DEVELOPMENTAL MECHANISMS OF LUNG PARENCHYMAL INJURY EMPHYSEMA AND FIBROSI - CELL TO CELL INTERACTION IN LUNG PARENCHYMA -
| Project/Area Number |
62480201
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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 ASSISTANT PROFESSOR.THE FIRST DEPARTMENT OF INTERNAL MEDICINE YAMAGATA UNIVERSIT, 医学部, 講師 (50004685)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Hideki ASSISTANT THE FIRST DEPARTMENT OF INTERNAL MEDICINE YAMAGATA UNIVERSITY SCHOOL O, 医学部, 助手 (10175193)
SATO Shinobu ASSISTANT PROFESSOR THE FIRST DEPARTMENT OF INTERNAL MEDICINE YAMAGATA UNIVERSIT, 医学部, 講師 (90113951)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1988: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1987: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Lung parenchymal injury / Pulmonary emphysema / Pulmonary fibrosis / Bleomycin-induced lung injury / Vitamin E / Elastase / タバコ煙 / 肺線維化 / 肺気腫化 / ブレオマイシン / 血清エラスターゼ活性 / 過酸化脂質 / SOD / BALF細胞 |
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| Research Abstract |
THIS PROJECT AIMED TO CLARIFY THE MECHANISMS TO PRODUCE A LUNG PARENCHYMAL INJURY, I,E, EMPHYSEMA AND FIBROSIS. TO PROCEED THIS PROJECT,WE HAVE ORIENTED TO TWO PATHOLOGICAL HYPOTHESES ON THE DEVELOPMENT OF LUNG PARENCHYMAL INJURY,ANOXIDANT-ANTIOXIDANT IMBALANCE THEORY AND A PROTEASE-ANTIPROTEASE IMBALANCE THEORY.
WE HAVE BEEN STUDIED FOLLOWING SUBJECTS ON EXPERIMENTAL MODELS OF LUNG PARENCHYMAL INJURY INDUCED BY INTRATRACHEALLY ADMINISTERED BLEOMYCIN (BLM). SUBJECTS OF EXPERIMENT: 1) EFFECT OF ANTIOXIDANT AGENT VITAMIN E (VE). 2) EFFECT OF EXOGENOUSLY ADMINISTERED PORCINE PANCREATIC ELASTASE (PPE). 3) EFFECT OF CIGARETTE SMOKE EXPOSURE. RESULTS: 1) DIETARY SUPPLEMENT OF VE DID NOT REDUCE BLM FIBROSIS. 2) VE DEFFICIENCY CONSEQUENTLY INDUCED THE EMPHYSEMATOUS CHANGE IN BLM-ADMINISTERED LUNG INJURY. 3) CIGARETTE SMOKE EXPOSURE MODIFIED BLM-INDUCED LUNG INJURY TO PRODUCE A EMPHYSEMA. 4) INTRAMUSCULARLY ADMINISTERED PPE REDUCED AN INDUCTION OF BLM INDUCED FIBROSIS. DISCUSSION: BECAUSE A SUPP
… More
LEMENTATION OF VE DID NOT INHIBIT THE DEVELOPMENT OF FIBROSIS,IT IS SPECULATED HYDROGEN PEROXIDE IS AN IMPORTANT ACTIVE OXYGEN SPECIES TO INCITE A LUNG FIBROSIS. OTHERWISE VITAMIN EDEFICIENCY CAUSED A SEVERE FIBROTIC CHANGE IN EARLY STAGE OF BLM TREATMENT, BUT CONSEQUENTLY INDUCED AN EMPHYSEMA. FROM THESE RESULTS, IT SEEMED A SINGLET OXYGEN ACTED AND INDUCED A SEVERE FIBROTIC CHANGE IN THE EARLY STAGE AND OTHER ACTIVE OXYGEN SPECIES SUCH AS PEROXIRADICAL, HYDROPEROXIRADICAL AND SUPEROXIDE ANION RADICAL WHICH COULD BE SCAVENGED BY VE FOLLOWED AN EMPHYSEMATOUS CHANGE. COEXIST OF CIGARETTE SMOKE EXPOSURE AND INTRATRACHEAL INSTILLATION OF BLM INFERED TO DEVELOPE AN EMPHYSEMATOUS LUNG INJURY. IN ELASTASE EXPERIMENT, IT IS ESTIMATED COEXIST OF LOCAL DISTANT ORGAN INFLAMMATION AND A LEVEL OF SERUM ELASTASE ACTIVITY AFFECT THE LUNG PARENCHYMAL INJURY. A HIGH LEVEL OF SERUM ELASTASE ACTIVITY RESTRAINED NEUTROPHIL INFILTRATION IN THE LUNG TISSUE. THESE RESULTS SUGGEST THAT ALTHOUGH PULMONARY FIBROSIS AND EMPHYSEMA HAVE BEEN CONSIDERED TO BE FINAL AND DIFFERENT FORMS OF PARENCHYMAL INJURY, EACH MAY PROCEED TO THE OTHER UNDER THE INFLUENCE OF SOME MODULATING FACTORS. Less
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Report
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Research Products
(23 results)
