| Project/Area Number |
06454272
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Shinshu University |
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Principal Investigator |
YOSHIMURA Kazuhiko Shinshu Univ., Associate Professor, 医学部附属加齡適応研究センター, 助教授 (70174985)
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| Co-Investigator(Kenkyū-buntansha) |
SANO Kenji Shinshu Univ., Assisstant professor, 医学部, 講師 (50205994)
CHANG Sung Koh Shinshu Univ., Assisstant professor, 医学部附属病院, 講師 (80143981)
KOBAYASHI Toshio Shinshu Univ., Assisstant professor, 医学部附属病院, 講師 (80020775)
HOWMA Tatsuji Shinshu Univ., Professor, 医学部附属加齡適応研究センター, 教授 (90020875)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥6,100,000 (Direct Cost: ¥6,100,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1994: ¥4,700,000 (Direct Cost: ¥4,700,000)
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| Keywords | interleukin-1beta / rabbit / isolated perfused lungs / filtration coefficient / prostaglandin / nitric oxide / Cyelooxygluase / インターロイキン1β / 肺微小血管透過性 / 水分濾過保数 / サイトカイン / インターロイキン-1β / プロスタグランデイン |
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| Research Abstract |
The effects of interleukin-1 beta (IL-1beta) on the pulmonary microvascular permeability and the prostaglandin (PG) E2 synthesis, and the role of nitric oxide (NO) in the microvascular response to IL-1 beta in the isolated non-blood perfused rabbit lungs were studied. Pulmonary microvascular permeability and the lung edema were assessed by the fluid filtration coefficient (Kf) and the wet to dry lung weight ratio (W/D ratio), respectively. Pulmonary capillary pressure was estimated by the double occlusion technique. The PGE2 concentration in the perfusate was measured by radioimmunoassay. The values of Kf were significantly increased at 30 min after administration of IL-1beta and continued with time. The W/D ratios in the lungs receiving IL-1beta were significantly higher than the control lungs. Pretreatment with either N^<omega>-nitro-L-arginine (L-NA,a non-selective NO synthase inhibitor, 0.3 mM) or aminoguanidine (AG,a selective inducible NO synthase inhibitor, 1 mM) abolished the IL-1beta -induced increases in Kf and W/D ratio. The IL-1beta injection stimulated the production of PGE2 in the lungs. Either L-NA or AG attenuated the IL-1beta -induced PGE2 production. These results suggest that NO derived from inducible NO synthase plays crucial roles in the IL-1beta -induced lung injury and the PGE2 production in the lungs.
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