Project/Area Number |
20591880
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Urology
|
Research Institution | Tottori University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
KINOSHITA Yukako 鳥取大学, 医学部, 助教 (50032214)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | 過活動膀胱 / 虚血 / SHR / 排尿筋過活動 / 膀胱血流 / NGF / 急性尿閉 / K_<ATP>チャンネル開口薬 / 膀胱平滑筋 / プレコンディショニング |
Research Abstract |
Bladder dysfunction in a rat model caused by acute urinary retention(AUR) needs more than two weeks of recovery period, and within two weeks of induction of AUR these rats may be used as a rat overactive bladder(OAB) model. A radical scavenger, edaravone reduces the oxidative stress and prevents the bladder dysfunction caused by AUR and subsequent catheterization. K_<ATP> channel openers, nicorandil and cromakalim prevent AUR-induced bladder dysfunction via activation of K_<ATP> channels with subsequent decrease in oxidative stress and decreased induction of apoptosis. Chronic administration of a K_<ATP> channel opener, nicorandil, anα_<1A>-blocker, silodosin, and a Rho kinase inhibitor, fasdil ameliorate hypertension-related bladder dysfunction in the SHR via improvement of bladder blood flow.
|