1987 Fiscal Year Final Research Report Summary
Pathophysiological studies of hypofibronectineamia and superoxide radical in multiple organ failure (MOF)
Project/Area Number |
61570599
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
General surgery
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Research Institution | Asahikawa Medical College |
Principal Investigator |
KASAI Shinichi Asahikawa Medical College, 医学部, 講師 (40091566)
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Co-Investigator(Kenkyū-buntansha) |
KATO Kazuya Asahikawa Medical College, 医学部, 助手 (70175280)
NONDO Keishi Asahikawa Medical College, 医学部, 助手 (60153714)
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Project Period (FY) |
1986 – 1987
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Keywords | MOF / fibronectine / superoxide radical / liver failure / severe sepsis / reticuloendothelial system / 網内系機能 |
Research Abstract |
Multiple organ failure (MOF) is a syndrome which may occur in patients after injuey or after operation. This syndrome is the natural result of improved surgical capability and care of patients, but is still sometimes fatal. Recently, it has been pointed out that the main pathophysiology of the syndrome is severe sepsis observed in injured or surgical patients. These patients are usually impaired reticuloendothelial host defense mechanisms and serum fibronectin of these patients is often low. While it has been noticed that the formation of oxygen-derived free radical may play an important part in somekinds of tissue injuries. Thus is this study, we design to investigate the patophysiological interrelationship between hypofibronectinemia and super oxide radical in MOF. 1. Plasma fibronectine in clinical patients; The were observed that the level of plasma fibronectine decreased remarkably in patients with severe sepsis and liver failure. The level also decreased just after surgical insertion, but it again increased in usual course by one week. 2. Experimental studies; i) Plasma fibronectine level decreased in rats with abdominal infection and the animals died by severe sepsis. ii) It was observed that super oxide radical played an important role in rat hepatic injury associated with ischemia and the injury was prevented by and administration of free radical scavenger (Alopurinol). iii) Severe hepatic failure in rats was induced by galactosamine and the level of ATP in the liver remarkably decreased, but the level was maintained within normal range by and administration of DBcAMP which was second messenger in the cell.
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Research Products
(13 results)