| Project/Area Number |
12557097
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
General surgery
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MIMURA Yoshikazu The University of Tokyo, The University of Tokyo Faculty of Medicine, Associate Professor (10175614)
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| Co-Investigator(Kenkyū-buntansha) |
OGAWA Toshihisa The University of Tokyo, Faculty of Medicine, Lecturer (80224111)
HIKI Naoki The University of Tokyo, Faculty of Medicine, Research Associate (30313026)
金内 一 東京大学, 医学部附属病院, 助手 (20242141)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥5,300,000 (Direct Cost: ¥5,300,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Hypoxia / Endotoxin / Tolerance / Cytokine / エンドトキシン耐性 / 無毒化エンドトキシン / 交感神経 / MLA / ラット |
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| Research Abstract |
Endotoxin (Et) tolerance is developed after the pretreatment in animals with sublethal dose of Et and is characterized by a reduced inflammatory cytokine response to subsequent Et challenge. The Et administration also attenuates ischemic injury of rat myocardial tissue flowing hypoxia described as a cross-tolerance. The objective of this study was : 1) to determine whether Et evokes cross-tolerance to rat systemic hypoxia as behaviors of cytokine and catecholamines ; 2) to estimate the circulatory and pulmonary performance in rat systemic hypoxia after endotoxin pretreatment. Wistar rats were pretreated with intraperitoneal injection of 10 /μg/kg/body wt of Et. Systemic hypoxia was achieved by continuous inhalation of the gas mixture (9% oxygen + 91% nitrogen) for 4h. Obtained results were as follows : 1) Et pretreatment prevented the drop of mean arterial pressure and the fall of arterial oxygen pressure during hypoxia : 2) Et pretreatment suppressed the hypoxia-induced cytokines hypersecretion ; 3) Et pretreatment suppressed the norepinephrine to the levels of normoxia. In conclusion, Et pretreatment improves the hypoxia-induced 1) inflammatory responses ; 2) reduction of oxygenation ; 3) anaerobic metabolism ; and 4) high activity of norepinephrine.
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