| Project/Area Number |
23791689
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Niigata University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | アクアポリン1 / CRPS / 虚血後慢性疼痛モデル / アクアポリン１ / 慢性疼痛 / 動物モデル / 遺伝子欠損マウス |
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| Research Abstract |
AQP1 water channel is involved in both edema formation and pain. Edema and pain are hallmarks of CRPS I, a debilitating chronic pain condition that can develop in 10-20% of patients following fractures or other similar injuries. This study was undertaken to find out if AQP1 protein is involved in the mechanism of CRPS. We investigated the role of AQP1 in the development of edema and hypersensitivity in CPIP model. A pharmacological approach that used acetazolamide, an inhibitor of AQP1 function was used. Mice that underwent CPIP procedure were given acetazolamide beginning the day before the injury and continuing for the observation period of 28 days. As we showed, acetazolamide had no effect on the extent of edema and the time course of its resolution following the reperfusion. Also, no differences in pain thresholds were found in mice receiving AQP1 inhibitor in mechanical and thermal sensory assays performed during 28-day postreperfusion period. Our results indicate that AQP is unlikely to be involved in the edema formation following ischemia-reperfusion injury. It is also unlikely to be involved in the development of pain hypersensitivity following such injury. They also suggest that targets other than AQP1 should be looked for pharmacological management of CRPS.
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