Analysis of pathophysiology in acute pancreatitis from the stand point of second attack theory

急性胰腺炎伴随着组织的破坏和消化，引起高细胞素血症和白细胞（巨噬细胞和中性粒细胞）和血管内皮的高反应性！细胞。中性粒细胞作为这种情况下的生物防御机制之一，浸润重要器官，如肺、肝和消化器官。当急性胰腺炎并发感染时，高反应性巨噬细胞释放大量促炎细胞因子，激活引物中性粒细胞作为第二次攻击”。中性粒细胞利用蛋白水解酶和氧化剂，损伤浸润的重要器官，引起远离胰腺的重要器官的细胞损伤和功能障碍。急性胰腺炎合并脓毒性并发症的多器官衰竭，至少部分是由炎症细胞因子和中性粒细胞激活引起的。

Acute pancreatitis is accompanied by destruction and digestion of tissues, causing hvpercytokinemia and hyperreactivity of leukocytes (macrophages and neutrophils) and vascular endothelia! cells. As one of the biological defense mechanisms in this condition, neutrophils infiltrate vital organs, such as lung, liver, and digestive organs. When acute pancreatitis is complicated by infection, hyperreactive macrophages release a large amount of proinflammatory cytokines that activate primed neutrophils as a second attack". Utilizing proteolytic enzymes and oxidant, neutrophils injure the infiltrated vital organs, causing cellular damage and dysfunction of vital organs distant from the pancreas. Multiple organ failure in acute pancreatitis with septic complications can develop, at least in part, by inflammatory cytokine and neutrophil activation.