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

抗血小板药物治疗可改善大鼠出口梗阻后的膀胱功能

基本信息

批准号：
22890012
负责人：
MATSUMOTO Seiji
金额：
$ 1.71万
依托单位：
Asahikawa Medical College
依托单位国家：
日本
项目类别：
Grant-in-Aid for Research Activity Start-up
财政年份：
2010
资助国家：
日本
起止时间：
2010 至 2011
项目状态：
已结题

项目摘要

[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.

[目的]探讨磷酸二酯酶3抑制剂（PDE3i）治疗膀胱出口梗阻（BOO）后膀胱功能障碍的改变。抗血小板药物PDE3i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Sprague-Dawley大鼠分为5组；1、2组，假手术大鼠（各3只）；3 ~ 5组，BOO大鼠（每6只），1、3组给药；2、51组，大剂量PDE3i；4组大鼠分别给予低剂量PDE3i。PDE3i从手术当天起在饮食中给予。在BOO 4周时，膀胱切除并解剖成四条纵条进行等长器官浴测定。测定各组膀胱条对电场刺激（EFS）、苯酚和氯化钾的收缩反应。[结果]与1、2组相比，BOO诱导3 ~ 5组膀胱重量显著增加。PDE3i组膀胱重量与载药组无显著差异。3组对EFS、carbachol和KCl反应的收缩力约为1组的20-40%。在BOO组中，PDE3i治疗剂量依赖性的收缩力增加了BOO引起的膀胱条收缩力的减少。【结论】PDE3i对4周BOO引起的大鼠收缩功能障碍具有小而显著的保护作用，但膀胱肿块的增加没有改变。PDE3i可有效预防梗阻膀胱的收缩功能障碍。