Quantification of neurological and other contributors to continence in female rats.

Smooth muscle, striated muscle, their central and peripheral innervations and control, and mucosal coaptation contribute to maintenance of continence. We used manual leak point pressure (mLPP) testing and electrical stimulation LPP (eLPP) testing in female rats to quantify the contribution of these factors to urethral resistance, a measure of continence. Abdominal muscles were electrically stimulated to induce leakage for eLPP. A Crede maneuver was applied for mLPP. These were repeated after complete T8 spinal cord injury (SCI) and/or bilateral pudendal nerve transection (PNT). After euthanasia, mLPP was repeated. MLPP was not significantly affected by opening the abdomen, suggesting that intra-abdominal pressure transmission contributes little to continence during slow pressure changes. ELPP was significantly higher than mLPP in intact rats, after PNT, and after SCI+PNT, suggesting that abdominal pressure transmission contributes to continence during rapid increases in intra-abdominal pressure. MLPP decreased significantly after PNT, indicating that urethral striated muscles contribute significantly to continence. ELPP decreased significantly after PNT with and without SCI, suggesting that supraspinal control significantly affects continence during rapid pressure changes, but not during slow pressure changes. MLPP after euthanasia was significantly decreased compared to mLPP after SCI+PNT, suggesting that urethral mucosal seal coaptation and tissue elasticity also contribute to continence. The urethra is a complex organ that maintains continence via a highly organized and hierarchical system involving both the central and peripheral nervous systems.

Pelvic floor muscles and the external urethral sphincter have different responses to applied bladder pressure during continence.

OBJECTIVES: To determine the functional innervation of the pelvic floor muscles (PFM) and whether there is PFM activity during an external pressure increase to the bladder in female rats. METHODS: Thirty-one female adult virgin Sprague-Dawley rats received an external increase in bladder pressure until urinary leakage was noted while bladder pressure was recorded (leak point pressure [LPP]) under urethane anesthesia. Six of the rats underwent repeat LPP testing after bilateral transection of the levator ani nerve. Another 6 rats underwent repeat LPP testing after bilateral transection of the pudendal nerve. Simultaneous recordings of PFM (pubo- and iliococcygeus muscles), electromyogram (EMG), and external urethral sphincter (EUS) EMG were recorded during cystometry and LPP testing. RESULTS: Thirteen rats (42%) showed tonic PFM EMG activity during filling cystometry. Eighteen rats (58%) showed no tonic PFM EMG activity at baseline, but PFM EMG could be activated by pinching the perineal skin. This activity could be maintained unless voiding occurred. The external increase in bladder pressure caused significantly increased EUS EMG activity as demonstrated by increased amplitude and frequency. However, there was no such response in PFM EMG. LPP was not significantly different after levator ani nerve transection, but was significantly decreased after pudendal nerve transection. CONCLUSIONS: PFM activity was not increased during external pressure increases to the bladder in female rats. Experimental designs using rats should consider this result. The PFM, unlike the EUS, does not contribute to the bladder-to-urethra continence reflex. PFM strengthening may nonetheless facilitate urinary continence clinically by stabilizing the bladder neck.

Effects of sphincterotomy and pudendal nerve transection on the anal sphincter in a rat model.

PURPOSE: Our objective was to define anal resting pressure and electromyography of the normal rat anal sphincter and investigate the short-term effects of both mechanical trauma to the anal sphincter muscles and pudendal nerve transection. METHODS: Forty-five virgin female Sprague-Dawley rats were randomly allotted to three groups: controls (n = 21), sphincterotomy (n = 12), and pudendal nerve transection (n = 12). Anal pressure was monitored using a saline-filled balloon connected to a pressure transducer. Anal pressure and electromyography of the anal sphincter with use of a needle electrode were recorded both before and after injury or succinylcholine administration. RESULTS: Anal pressure data were consistent with rhythmic pressure contractions. Succinylcholine significantly reduced both pressure and electromyography signals. Electromyography amplitude and frequency decreased after nerve transection but not after sphincterotomy. The histology showed that the rat anal anatomy has muscular components that compare with human anatomy. The sphincterotomy group showed injury to the anal sphincters and the sphincter anatomy of the nerve transection group appeared similar to the control group. The anal pressure wave appears to be created by synergistic activity of both striated and smooth muscle of the anal sphincter. CONCLUSION: The female rat is a suitable and reliable model for studying effect of direct and indirect injury to the anal sphincters.

Electrophysiological function during voiding after simulated childbirth injuries.

During vaginal delivery dual injuries of the pudendal nerve and the external urethral sphincter (EUS), along with other injuries, are correlated with later development of stress urinary incontinence. It is not known how combinations of these injuries affect neuromuscular recovery of the micturition reflex. We investigated the EUS electromyogram (EMG) and the pudendal nerve motor branch potentials (PNMBP) during voiding 4 days, 3 weeks or 6 weeks after injury; including vaginal distension (VD), pudendal nerve crush (PNC), both PNC and VD (PNC+VD), and pudendal nerve transection (PNT); and in controls. Pudendal nerve and urethral specimens were excised and studied histologically. No bursting activity was recorded in the EUS EMG during voiding 4 days after all injuries, as well as 3 weeks after PNC+VD. Bursting activity demonstrated recovery 3 weeks after either VD or PNC and 6 weeks after PNC+VD, but the recovered intraburst frequency remained significantly decreased compared to controls. Bursting results of PNMBP were similar to the EMG, except bursting in PNMBP 4 days after VD and the recovered intraburst frequency was significantly increased compared to controls after PNC and PNC+VD. After PNT, neither the EUS nor the pudendal nerve recovered by 6 weeks after injury. Our findings indicate bursting discharge during voiding recovers more slowly after PNC+VD than after either PNC or VD alone. This was confirmed histologically in the urethra and the pudendal nerve and may explain why pudendal nerve dysfunction has been observed years after vaginal delivery.