Presentation Authors: Shinji Fujii*, Shinichi Yamashita, Natsuho Hayashi, Goto Takuro, Juntaro Koyama, Takuma Sato, Shuichi Shimada, Yoshihide Kawasaki, Hideaki Izumi, Naoki Kawamorita, Koji Mitsuzuka, Akihiro Ito, Yoichi Arai, Sendai, Miyagi, Japan
Introduction: Many elderly men suffer from benign prostatic hyperplasia (BPH) due to aging, but the pathogenesis of BPH remains to be completely elucidated. Recently, chronic ischemia in the prostate has been suggested to be related to BPH. Thus, we evaluated the impact of chronic ischemia on the development of prostatic hyperplasia and the efficacy of phosphodiesterase type 5 (PDE5) inhibitor for hyperplasia in a rat model with chronic ischemia induced by local atherosclerosis.
Methods: Eighteen male Sprague-Dawley rats weighing 450-500 g were divided into 3 groups: sham operation, regular diet, placebo (SRP group; n = 6); arterial endothelial injury, high cholesterol diet, placebo (AHP group; n = 6); or arterial endothelial injury, high cholesterol diet, and tadalafil as a PDE5 inhibitor (AHT group; n = 6). The endothelial injury in the common iliac arteries was performed using a 2-Fr Fogarty arterial embolectomy catheter through an incision in the femoral artery into the common iliac artery. Diet and oral drugs were administrated for 8 weeks after surgery. At 8 weeks, blood flow to the ventral prostate (VP) was measured using laser speckle blood flow analysis, and the VP was histologically evaluated.
Results: Mean VP weights were 639 Â± 43 mg in the AHP group and 460 Â± 54 mg in the SRP group, showing a significant enlargement in VP for the AHP group compared with the SRP group (p = 0.03). Importantly, mean VP weight was 449 Â± 62 mg in the AHT group, significantly smaller than that in the AHP group (p = 0.03) and similar to that in the SRP group. Prostatic blood flow was significantly lower in the AHP group than in the SRP group (p < 0.01). Interestingly, the blood flow was significantly higher in the AHT group than in the AHP group (p = 0.02). Histologically, mean interstitial area in the prostate of the AHP group was significantly increased compared with that of the SRP group (p < 0.01). Moreover, tadalafil administration attenuated the increase in interstitial area in the prostate (P < 0.01).
Conclusions: Enlargement of the VP resulted from chronic ischemia induced by local arteriosclerosis. Also, administration of tadalafil attenuated VP enlargement. Chronic ischemia in the prostate might thus contribute to the development of BPH, and PDE5 inhibitors might provide an innovative approach to preventing BPH.