Effect of tadalafil on chronic pelvic pain and prostatic inflammation in a rat model of experimental autoimmune prostatitis

The Prostate ◽  
2018 ◽  
Vol 78 (10) ◽  
pp. 707-713 ◽  
Author(s):  
Ken Okamoto ◽  
Maki Kurita ◽  
Hiroshi Yamaguchi ◽  
Yuki Numakura ◽  
Michiko Oka
The Prostate ◽  
2019 ◽  
Vol 79 (12) ◽  
pp. 1466-1476 ◽  
Author(s):  
Li‐Gang Zhang ◽  
Jing Chen ◽  
Jia‐Lin Meng ◽  
Yong Zhang ◽  
Yi Liu ◽  
...  

Andrologia ◽  
2015 ◽  
Vol 48 (3) ◽  
pp. 243-251 ◽  
Author(s):  
X.-J. Wang ◽  
L.-L. Xia ◽  
T.-Y. Xu ◽  
X.-H. Zhang ◽  
Z.-W. Zhu ◽  
...  

2008 ◽  
Vol 294 (4) ◽  
pp. R1268-R1275 ◽  
Author(s):  
Charles N. Rudick ◽  
Anthony J. Schaeffer ◽  
Praveen Thumbikat

Pain is the hallmark of patients with chronic prostatitis (CP) and chronic pelvic pain syndrome (CPPS). Despite numerous hypotheses, the etiology and pathogenesis remain unknown. To better understand CP/CPPS, we used a murine experimental autoimmune prostatitis model to examine the development, localization, and modulation of pelvic pain. Pelvic pain was detected 5 days after antigen instillation and was sustained beyond 30 days, indicating the development of chronic pain. The pain was attenuated by lidocaine treatment into the prostate, but not into the bladder or the colon, suggesting that pain originated from the prostate. Experimental autoimmune prostatitis histopathology was confined to the prostate with focal periglandular inflammatory infiltrates in the ventral, dorsolateral, and anterior lobes of the mouse prostate. Inflammation and pelvic pain were positively correlated and increased with time. Morphologically, the dorsolateral prostate alone showed significantly increased neuronal fiber distribution, as evidenced by increased protein gene product 9.5 expression. Pelvic pain was attenuated by treatment with the neuromodulator gabapentin, suggesting spinal and/or supraspinal contribution to chronic pain. These results provide the basis for identifying mechanisms that regulate pelvic pain and the testing of therapeutic agents that block pain development in CP/CPPS.


Pain ◽  
2014 ◽  
Vol 155 (7) ◽  
pp. 1328-1338 ◽  
Author(s):  
Kenny Roman ◽  
Joseph D. Done ◽  
Anthony J. Schaeffer ◽  
Stephen F. Murphy ◽  
Praveen Thumbikat

BMC Urology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ozgu Aydogdu ◽  
Pinar Uyar Gocun ◽  
Patrik Aronsson ◽  
Thomas Carlsson ◽  
Michael Winder

Abstract Background The aim of the current study was to investigate the effects of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) on bladder function via prostate-to-bladder cross-sensitization in a rat model of lipopolysaccharide (LPS)-induced prostate inflammation. Methods Male rats were intraprostatically injected with LPS or saline, serving as control. Micturition parameters were examined in a metabolic cage 10 or 14 days later. Subsequently, to evaluate bladder function, cystometry was performed. Micturition cycles were induced by saline infusion and cholinergic and purinergic contractile responses were measured by intravenous injection with methacholine and ATP, respectively. Thereafter, the prostate and bladder were excised and assessed histopathologically for possible inflammatory changes. Results Metabolic cage experiments showed increased urinary frequency in rats with LPS-induced CP/CPPS. Cystometry showed a significant increase in the number of non-voiding contractions, longer voiding time and lower compliance in CP/CPPS animals compared to controls. Induction of CP/CPPS led to significantly reduced cholinergic and purinergic bladder contractile responses. Histopathological analysis demonstrated prostatic inflammation in CP/CPPS animals. There were no significant differences between the groups regarding the extent or the grade of bladder inflammation. Prostate weight was not significantly different between the groups. Conclusions The present study shows that prostate-to-bladder cross-sensitization can be triggered by an infectious focus in the prostate, giving rise to bladder overactivity and alterations in both afferent and efferent signalling. Future studies are required to fully understand the underlying mechanisms.


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