Analysis of pathophysiology in acute pancreatitis from the stand point of systemic inflammatory response syndrome

从全身炎症反应综合征角度分析急性胰腺炎的病理生理学

• 批准号: 07457258
• 负责人: OGAWA Michio
• 金额: $ 4.8万
• 依托单位: Kumamoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1996
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07457258/
• 关键词: acute pancreatitis; SIRS; cytokine; organ dysfunction; infection; neutrophil; 好中球; 炎症性サイトカイン; 多臓器不全

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.

全身性炎症反应综合征（SIRS）是临床症状，由高胞菌血症诱导。与MILED病例相比，严重急性胰腺炎患者（92％）（22％），SIRS的畸形更为常见。 SIRS的延长（超过1W），并增加阳性SIRS标准（超过3）夸大了死亡率（分别为35％和39％）。使用Cerulein注射引起的大鼠胰腺炎模型，分析了肺损伤的机制。胰腺炎诱导后，支气管肺泡巨噬细胞启动。巨噬细胞增强了脂多糖暴露后的细胞因子诱导的嗜中性粒细胞趋化剂（CINC），一种中性粒细胞的趋化因子。 CINC的增强表达可能会调节与败血症复杂的胰腺炎相关肺损伤的发病机理。这些结果表明，全身细胞因子反应可能与急性胰腺炎的严重程度有关。

项目成果

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Ogawa M,et al.: Increased cytokine release in severe acute pancreatitis is closely related to the development of organ failure.The Immune Consequences of Trauma, Shock and Sepsis. Vol.II.Faist E,Baue AE,Schildberg FW (eds.), Monduzzi Editore (Bologna), 33

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