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.

全身炎症反应综合征(SIRS)是由高细胞分裂素血症引起的临床症状。重症急性胰腺炎患者SIRS发生率(92%)明显高于轻型患者(22%)。SIRS延长(>1周)和阳性SIRS增加(>3个)分别夸大死亡率(分别为35%和39%)。采用雨蛙素诱导的大鼠胰腺炎模型，分析肺损伤的机制。在胰腺炎诱导后，支气管肺泡巨噬细胞被激活。巨噬细胞在脂多糖暴露后，增加了细胞因子诱导的中性粒细胞趋化因子(CINC)的产生，这是一种中性粒细胞的趋化因子。CINC表达增强可能参与了胰腺炎相关肺损伤并发脓毒症的发病机制。这些结果提示，全身细胞因子反应可能与急性胰腺炎的严重程度有关。

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