| Project/Area Number |
61570371
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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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 |
HIRAYAMA Jiro (1987-1988) Shinshu University Hospital, Physician Speciality, 医学部付属病院, 助手 (90156696)
吉村 一彦 (1986) 信大, 医学部, 助手 (70174985)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAI Akio Shinshu University Medical School, Institute of Cardio-vascular Disease, Associa, 医学部付属心脈管研究施設, 助教授 (70020758)
YOSHIMURA Kazuhiko Shinshu University Medical School, Physician Speciality, 医学部, 助手 (70174985)
KUBO Keishi Shinshu University Medical School, Assistant Professor, 医学部, 講師 (80143965)
FUKUSHIMA Masao Shinshu University Hospital, Physician Speciality, 医学部付属病院, 助手 (30173339)
KOBAYASHI Toshio Shinshu University Hospital, Assistant Professor, 医学部付属病院, 講師 (80020775)
草間 昌三 信州大学, 医学部, 教授 (70020708)
平山 二郎 信州大学, 医学部附属病院, 助手 (90156696)
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| Project Period (FY) |
1986 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1988: ¥100,000 (Direct Cost: ¥100,000)
Fiscal Year 1987: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1986: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Chronic lung lymph fistula / Awake sheep / Lung injury(increased permeability pulmonary edema) / Endotoxemia / Pulmonary microair embolism / Paraquat toxiciyt / ARDS(adult respiratory distress syndrome) / エンドトキシン / パラコート / 血管透過性肺水腫 / 白血球 / 透過性亢進型肺水腫 / ロイコトリエン【B_4】 / エンドトキシン肺傷害 / 肺循環動態 / 肺リンパ動態 / 肺血管障害 |
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| Research Abstract |
We studied the role of vasoactive substances in the pathogenesis of increased permeability pulmonary edema in sheep with chronic lung lymph fistula. Pulmonary edemas were produced by endotoxemia, pulmonary microair embolism and paraquat toxicity.
1. Endotoxemia Pretreatment of PAF(platelet activating factor)antagonist did not prevent the process induced by escherichia coli endotoxin. So PAF may be not related to this injury. Leukotriene B_4 increased significnatly in lung lymph and plasma. Cyclic AMP may be concerned with the development of endotoxin-induced lung injury, since dibutyryl cyclic AMP(db cAMP)which was penetrated in the cell supressed the process of this injury.
2. Pulmonary micro air embolism Because pretreatment of db cAMP prevented the increased pulmonary edema after air embolism, cyclic AMP may be related to the development of this injury.
3. Paraquat toxicity Thromboxane B_4 and 6-keto PGF_<1 > did not change in lung lymph and plasma after paraquat administration. So these prostanoids are not related to the pathogenesis of paraguat toxocity.
These three lung injuries are thought to be good models of ARDS(adult respiatory distress syndrome). The findings of this study may suggest that the mechanisms of increased pulmonary edema are different in each lung injury in sheep.
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