- 作者：Seiji Matsumoto ; matsums@asahikawa-med.ac.jp" class="auth_mail ; Masaki Watanabe ; Kazumi Hashizume ; Naoki Wada ; Jun-ichi Hori ; Masafumi Kita ; Tatsuya Iwata ; Hidehiro Kakizaki
- 刊名：Urology
- 出版年：March, 2014
- 年：2014
- 卷：83
- 期：3
- 页码：675.e7-675.e11
- 全文大小：962 K
Objective
To investigate whether bladder dysfunction after bladder outlet obstruction (BOO) could be altered by treatment with cilostazol, a phosphodiesterase 3 inhibitor (PDE3i).Methods
Twelve-week-old female Sprague-Dawley rats were divided into 5 groups: groups 1 and 2, sham-operated rats and groups 3-5, BOO rats. Group 1 and 3 rats were given normal diet, group 2 and 5 rats were given high-dose PDE3i diet, and group 4 rats were given low-dose PDE3i diet. PDE3i was given within diet from the day of surgery. Four weeks after BOO, the bladder was excised and dissected into 4 longitudinal strips for isometric organ-bath assay. Contractile responses of bladder strips to electrical field stimulation (EFS), carbachol, and potassium chloride (KCl) were determined for each group.
Results
BOO induced a significant increase in bladder weight in groups 3-5 compared with groups 1 and聽2. PDE3i treatment did not affect bladder weight in sham or BOO rats. Contractile forces in response to EFS, carbachol, and KCl in group 3 were about 20%-40% of those in group 1. Contractile responses to EFS or KCl in PDE3i-treated BOO rats were not significantly different from those in group 3. Only high dose of PDE3i treatment in BOO rats caused a statistically significant increase in the response to carbachol compared with group聽3.
Conclusion
PDE3i has a small but significant protective effect on the contractile dysfunction induced by a 4-week BOO in rats, although the increase in bladder mass was not altered. PDE3i could be a聽useful protection against contractile dysfunction of the obstructed bladder.