| Project/Area Number |
09671619
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | Kanazawa University |
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Principal Investigator |
KOMATSU Kazuto University Hospital, Kanazawa University Assistant Professor, 医学部・附属病院, 助手 (80291368)
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| Co-Investigator(Kenkyū-buntansha) |
KOH Eitetsu University Hospital, Assistant Professor, 医学部・附属病院, 助手 (90283134)
YOKOYAMA Osamu University Hospital, Assistant Professor, 医学部・附属病院, 講師 (90242552)
NAMIKI Mikio School of Medicine, Professor, 医学部, 教授 (70155985)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1998: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Stroke / neurogeric bladder / bladder overactivity / NMDA / antisense / glutamate / stroke |
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| Research Abstract |
ROLE OF NMDA AND AMPA/KINATE RECEPTOR CHANNELS IN THE - PREVENTION OF BLADDER OVERACTIVITY AFTER CEREBRAL INFARCTION
INTRODUCTION AND OBJECTIVES : To investigate the role of glutamatergic receptors in detrusor hyperreflexia after cerebrovascular disease, we examined the effect of two different types of glutamate receptor antagonists on bladder function after focal cerebral infarction in rat model.
METHODS : Focal cerebral infarction was produced with a middle cerebral artery occlusion (MCAO) technique on the left side in female S-D rats under halothane anesthesia. Cystometric examination was performed on unanesthetized rats through a catheter implanted in the dome of the urinary bladder. Entire experiments was designed to allow for observation of acute phase (0 to 8 hours) reaction after MCAO.Two kinds of glutamate receptor antagonists were administrated intravenously before or after MCAO.
RESULTS : Bladder capacity of conscious rats was significantly reduced just after MCAO and remained comparatively small for 8 hours. Intravenous administration of N -methyl-d-aspartate (NMDA) receptor antagonist MK-801. (0.5 mg/kg) prior to MCAO prevented the reduction in bladder capacity. This effect becaome gradually observable about 4 hours after MCAO.The bladder capacity of rats given a-amino -3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kinate receptor antagonist NBQX (10, 30 mg/kg) prior to MCAO was not different from that of rats with vehicle administration followed by MCAO.Administration of MK-801(0.5 mg/kg) or NBQX (30 mg/kg) after MCAO did not inhibit the reduction in bladder capacity.
CONCLUSIONS : Our results suggest that glutamate may play a part in the pathogenesis of voiding dysfunction after cerebrovascular disease, and that the NMDA receptor may play a more dominant role than the AMPA/kinate receptor in evoking bladder overactivity after MCAO.
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