1996 Fiscal Year Final Research Report Summary
Vasospasum induced bacterial translocation following intraabdominal hemorrhage
| Project/Area Number |
06671318
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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 |
Digestive surgery
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| Research Institution | Kansai Medical University |
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Principal Investigator |
CHISHIRO Takao Medical department Kansai Medical University, Associate Professor, 医学部, 助教授 (30105796)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Tohru Medical department Kansai Medical University, Lecturer, 医学部, 講師 (20240111)
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| Project Period (FY) |
1994 – 1996
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| Keywords | Mesenteric blood flow / Vasospasum / Intraabdominal hemorrhage / Superoxide radical / Intestianl ischemia / Bacterial translocation / bacterial traslocation |
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| Research Abstract |
Transmucosal passage of bacteria in critically ill patients may lead to a significant incidence of systemic sepsis. Bacterial translocation is increased in animal models where nutrients are given by the parenteral route, while enteral feeding reverses this. Translocation is also considerably increased in response to a non-lethal endotoxin challenge. Disordera of mucosal blood flow may contribute to gut barrier dysfunction in bacterial translocation. It is well known that subarachnoid hemorrhage induces arterial vasoconstriction. This study was performed to investigate the mechanisms by which mesenteric microcirculation and oxygen radical induced by abdominal hemorrhage canses intestinal mucosal injury and bacterial translocation. Fresh blood cells stimulated by lipopolysaccharide occured a statistically significantly vasoconstriction and lower blood flow on 6 hours after versus controls and nonstimulated groups. Then stimulated blood cells increased statistically significantly the histological damage of intestinal epithelial mucosa, % xanthine oxidase activity, catalase activity, lipid peroxidation, and bacterial inversion of the liver, spleen, portal vein, and systemic sepsis on 6 hours after versus controls and nonstimulated groups.
We believe that this bacterial inversion in indicative of decreased mesenteric perfusion due to fresh stimulated blood cells, and oxygen free radicals may be potential factors in the development of gut barrier failure.
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