论文部分内容阅读
采用胰管内逆行注入不同浓度牛磺胆酸钠造成程度不同的大鼠急性胰腺炎（ＡＰ）的模型，观察不同程度ＡＰ大鼠早期肿瘤坏死因子（ＴＮＦ）、内毒素（ＬＰＳ）及酶学的改变，结果表明轻、重胰腺炎（ＡＥＰ、ＡＮＰ）组ＬＰＳ水平造模后２４小时后明显升高，升高的程度以重型组最剧。轻、重胰腺炎组血中ＴＮＦ水平造模术后均急剧升高，两组相比有显著性变化。各组血中淀粉酶的水平术后１２小时达到高峰。说明在ＡＰ的早期，胰酶的活化，细胞因子的诱生参与机体超强的炎症反应过程，是造成ＡＰ早期病理损害的主要原因。而来自肠源性细菌的严重感染和内毒素血症导致了后期病理生理的恶性循环，形成急性胰腺炎病损变化的第二个“高峰”。
Acute pancreatitis (AP) induced by different concentrations of sodium taurocholate in rats was retrogradely injected into the pancreatic duct to observe the changes of tumor necrosis factor (TNF), endotoxin (LPS) and enzymology Changes, the results showed that light and severe pancreatitis (AEP, ANP) group LPS levels significantly increased 24 hours after modeling, the degree of increase in the most severe group. The levels of TNF in blood of patients with mild and severe pancreatitis increased sharply after modeling, and there were significant changes between the two groups. The levels of amylase in each group peaked at 12 hours after operation. In the early stage of AP, trypsin activation and induction of cytokines are involved in the superficial inflammatory reaction process, which is the main reason for the early pathological damage of AP. Serious infections and endotoxemia from gut-derived bacteria lead to a vicious cycle of later pathophysiology, forming the second “peak” in the changes in lesions of acute pancreatitis.