To test a neurogenic hypothesis for external urethral sphincter (EUS) dysfu
nction associated with urinary incontinence, the proximal pudendal nerve wa
s crushed in anesthetized retired breeder female rats (n = 5) and compared
with a sham lesion group (n = 4). Outcome measures included concentric need
le electromyograms (EMGs) from the target EUS, voiding patterns during a 2-
hour dark period, and micturition data over a 24-hour period. Fast Blue (FB
) was introduced to the crush site at the time of injury and Diamidino Yell
ow (DY) to the EUS at the time the rats were killed (3 months post-operativ
e), when histological analysis of the nerve and urethra was also performed.
EMG records indicated the EUS motor units undergo typical denervation chan
ges followed by regeneration and recovery. Voiding patterns from the crush
group show a significant increase of small urine marks in the front third o
f the cage. At 1-2 weeks post-op, the frequency of voids was significantly
increased in the crush group compared to pre-op and late post-op time perio
ds. The mean volume voided in the light phase at the early post-op time was
significantly increased in the sham group. Light and electron microscopic
patterns seen in nerve and muscle suggest the regenerating motor units main
tain a structural integrity. Motoneurons in the lower lumbar cord were labe
led with either DY (14.5 +/- 6.8), FB (31.7 +/- 23.7), or both (35.0 +/- 17
.5) tracers, indicating similar to 54% of che crushed pudendal neurons rege
nerated to the EUS. In conclusion, several measures suggest this reversible
crush lesion induces mild urinary incontinence. This animal model is promi
sing for further development of hypotheses regarding neural injury, the pat
hogenesis of incontinence, and strategies aimed at prevention and treatment
. (C) 2000 Wiley-Liss, Inc.