1988 Fiscal Year Final Research Report Summary
Pathogenesis of multiple organ failure in severe acute pancreatitis,with special interest to lipid peroxide
| Project/Area Number |
62570603
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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 | Mie University |
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Principal Investigator |
YOSHIFUMI KAWARADA College of Medical Sciences Mie University, Professor, 医療技術短期大学部, 教授 (40024814)
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| Co-Investigator(Kenkyū-buntansha) |
KAZUNORI OKAMURA Mie University School of Medicine, Assistant, 医学部, 助手 (50194387)
SHUJI ISAJI Mie University Hospital, Assistant, 医学部附属病院, 助手 (70176121)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Acute pancreatitis / Multiple organ failure / Lipid peroxide / Phospholipase A_2 / 細胞膜流動性 |
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| Research Abstract |
This experimental study was undertaken to clarify the role of phospholipase A2 (PLA2) and lipid peroxide in the pathogenesis of renal and respiratory failures in acute pancreatitis.
[Material and Methods] Acute pancreatitis was induced in dogs by injecting autologous gallbladder bile into the main pancreatic duct. In another experiment, pancreatic enzymes such as PLA2 were infused into the renal or pulmonary artery of dogs. In both experiments, the kidney and lung were evaluated functionally and morphologically. PLA2 activity and the content of lipid peroxide was measured in blood and tissues.
[Results] I.Pathogenesis of Renal Failure: In experimental acute pancreatitis, PLA2 activity in peripheral blood increased markedly after on hour, and urinary excretion of renal tubular enzymes significantly increased after 3 hours, showing renal tubular damage. PLA2 activity and lipid peroxide in renal tissue homogenate demonstrated marked increase after one hour. PLA2 activity in brush border Mem
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branes, which were separated from the renal tubular cells, increased after 3 hours. Membrane fluidity of the brush border membranes decreasaed significantly after 3 hours. PLA2 infusion into the renal artery produced similar results to those in experimental pancreatitis.
II. Pathogenesis of Respiratory Failure: In experimental pancreatitis, PaO2 decreased significantly with marked elevation of Qs/Qt. The lecels of lipid peroxide, free fatty acid and phospholipid were significantly higher in the pulmonary venous blood than those in the pulmonary arterial blood. The ratio of lysolecithin to total phospholipid in the bronchioalveolar lavege fluid increased markedly, demonstrating the destruction of pulmonary surfactant. PLA2 infusion into the pulmonary artery produced similar results to those in experimental pancreatitis.
[Conclusion] It is considered that PLA2 plays an important role in the pathogenesis of renal and respiratory failures in acute pancreatitis, because it has a damaging effect to cell membranes of renal tubules as well as to the pulmonary surfactant, with concomitant production of lipid peroxide causing further cell damage. Less
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