Lower urinary tract symptoms due to intrapelvic nerve impairment are frequent complications of pelvic surgery. We recently reported a novel neurogenic bladder rat model by damaging  the accessory nerve (ACN), which is one of the intrapelvic nerves. Bilateral ACN injury (BACNI) causes overflow urinary incontinence and bladder fibrosis in the short term. In this study, we examined the effects of BACNI on detrusor muscle contractility without overdistension of the bladder.

We randomly categorized ten-week-old male Wistar/ST rats into the sham, BACNI, and BACNI+low-pressure (LP) groups. BACNI was induced by crushing the ACN bilaterally for one min using reverse-action tweezers. In the sham group, the bilateral ACN was identified but was not crushed. A polyethylene catheter was then inserted into the bladder dome to drain urine. In the BACNI+LP group, the urine was continuously drained to avoid bladder overdistension. While in the sham and BACNI groups, the tip of the catheter was closed and urine was not drained. After a 4-hour operation, residual urine volume in the BACNI and BACNI+LP groups was measured. The bladder was then excised, and detrusor muscle contractility was evaluated using an isometric tension study. Bladder contractile responses to cumulative administration of carbachol (CCh; 10^9‐3×10^5 M) and electrical field stimulation (EFS; 1‐64 Hz) were measured. The maximum response (Emax) and the concentration that induced half the response of Emax (EC50) of CCh were analyzed from dose-response curves. In EFS evaluation, the cholinergic component was calculated as the difference between the contractile responses to EFS without inhibitors and with atropine, a cholinergic inhibitor. One-way analysis of variance (ANOVA) followed by Dunnett’s multiple comparison test was used to compare the contractile responses. Welch’s t-test was used to compare the residual urine volume.

Large residual urine volume and overflow urinary incontinence were observed in the BACNI group, while little residual urine was observed in the BACNI+LP group (BACNI, 1.61 ± 0.82 mL; BACNI+LP, 0.07 ± 0.05 mL; P<0.01). Contractile responses to EFS were significantly decreased in the BACNI and BACNI+LP groups compared with those in the sham group (Fig. 1A). The cholinergic component-induced contractile responses to EFS were lower in the BACNI and BACNI+LP groups than in the sham group (Fig. 1B). The dose-response curves for CCh are shown in Fig.2A. Emax was lower in the BACNI and BACNI+LP groups than in the sham group, while there were no differences in the EC50 between the three groups (Fig. 2B, 2C).

BACNI caused bladder overdistension and weakened detrusor muscle contraction in the EFS. The cholinergic component of the EFS and contractile responses to CCh decreased soon after BACNI, suggesting that cholinergic signaling is attenuated. Urine was drained intermittently after BACNI, except for the effects of bladder overdistension on detrusor muscle contractility. The detrusor muscle contraction was weakened after BACNI,although the intravesical pressure remained low.

Detrusor muscle contractility is impaired immediately following intrapelvic nerve injury but not as a result of overdistension of the bladder.