| Project/Area Number |
12832023
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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 Institution | Nagoya University |
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Principal Investigator |
KOEDA Tomoko School of Health Sciences,Nagoya University, Research Associat, 医学部, 助手 (20223050)
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| Co-Investigator(Kenkyū-buntansha) |
IDA Kunio School of Health Sciences,Nagoya University, professor, 医学部, 教授 (10115529)
MIZUMURA Kazue Research Institute of Environmental Medicine, Nagoya University, professor, 環境医学研究所, 教授 (00109349)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Adjuvantinflammation, / blood flow, / sympathetic nerve stimulation, / noradrenaline. / substance P, / pain / thermotherapy, / cold therapy, / 足容積 / 温熱刺激 / アジュバント炎症ラット / 血流増加反応 / α_1受容体 / α_2受容体 / NK-1受容体 |
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| Research Abstract |
Previous study demonstrated that the electrical stimulation of the lumbar sympathetic trunk (SS), which normally induces a blood flow (BF) decrease, induced a BF increase in about 50 % of adjuvant-inflamed polyarthritic rats. To address the mechanism for this BF-increase response, we examined whether noradrenaline (NA) plays any role in this changed response to the SS, and which receptor subtype is involved. The BF-increase response to NA was significantly reduced after the close-arterial injection of either al or a2-adrenoceptor antagonist. In contrast the BF increase response to the SS was not reduced by a single administration of either al or a2-adrenoceptor antagonist, and it was significantly suppressed when CH-38083 was injected after prazosin. These results suggest that the BF-increase response to the SS involves other mechanism(s) than NA yet to ;be identified.
Secondary, we examined in the adjuvant-monoarthritic model whether pain behaviors and foot volumes are affected by repetitive warm or cold treatment, which are often used in clinical practice. Both treatments were started after induction of inflammation. Warm treatment was carried out by immersing the both hindlimbs distal to ankle joints into 40 ℃ water bath for 20 min everyday for 14 days. Rats of the cold treatment group were held in a box the temperature of which was 5 ℃ for 30 min everyday for 21 days. We examined pain behaviors and foot volume in 24 hours after the each treatment every other day. The pain behaviors and foot volume were not affected by the present warm treatment. In contrast pain behaviors worsened and the foot volume increased after the cold treatment. After these experiments, we examined acute BF responses to warm and cold treatments. The BF in the injected side increased less than the non-injected side.
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