Effects of pudendal nerve injury in the female rat

Citation
Jm. Kerns et al., Effects of pudendal nerve injury in the female rat, NEUROUROL U, 19(1), 2000, pp. 53-69
Citations number
43
Categorie Soggetti
Urology & Nephrology
Journal title
NEUROUROLOGY AND URODYNAMICS
ISSN journal
07332467 → ACNP
Volume
19
Issue
1
Year of publication
2000
Pages
53 - 69
Database
ISI
SICI code
0733-2467(2000)19:1<53:EOPNII>2.0.ZU;2-T
Abstract
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.