1996 Fiscal Year Final Research Report Summary
Analysis of pathophysiology in acute pancreatitis from the stand point of systemic inflammatory response syndrome
| Project/Area Number |
07457258
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
OGAWA Michio Kumamoto University School of Medicine Professor, 医学部, 教授 (30028691)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Yasuo Kumamoto University School of Medicine, Assistant Professor, 医学部・附属病院, 講師 (90253757)
MORI Katsutaka Kumamoto University College of Medical Science Professor, 医療技術短期大学部, 教授 (10040213)
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| Project Period (FY) |
1995 – 1996
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| Keywords | acute pancreatitis / SIRS / cytokine / organ dysfunction / infection / neutrophil / 好中球 |
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| Research Abstract |
Systemic inflammatory response syndrome (SIRS) is clinical symptome which are induced by hypercytokinemia. The incidense of SIRS was more common in patients with severe acute pancreatitis (92%) compared with miled cases (22%). Prolongation of SIRS (more then 1w) and increase in positive SIRS-criteria (more than 3) exaggerated the mortality rate (35 and 39%, respectively).
Using rat pancreatitis model induced by cerulein injection, the mechanism of lung injury was analyzed. Bronchoalveolar macrophages were primed following the induction of pancreatitis. The macrophages enhanced the production of cytokineinduced neutrophil chemoattractant (CINC), a chemokine for neutrophils, after lipopolysaccharide exposure. Enhanced expression of CINC may modulate the pathogenesis of pancreatitis-associated lung injury complicated with sepsis. These results suggest that systemic cytokine reactions may be associated with the severity of acute pancreatitis.
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