| Project/Area Number |
12671467
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Kobe University |
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Principal Investigator |
NISHINA Kahoru KOBE UNIV.M GRADSCH. MED., DEPT. OF ANESTHESIA & PERIOPERATIVE MEDICINE, INSTRUCTOR, 大学院・医学系研究科, 助手 (20311780)
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| Co-Investigator(Kenkyū-buntansha) |
MIKAWA Katsuya KOBE UNIV., GRAD. SCH. MED., DEPT. OF ANESTHESIA & PERIOPERATIVE MEDICINE, INSTRUCTOR, 大学院・医学系研究科, 助教授 (40229662)
尾原 秀史 神戸大学, 医学部, 教授 (80030998)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | ACUTE LUNG INJURY / APOPTOSIS / REGENERATIVE MEDICINE / INFLAMMATORY CELLS / ALVEOLAR EPITHELIUM / PULMONARY FIBROSIS / GROWTH FACTOR / 急性肺傷害 / 呼吸窮迫症候群 / ケモカイン / 好中球 / II型肺胞上皮細胞 |
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| Research Abstract |
Therapy for acute lung injury consists of [1] cessation of alveolar inflammation, [2] repairment of alveolar epithelium, and [3] prevention of lung fibrosis. We first investigated the effects of rolipram (PDE-IV inhibitor), lidocaine, midazolam, propofol, ketamine (anesthetics) on apoptosis of neutrophils and alveolar type II pneumocytes. Anti-Fas antibody-induced apoptosis of neutrophils was enhanced by rolipram and not by the anesthetics. Endotoxin-induced apoptosis of type II pneumocytes was inhibited by rolipram and propofol. We secodly assessed the effects of these drugs on proliferation of rat cultured type II pneumocytes. Rolipram increased spontaneous proliperation and enhanced KGF/HGF-induced proliferation. Immunohistochemical analysis using BrdU antibody revealed that rolipram increased DNA synthesis in type II pneumocytes in mice treated with KGF/HGF. Acute lung injury was induced by intraperitoneal endotoxin (10 mg/kg) in mice. Rolipram attenuated the pathological changes of the lung injury. This successful result of rolipram may be due to the effect of the drug on neutrophils and the alveolar epithelial cells.
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