| Budget Amount *help |
¥2,678,000 (Direct Cost: ¥2,060,000、Indirect Cost: ¥618,000)
Fiscal Year 2011: ¥728,000 (Direct Cost: ¥560,000、Indirect Cost: ¥168,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Research Abstract |
[Aim] To investigate whether bladder dysfunction after bladder outlet obstruction (BOO) could be altered by treatment with a phosphodiesterase 3 inhibitor (PDE3i). PDE3i, the antiplatelet agents, has been used to improve perfusion of the heart and brain.
[Materials and methods] In all, 12-week-old female Sprague-Dawley rats were divided into five equal groups ; group 1 and 2, sham operated rats (each 3 rats); group 3-5, BOO rats (each 6 rats), and group 1 and 3 rats given vehicle ; group 2 and 51, rats given high dose PDE3i ; group 4 rats given low dose PDE3i, respectively. PDE3i was given within diet from the day of surgery. At 4-weeks BOO, 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 3-5 compared with group 1 and 2. Bladder weights of PDE3i groups were not significantly different from vehicle groups. The contractile forces in response to EFS, carbachol and KCl in group 3 were about 20-40% of those in group 1. In BOO groups, the contractile forces in PDE3i treatment dose-dependency increase the BOO-induced reduction of contractile force in the bladder strips.
[Conclusion] PDE3i has a small but significant protective effect on the contractile dysfunction induced by 4-weeks BOO in rats, although the increase in bladder mass was not altered. PDE3i could be a useful protection against contractile dysfunction of the obstructed bladder.
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