| Project/Area Number |
11671858
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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 |
Functional basic dentistry
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| Research Institution | Kanagawa Dental College |
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Principal Investigator |
TODOKI Kazuo Kanagawa Dental College, Pharmacology, lecturer, 歯学部, 講師 (90139577)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Syun-suke Kanagawa Dental College, Pharmacology, lecturer, 歯学部, 講師 (60206810)
KOBAYASHI Yutaka Kanagawa Dental College, Pharmacology, lecturer, 歯学部, 講師 (50130919)
OKABE Eiichiro Kanagawa Dental College, Pharmacology, Professor, 歯学部, 教授 (50097276)
SHOJI Hirofumi Kanagawa Dental College, Pharmacology, Instructor, 歯学部, 助手 (90277913)
LEE Chang-il Kanagawa Dental College, Pharmacology, lecturer, 歯学部, 講師 (60220795)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | nitric oxide / reactive hyperemia / Ischemia / electrochemical probe / gingival blood flow / L-NAME / Laser Lppler flowmetry / in vivo / ルミノール / デフェロキサミン / フリーラジカル / カタラーゼ / ペルオキシダーゼ / 化学発光 / 口腔組織 / 活性酸素 / nitric oxide / 歯肉 / 局所循環調節 / (1)活性酸素フリーラジカル / (2)ルミノール / (3)化学発光 / (4)デフェロキサミン / (5)バイオセンサー / (6)Cu,Zn-SOD / (7)ペルオキシダーゼ / (8)フェントン反応 |
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| Research Abstract |
Reactive hyperemia, the local vasodilatation which occurs in response to oxygen debt and accumulation of metabolic waste products due to interruption of blood flow ; active hyperemia, and the increased blood flow in an organ during a period of activity. The microcirculation is controlled partly by sympathetic nerve and partly by vasoactive substances secreted locally by the endothelial cells. The most important of the latter is nitric oxide(NO), which facilitates flow by causing relaxation of vascular smooth muscle. In the present study, we investigated the role of NO in the regulation of local circulation in gingival tissue during reactive hyperemia, using laser Doppler flowmetry and NO electrochemical technique.
METHODS : The experiments were performed in beagle dogs under anesthesia by sodium pentobarbital (25 mg/kg, i.v.). Gingival blood flow (GBF) was measured in attached gingival tissue of right mandibular canine tooth using a laser Doppler flowmeter. Reactive hyperemia was elicit
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ed by release of occlusive compression (30, 60 and 300 sec period), which laser Doppler flowmeter probe was applied against to the gingival tissue at a force that caused less than GBF 2 ml/min/100 g. In order to perform pharmacological consideration of reactive hyperemia generated in gingival tissue, intra-arterial bolus injection of various drugs were given.
RESULTS : The GBF increased depending on occlusion durations of 30, 60, and 300 sec by compressing of gingival tissue. The reactive hyperemia was significantly suppressed by pretreatment with N ω-nitro-L-arginine methyl ester (L-NAME, 60 mg/kg, i.a.), an inhibitor of NO synthase, but not by atropine (muscarinic antagonist), propranolol(β-blocker), pilylamine (H1-blocker), cimetidine (H2-blocker). The L-NAME-suppressed reactive hyperemia in gingiva was partially recovered by the treatment with L-arginine (60 mg/kg, i.a.), the substrate of NO synthase. Furthermore, NO could be detected using NO-selective electrode during reactive hyperemia in gingival tissue.
CONCLUSIONS : These results suggest that NO function as nonadrenergic noncholinergic (NANC) mediator is involved in the vasodilation during reactive hyperemia in gingival tissue, and deals with the maintenance of homeostasis in gingival circulation. Less
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