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Eviprostat is a phytotherapeutic agent that has been used widely for more than 40 years in the treatment of benign prostatic hyperplasia (BPH) in Japan and Germany, and is known to have antioxidant activity. The present study investigated the effect of Eviprostat on the levels of the urinary oxidative stress marker 8-hydroxy-2'-deoxyguanosine (8-OHdG) in a rabbit model of surgical partial bladder outlet obstruction (PBOO) and in patients with lower urinary tract symptoms (LUTS) associated with BPH. In the rabbit model, 8-OHdG levels in urine collected after 3 weeks of PBOO were 3.8-fold higher than in the urine of sham-operated rabbits. When twice-daily Eviprostat was administered orally throughout the 3-week PBOO period, the increase in urinary 8-OHdG levels was suppressed by 70%. In the clinical study, nine patients who received Eviprostat for 4 weeks showed 2.5-fold lower urinary 8-OHdG levels than before treatment. During Eviprostat treatment, the total International Prostate Symptom Score (IPSS) decreased from 16.56 +/- 2.74 to 13.67 +/- 2.30 and the quality of life score from 4.22 +/- 0.40 to 3.22 +/- 0.46. The findings provide evidence that the antioxidant activity of Eviprostat is responsible for its beneficial effects in the treatment of BPH.

OBJECTIVE To examine the correlation between partial bladder outlet obstruction (PBOO) and bladder carcinogenesis. MATERIALS AND METHODS Female Wistar rats (6 weeks old) were divided into three groups of 10 each: group 1 was exposed to n‐butyl‐n‐butanol nitrosamine (BBN, a carcinogen) in drinking water for 8 weeks; group 2 had PBOO induced surgically after exposure to BBN for 8 weeks; group 3 had a sham operation and the rats drank normal water (control group). After 20 weeks, all of the rats were killed humanely and their bladders analysed. RESULTS There were no significant differences in body weight among the groups. The bladder weight of group 2 was significantly greater than either group 1 or group 3. Histopathologically, bladder smooth muscle hypertrophy was the major cause of the increased bladder weight for group 2. In group 2 there were increases in bladder wall thickness and many nipple‐shaped urothelial tumours. Basic fibroblast growth factor and hypoxia‐inducible factor‐1α expression were significantly greater in group 2 than in groups 1 and 3. CONCLUSIONS Exposure of the bladder to carcinogens during bladder hyperplasia and hypertrophy induced by PBOO results in a greater incidence of superficial bladder carcinoma.

OBJECTIVES To investigate whether vardenafil, a phosphodiesterase 5 (PDE‐5) inhibitor, would protect the bladder from decompensatory changes in a 4‐week rat bladder outlet obstruction (BOO) model, as evidence has been accumulating that PDE‐5 inhibitors improve lower urinary tract symptoms (LUTS) in patients with benign prostatic hyperplasia (BPH). MATERIALS AND METHODS In all, 50 12‐week‐old female Sprague‐Dawley rats were divided into five equal groups; group 1, sham operated vehicle control rats; group 2, BOO vehicle rats; group 3–5, BOO rats given oral vardenafil at 5, 20, 80 mg/L, respectively. Vardenafil was given in drinking water from the day of surgery. At 4‐weeks after the introduction of BOO, vardenafil was washed‐out by giving water for 24–48 h, and then the bladder was excised and dissected into four longitudinal strips for isometric organ‐bath assay. Contractile responses of bladder strips to electrical field stimulation (EFS), carbachol and KCl was determined for each group. RESULTS BOO induced a significant increase in bladder weight in group 2 compared with group 1. Bladder weights of groups 3–5 were not significantly different from that of group 2. The contractile forces in response to EFS, carbachol and KCl in group 2 were 30.7–51.7% of those in group 1. Vardenafil treatment in groups 3–5 generally did not block the BOO‐induced reduction of contractile force in the bladder strips. However, treatment with a high dose of vardenafil resulted in a significant increase in the contractile response to carbachol (78.4% group 5 vs 51.7% group 2). CONCLUSION Chronic treatment with a high dose of vardenafil protected the rat bladder from BOO‐induced contractile dysfunction to carbachol.

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