The anti platelet agents treatment improves bladder function after outlet obstruction in rat

[Aim]研究磷酸二酯酶3抑制剂（PDE 3 i）治疗是否可以改变膀胱出口梗阻（BOO）后的膀胱功能障碍。PDE 3 i是一种抗血小板药物，已被用于改善心脏和大脑的灌注。【材料与方法】将12周龄雌性SD大鼠分为5组，每组3只，分别为假手术组（1、2组）、BOO组（3-5组）、溶媒组（1、3组）、高剂量PDE 3 i组（2、51组）、低剂量PDE 3 i组（4组）。从手术当天开始，在饮食中给予PDE 3 i。在4周BOO时，切除膀胱并切成四个纵向条带用于等距器官浴测定。测定各组膀胱条对电场刺激（EFS）、卡巴胆碱和KCl的收缩反应。[结果]与第1、2组相比，第3-5组膀胱重量明显增加。PDE 3 i组的膀胱重量与媒介物组无显著差异。第3组对EFS、卡巴胆碱和KCl的收缩力约为第1组的20-40%。在BOO组中，PDE 3 i处理剂量依赖性的收缩力增加了BOO诱导的膀胱条收缩力的降低。[结论] PDE 3 i对4周BOO所致大鼠膀胱收缩功能障碍有明显的保护作用，但对膀胱重量的增加无明显影响。PDE 3 i可能是一个有用的保护，对收缩功能障碍的梗阻膀胱。

[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.