1996 Fiscal Year Final Research Report Summary
MODULATION OF NEURO-ENDOCRINE-IMMUNE RESPONSES IN SURGICAL STRESS
Project/Area Number |
07457246
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General surgery
|
Research Institution | THE UNIVERSITY OF TOKYO |
Principal Investigator |
SAITO Hideaki THE UNIVERSITY OF TOKYO,DEPT.OF SURGERY,ASSOCIATE PROFESSOR, 医学部・附属病院, 助教授 (30134555)
|
Co-Investigator(Kenkyū-buntansha) |
FURUKAWA Satoshi THE UNIVERSITY OF TOKYO,DEPT.OF SURGERY,ASSISTANT, 医学部・附属病院, 医員
はん 一秀 東京大学, 医学部・附属病院, 医員
FUKATSU Kazuhiko THE UNIVERSITY OF TOKYO,DEPT.OF SURGERY,ASSISTANT, 医学部・附属病院, 医員
INOUE Tomomi THE UNIVERSITY OF TOKYO,DEPT.OF SURGERY,ASSISTANT, 医学部・附属病院, 医員
INABA Tsuyoshi THE UNIVERSITY OF TOKYO,DEPT.OF SURGERY,ASSISTANT, 医学部・附属病院, 助手 (80272582)
ILL-SON Han THE UNIVERSITY OF TOKYO,DEPT.OF SURGERY,ASSISTANT
|
Project Period (FY) |
1995 – 1996
|
Keywords | SURGICAL STRESS / CYTOKINES / BIOLOGICAL RESPONSES / HOST DEFENSE / TNF / IL-1 / SURGICAL NUTRITION / NITRIC OXIDE |
Research Abstract |
The purpose of this research was how to modulate neruo-endocrine-immune responses in surgical stress. The result is as follows : 1. Nutritional routes and glutamine supplementation : Both antecedent enteral nutrition and Ala-Gln enriched TPN enhance local, systemic and remote organ immune responses to intraperitoneal bacterial chalenge. On the basis of our findings, critical illness whenever the enteral route is feasible. Ala-Gln enriched TPN may be an option for enhancing host defense when enteral nutrition can not be tolerated. 2. Growth hormone and Insulin-like growth factor 1 : GH and IGF-1 enhance phagocytosis and the E.coli-killing activity of PECs, via a modestly increased plasma capacity to support these activities, as well as by a strong direct action. 3. Nitric oxidase inhibitor and NO donor : Administration of L-NAME increased neutrophil adhesion in the lung, while decreasing that in the peritoneum. NO inhibition may be ditrimental, due to neutrophil sequestration, in this peritonitis model. NO donor administration prevented neutrophil adhesion in the lung, but decreased neutrophil adhesion in the peritoneal cavity.
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Research Products
(20 results)