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

全身性炎症反应综合征（SIRS）是由高细胞分裂血症引起的临床症状。SIRS的发生率在重症急性胰腺炎患者中更为常见（92%），而在轻度胰腺炎患者中（22%）。SIRS的延长（超过1w）和SIRS阳性标准的增加（超过3个）使死亡率升高（分别为35%和39%）。采用丙核蛋白致大鼠胰腺炎模型，分析其肺损伤机制。诱导胰腺炎后，支气管肺泡巨噬细胞被激活。脂多糖暴露后，巨噬细胞增强了细胞因子诱导的中性粒细胞趋化因子（CINC）的产生，CINC是中性粒细胞的趋化因子。CINC表达增强可能调控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。

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.