Abstract

INTRODUCTION AND OBJECTIVES: It has been recognized that lumbar canal stenosis (LCS) compromised neurological function is a common problem in elderly patients and may cause underactive bladder (UAB). However, the mechanism and molecular change underlying the UAB is not clear. METHODS: One small hole was drilled at the fifth lumbar vertebral arch (sham), and a rectangular piece of silicone rubber was inserted into the L5iVL6 epidural space (LCS) of female Sprague-Dawley rats. LCS rats underwent bladder expression twice a day. Before and after surgery, a metabolic cage study was performed. Continuous cystometry (CMG) was performed at day 14, or 28 under urethane anesthesia. The bladder was then harvested for histology, expression of M2 and M3 receptors, NGF, and agrin by western blotting. Some animals received intravesical PGE2 instillation. RESULTS: LCS induced acute urinary retention and progressive increase of bladder weight. The LCS rats showed a significant decrease in voided volume and a significant increase in postvoid residual urine compared with Sham rats. CMG showed that the LCS bladder was no contraction, high compliance and overflow incontinence. Intravesical PGE2 induced decreased bladder compliance, but no recovery of bladder contraction in the LCS rats. In contrast, there was a significant decrease in intercontraction interval (ICI) and increased in contraction amplitude in response to PGE2 in sham rats. LCS rats showed no obvious difference in detrusor morphology (Fig 1), M2, M3 receptor, NGF, and agrin compared with the sham rats. CONCLUSIONS: LCS induced UAB model preserved bladder morphology and functional receptor. It might be a useful model for the mechanism and treatment of neurogenic UAB.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call