Purpose: To establish a male rat model of neurogenic bladder after bilateral pelvic nerve injury (BPNI) and investigate the factors associated with onset of neurogenic bladder.
Methods: Twenty-four 8-week-old male Sprague-Dawley rats were randomly divided into three groups (n = 8 rats per group). Rats in 4-week and 8-week nerve injury group underwent BPNI, while rats in the sham group underwent a sham operation. Bladder functional analysis were performed and then bladders tissues were harvested for morphological examination and investigating the mRNA expression levels of target genes in all rats.
Results: The bladder weight significantly increased in rats following BPNI. Functional analysis revealed non-voiding contractions and decreased detrusor contractility following BPNI, manifested as elevated post-void residual and bladder capacity while reduced maximum voiding pressure and voiding efficiency. The collagen area in bladder tissue and mRNA expression levels of target genes significantly increased at 4 or 8 weeks post-BPNI except Smad3. At 4 weeks post-BPNI, expression levels of vesicular acetylcholine transporter were reduced, then returned to baseline at 8 weeks. Expression levels of tyrosine hydroxylase were reduced at both 4 and 8 weeks post-BPNI.
Conclusions: A neurogenic bladder animal model was successfully established by performing BPNI in male rats, characterized by impaired voiding function, bladder detrusor fibrosis, and reduced neurotransmitter release.
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