1999 Fiscal Year Final Research Report Summary
Mechanism of multiple organ failure caused by interaction of nitric oxide and oxidant stress
| Project/Area Number |
10671142
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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 |
General surgery
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| Research Institution | KINKI UNIVERSITY |
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Principal Investigator |
YONEKURA Takeo Kinki University School of Medicine, Assistant Professor, 医学部, 講師 (00258021)
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| Co-Investigator(Kenkyū-buntansha) |
IMANO Motohiro Kinki University School of Medicine, Assistant Professor, 医学部, 講師 (00278681)
KUBOTA Akio Kinki University School of Medicine, Assistant Professor, 医学部, 講師 (10161671)
OOYANAGI Harumasa Kinki University School of Medicine, Chief Professor, 医学部, 教授 (00030958)
HOKI Masanori Kinki University School of Medicine, Assistant Professor, 医学部, 講師 (40278685)
HIROOKA Shinji Kinki University School of Medicine, Assistant, 医学部, 助手 (10268394)
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| Project Period (FY) |
1998 – 1999
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| Keywords | nitric oxide / oxidant stress / ischemia reperfusion injury / glutathione / sepsis / hyperendotoxemia / drug delivery system |
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| Research Abstract |
Research 1 : Interaction of nitric oxide (NO) and free radical is suspected the cause of multiple organ failure in ischemia reperfusion injury. In this research, we evaluated effect of nitric oxide on oxidant stress to estimate mechanism of cellular injury in ischemia reperfusion using partial hepatic ischemia-reperfusion model. Rats were subjected to ischemia and reperfusion in the lateral lobe of the liver. After continuous administration of NG-nitro-L-arginine methyl ester (L-NAME), L-arginine (L-Arg) or saline, we evaluated tissue blood flow and concentrations of oxidized and reduced glutathione in the I/R-lobe and the non-I/R-lobe in each group. Inhibition of NO production deteriorated tissue blood flow, hepatic injury and oxidant stress in both the I/R-lobe and the non-I/R-lobe. Administration of L-Arg had only transient increase of tissue blood flow in the I/R-lobe, moreover deteriorated hepatic injury and oxidant stress.
Research 2 : Sepsis often causes multiple organ failure. To reveal the mechanism of septic organ failure, we developed a novel reproducible septic animal model applying drug delivery system (DDS). Rats implanted with DDS contained with lipopolysaccharide maintained high blood levels of endotoxin for 72 hours, and also exhibited septic condition.
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