1987 Fiscal Year Final Research Report Summary
A study on the development of liver disorder using experimental peritonitis models
| Project/Area Number |
61570653
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Digestive surgery
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
YOKOYAMA Takashi Associate Professor, Hiroshima University School of Medicine, 医学部, 助教授 (60034104)
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| Co-Investigator(Kenkyū-buntansha) |
KODAMA Takashi Assistant, Hiroshima University Hospital, 医学部附属病院, 助手 (20161945)
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| Project Period (FY) |
1986 – 1987
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| Keywords | Experimental model of severe peritonitis / right lymph duct drainage / endotoxin / liver damage / 組織血流 |
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| Research Abstract |
A study on the mechanism and its process of the liver disorder was made with the emphasis on the changes of endotoxin (Et) in the blood using our experimental peritonitis models. The models were divided into 3 groups as follows.
Group I : Peritonitis was induced by teh intraabdominal administration of physiological saline solution with thoracic duct drainage,
Group II : Peritonitis was induced by the intraabdominal administration of Et (Difco B_5, 0.5 mg/kg) without thoracic and right lymph duct drainage,
Group III : Peritonitis was induced by the intraabdominal administration of the same amount of Et as Group II with thoracic and right lymph duct drainage.
The examination on the following parameters of each groups was made for three hours after the administration; 1) observation of blood flow dynamics, 2) determination of leucocyte count and platelet count of the systemic blood, 3) determination of <beta>-glucronidase value, transaminase value, leucocyte chemiluminescence value, 4) MDA va
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lue in the lymph fluid, and 5) quantitative analysis of Et in the lymph fluid of the righ tlymph duct, throacic duct, portal blood, and systemic blood.
Liver disorder was not observed in Group I with no change in any of th eparameters. In Group II, GOT and LDH were significantly elevated in 30 minutes of the administration. From 60 minutes after the administration, there was significant decrease of arterial pressure and blood flow volume in the hepatic and intestinal tissues. After 120 minutes, a significant drop of cardiac output was observed. No significant changes of MDA value in the lymph fluid could be demonstrated. In Group III, liver disorder could not be observed and the changes in the various parameters were minimal.
Consequently, it is considered that it is produced by chemical mediators which are released following interaction with complement, coagulant factors, and such mesodermal cells as leucocytes, platelets, and macrophage. Within the entire course of the present experiment of less than three hours, cell damage due to active oxygen and lipid peroxides could not be observed. Less
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