Recovery of Lower Urinary Tract Function After Periurethral Nerve Injury
Drs. C. Wai, B. Vakili, M. Boreham, J. Schaffer, A. Word
University of Texas Southwestern
Dallas, Texas

Objective:   To determine the temporal relationship between periurethral nerve injury and changes in contractile function of the female lower urinary tract
Materials and Methods:   Branches of the pudendal and pelvic nerves 2-5mm lateral to the urethra were microdissected and transected in 19 young virginal female rats (NI).  The identical surgical technique (except for nerve transection) was performed in 18 sham-operated controls (SH).  Urethra, bladder base and dome were harvested for neurophysiologic studies 3, 7, 14 and 21 days after nerve injury.  Maximal responses to transmural electric field stimulation (EFS) were used to study nerve-mediated contractions.
Results:   Force of nerve-mediated contractions in the striated external urethral sphincter as well as the longitudinal urethral smooth muscle were similar in NI and SH at all time points.  However, 72 h after NI, nerve-mediated contractions were impaired significantly in the bladder base and dome (BASE, 32 ± 10 (NI) vs 91 ± 20 (SH) g/cm², P £ 0.02; DOME, 137 ± 19 (NI) vs 399 ± 53 (SH) g/cm², P £ 0.002).  By day 21, nerve-mediated contractions of both base and dome were completely restored.  This dramatic improvement in bladder function occurred between day 14 and 21.  In the dome, the rate of force development after EFS was slower 72 h after NI (167 ± 24 compared with 319 ± 48 g/cm²/sec, P £ 0.02).  Rates of contraction normalized by 21d.  Although maximal force generation and rates of contraction normalized with time, rates of relaxation were significantly compromised 21 d after NI (77 ± 6 compared with 130 ± 16 g/cm²/sec, P £ 0.03). 
Conclusions:   These studies may contribute to our understanding of the pathophysiology of post-operative urinary retention after gynecologic surgeries.  In our rat model, damage to the periurethral nerves resulted in an initial impairment of nerve-mediated contractions in the bladder base and dome followed by time-dependent recovery of force and rate of contraction.  Urethral contractions were unaffected.  This model may also shed light on the pathophysiology of genuine stress incontinence.  External urethral sphincter and urethral smooth muscle contractions were intact after isolated injury to periurethral nerves.  Thus, although periurethral NI has been associated with GSI, nerve injury may not be the sole pathophysiologic factor in this disorder.
Key words:  Nerve injury, incontinence, smooth muscle, urinary retention