were to examine voiding and the EUS electromyogram (EMG) in a durable SUI model in rats with bilateral or unilateral pudendal nerve transections. In addition, the effects of denervation on urethral anatomy were investigated. METHODS: A leak point pressure (LPP) test was first used to demonstrate that pudendal nerve transection induced SUI. Cystometry exhibited changes in voiding function and EUS-EMG measurements provided a quantitative evaluation of EUS activity during voiding. The morphological changes in sections through the mid-urethra were assessed with hematoxylin and eosin (H&E) staining. RESULTS: A significant decrease in average LPP was detected in rats 6 weeks after bilateral pudendal nerve transection (BPNT). Abnormal urodynamic measurements including a decrease in contraction amplitude and voided volume as well as an increase in contraction duration, and residual volume all indicated inefficient voiding. In addition EUS-EMG silent periods were reduced and the frequency of EUS-EMG bursting during voiding was increased. Atrophy of striated muscle in the EUS was also detected in rats with pudendal nerve transection(s). CONCLUSIONS: Our results indicate that pudendal nerve transection in rats decreases urethral outlet resistance and causes striated muscle atrophy in the EUS, EUS-EMG abnormalities and inefficient voiding. The results demonstrate that BPNT is a durable model for SUI.
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