| Project/Area Number |
61480200
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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 | KINKI UNIVERSITY |
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Principal Investigator |
NAGASAKA Yukio M.D. 4th,DEPT. OF INTERNAL MEDICINE, KINKI UNIVERSITY, SCHOOL OF MED., 医学部第4内科学教室, 講師 (40180468)
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| Co-Investigator(Kenkyū-buntansha) |
波津 竜平 近畿大学, 医学部第4内科学教室, 助手
藤本 和久 近畿大学, 医学部第4内科学教室, 助手
UENISHI Hiroki M.D. same as the above, 医学部第4内科学教室, 助手 (60176609)
TOHDA Yuji M.D. 4th DEPT. OF INTERNAL MED., KINKI UNIVERSITY, 医学部第4内科学教室, 助手 (50167524)
FUJIMOTO Tomohisa M.D. same as the above (20181399)
HAZU Ryuhei M.D. same as the above
志波 邦夫 近畿大学, 医学部第4内科学教室, 助手 (60167442)
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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 |
¥6,800,000 (Direct Cost: ¥6,800,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥5,300,000 (Direct Cost: ¥5,300,000)
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| Keywords | HYPOXIC PULMONARY VASOCONSTRICTION / MICROVASCULAR PRESSURE / BRONCHOSPASM LEUKOTRIENES / VASOACTIVE SUBSTANCES / 気道攣縮 / 肺微小循環 / 気道粘膜浮腫 / アセチルコリン / ヒスタミン / PAF / 気道過敏性 / 気管支喘息 / 血管透過性 / 肺水腫 / LTC_4 / LTD_4 / 猫摘出還流肺 / 摘出肺還流 / 猫肺 / 肺微小血管圧 / 肺微小血管穿利法 / Servoーnull法 / 気道および肺血管攣縮 / 換気血流調節 / 肺化学伝達物質 / 肺循環 / 肺循環、気道同時評価 / マイクロパンクチャー / 肺徴小血管圧 / 肺血管作動物質 / 気道収縮物質 |
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| Research Abstract |
To investigate the role of hypoxia and various vasoactive substances on pulmonary microcirculation, we used isolated perfused cat lung model developed by head investigator (Nagasaka et al. Circ. Res. 54:90,1984). We also investigate the role of pulmonary microcirculation during bronchospasm using the same animal model. At first, the role of leukotrienes, (LTC4 ＆ D4) on hypoxic pulmonary hypertension ( HPV ) was analysed by suing selective receptor blocker of leukotrienes ( ONO 1078 ). During control normoxic perfusion, ONO 1078 reduced pulmonary vascular tone slightly partially by reducing pulmonary venous tone as evidenced by decreased venular pressure. Although ONO 1078 reduced pulmonary vascular tone during normoxia, it did not affect HPV. In our preliminary study, we found LTD4, not LTD4 increased pulmonary vascular resistance significantly. It was concluded that our animal model respoded to LTD4 however blocking leukotrienes did not ablish HPV and leukotirenes ded not play a signi
… More
ficant role in HPV in perfused cat lung.
Following that study we investigated effect of bronchospasm on pulmonary microcirculation. Bronchospasm was induced by instillating acetylcholine, histamine or PAF. When bronchospasm was induced by acetylcholine, there was no singnificant increase of pulmonary venular pressure. However, when bronchospasm was induced by histamine or PAF, there were slight but significant increase of pulmonary venular pressure. AS most of bronchial circulation draines into pulmonary venous system, increase of pulmonary venous tone ( increase of pulmonary venular pressure ) must increase bronchial microvascular pressure. We conclude that bronchospasm itself ded not affect pulmonar venular pressure thus bronchial microvascular pressure. Although bronchospasm itself did not increase bronchial microvascular hydrostatic pressure, some vasoacitve substance ( e.g. histamine and acetylcholine ) increase microvascular pressure probably by its direct effect on pulmonary vasculature. So the latter substances may act as aggravating factors of bronchial mucosal edema by increasing microvascular hydrostatic pressure especially when microvascular permeability was increased such as the case in bronchial asthma. Less
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