1988 Fiscal Year Final Research Report Summary

Disseminated intravascular coagulation and organ failure inthe depressant state of reticuloendothelial function after hepatic resection

Research Project

Project/Area Number	61570642
Research Category	Grant-in-Aid for General Scientific Research (C)
Allocation Type	Single-year Grants
Research Field	Digestive surgery
Research Institution	Fukui Medical School
Principal Investigator	SHIMADA Hiroshi Fukui Medical school. Lecturer, 医学部, 講師 (90117747)
Co-Investigator(Kenkyū-buntansha)	NAKAGAWARA Gizo Fukui Medical school. Professor, 医学部, 教授 (10019549)
Project Period (FY)	1986 – 1988
Keywords	Hepatic failure / Phagocytic function / Endotocemia / Kupffer cell / chemical mediator
Research Abstract	In order to clarify the mechanism of liver failure after hepatic resection, pathophysiology of hepatic resection in 89 cases was clinically investigated from the point of endotoxemia and phagocytic function (phagocytic K value, serum CH50 and fibronectin), and estrogen concerning the enhancement of Kupffer cell phagocytic function for endotoxin and the mechanism of altered hepatic function in endotoxemia was experimentally studied in vivo and in vitro. It was concluded that endotoxemia in the presence of a self defence dysfunction a trigger for organ failure. The experimental study showed estrogen had the function of the enhancement of Kupffer cell phagocytosis for endotoxin, and from the another experimental result hepatic damage in endotoxemia was thought to be caured by the cytotoxic effect fia mediator secreted from Kupffer cells which blocked by dexamethazone.

(4 results)