Mechanism of airway hyperresponsiveness after lung transplantation
| Project/Area Number |
21592011
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Kawasaki Medical School (2011)
Hoshi University (2009-2010) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
CHIBA Yoshihiko 星薬科大学, 薬学部, 准教授 (00287848)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 移植 / 再生医療 / シグナル伝達 / アレルギー / 気道過敏性 / カルシウム感受性 / 免疫抑制剤 / 筋弛緩薬 |
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| Research Abstract |
It has been reported that an airway hyperresponsiveness(AHR) was observed in the non-asthmatic recipients who received lung transplantation. The mechanism of AHR after lung transplantation is unclear, and various factors seem to be involved in. Immunosuppressants are commonly used in transplanted patients to prevent the acute transplant rejection. These agents are reported to cause hypertension, suggesting they may cause vascular smooth muscle contraction. Both cyclosporine A and tacrolimus had no effect on the contraction in rat airway smooth muscle. And, effect of sugammadex, novel agent for reversal of neuromuscular blockade, was also examined. Sugammadex also failed to show significant contractile effects on rat airway smooth muscle. These result showed that the mechanism of AHR after lung transplantation is complicated and need further investigation.
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Report
(4 results)
Research Products
(48 results)
