Presentation Authors: Shinsuke Mizoguchi*, Yoko Ikeda, Anthony J. Kanai, Pittsburgh, PA, Kenichi Mori, Mimata Hiromitsu, Oita, Japan, Jianshu Ni, Masahiro Kurobe, Tetsuichi Saito, Donaldo B. DeFranco, Zhou Wang, Naoki Yoshimura, Pittsburgh, PA
Introduction: Prostatic inflammation has a positive relationship with male lower urinary tract symptoms with benign prostatic hyperplasia. Although pelvic neural cross-talk is reportedly involved in overlaps of pelvic organ disorders, it is unclear whether pelvic nerve afferent pathways are implicated to bladder overactivity after prostatic inflammation. Therefore we investigated changes in pelvic nerve activity directly by in vitro single-fiber nerve recordings as well as bladder function and NGF expression in the bladder mucosa following prostatic inflammation using a rat model with unilateral pelvic nerve transection.
Methods: (1) Adult male Sprague-Dawley rats were used for in vitro single-unit bladder afferent nerve recordings. One week after induction of prostatic inflammation by 5% formalin injection into bilateral ventral lobes of the prostate (VP), the bladder with associated pelvic nerves (L6-S2 levels) were excised en bloc. The bladder was cut to form a sheet and the dome was connected to a tension transducer to record electrical signals of the nerves in response to computer-controlled bladder stretch.(2) To assess involvement of the pelvic nerve in bladder overactivity after prostatic inflammation, male rats underwent transection of the right side of the pelvic nerve (rPNT group). Following rPNT, rats received formalin injection into either contralateral side (rPNT-L group) or ipsilateral side (rPNT-R group) of the VP. One week after surgery, bladder activity and NGF levels of the bladder mucosa were evaluated by awake cystometry and by Western blot, respectively.
Results: In vitro single nerve recordings, bladder stretch-evoked firings were increased in rats with prostatic inflammation compared to controls (Fig. 1). In cystometric evaluation, non-voiding contractions (NVCs) and NGF expression in the bladder mucosa were significantly increased in rPNT-L rats, but not in rPNT-R rats, compared to rPNT only rats.
Conclusions: We demonstrated bladder afferent nerve sensitization and blockade of bladder overactivity by ipsilateral PNT evident as no significant changes in NVCs or NGF levels in rPNT-R rats after prostatic inflammation. These results indicate that the development of bladder overactivity following prostatic inflammation is mediated by pelvic nerve afferent pathways.
Source of Funding: NIH U54DK112079