Establishment of animal model manifested as bladder neurogenic changes generated by bilateral pelvic nerve injury in male rats

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.