| Project/Area Number |
01480233
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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 | Yamagata University School of Medicine |
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Principal Investigator |
TAKAHASHI Keiji Yamagata University School of Medicine, Department of Laboratory Medicine, Associate Professor, 医学部, 助教授 (50004685)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Hideki Yamagata University School of Medicine, the First Department of Internal Medicin, 医学部, 助手 (10175193)
SATO Shinobu Yamagata University School of Medicine, the First Department of Internal Medicin, 医学部, 助教授 (90113951)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1991: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1990: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1989: ¥3,600,000 (Direct Cost: ¥3,600,000)
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| Keywords | Air Pollution / Road Dust / Tobacco Smoke / Aging / Lung Parenchymal Injury / Pulmonary Emphysema / Pulmonary Fibrosis / 肺サ-ファクタント / 肺線維化 / 肺気腫化 / スパイクタイヤ粉塵 / 肺組織弾性特性 / BAL / 肺組識傷害 / 加令 / 肺組識弾性特性 / ブレオマイシン肺傷害 / 肺の線維化 / 肺の気腫化 / 肺組織障害 / ブレオマイシン肺障害 |
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| Research Abstract |
Purpose : this project aimed to evaluate the synergistic effects of the chronic inhalation of road dust and tobacco smoke and the aging effects to induce the chroniclung deseases, such as pulmonary emphysema and pulmonary fibrosis.
Method : because oxidant-antioxidant inbalance might be a mechanism to induce the lung parenchymal injury and the antioxidant enzyme systems in the lung are most similar to that of the human lung, 8 weeks old male hamsters have been used in this experiment. after raising of 10 or 46 weeks, the animals were exposed to the tobacco smoke (S24, S60) and to the road dust by studded tire (D24, D60) during 1j weeks. the another group of the animals were exposed to the them both, the tobacco smoke and road dust, during the 14 weeks (SD24). the following subjects were studied in each groups. 1) pressure- volume (pv) curves of escised lung. 2) lengthy-tension (lt) relationships of alveolar wall. 3) morphometry of light-micrograh and electron-microscopic observations. 4
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) cellular analysis of broncho-alveolar lavage (bal) fluid. 5) collagen and elastin component of the lung tissue.
Results and discussion : aging effect -- no significant difference was observed in the P-V curves with aging. but in the analysis of L-T relationship, the distensibility was decreased with aging by the qualitative changes of collagen and elastic fibers and resting length of alveolar wall was also increased with aging. these results suggest the mechanical properties of surfactant ant alveolar wall have been changed with aging. each changes with aging counteract to keep a balance to minimize the mechanical change of whole lung. effects of tobacco smoke exposure and aging -- in the aged lung, the tobacco smoke exposure (S60) brought about the increment of static compliance, the enlargement of alveolar air space and the decrease of elasticity of collagen component in the alveolar wall. effect of road dust and tobacco smoke exposure -- in both the group D24 and SD2j, there was no significant difference in P-V curves. in the analysis of L-T curves in D24, the elasticity of alveolar wall was increased by the quantitative changes of collagen fibers. the mechanical properthes of alveolar wall in SD24 showed less distensibility by the qualitative change of collagen component and was similar to that of pulmonary emphysema in the human lung. mean linear intercept was significantly smaller in D24. these results suggest that the exposure of road dust induces a fibrotic change of the lung tissue and the exposure of both, road dust and tobacco smoke ; induces an emphysematous changes of the lung with aging. Less
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