Influence of stress in acute pancreatitis and correlation with stress-induced gastric ulcer
Influence of stress in acute pancreatitis and correlation with stress-induced gastric ulcer
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DOI：
10.1159/000079956
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发表时间：
2004-01-01
期刊：
影响因子：
3.6
通讯作者：
Tiscornia, O
中科院分区：
文献类型：
--
作者：
Cosen-Binker, LI;Binker, MG;Tiscornia, O
背景和目的：在全身适应综合征中，胃损伤是应激的首发表现。我们假设，急性胰腺炎(AP)是一种炎症性急性疾病，如果在应激后解除连锁，将会加剧。由于儿茶酚胺能释放导致胰腺内胆碱能张力的过度诱导，胰腺细胞对CCK的反应增强，内脏超敏反应将被增强。我们的目的是研究AP前的应激对后期AP的影响，以及AP在胃溃疡等基础疾病中的作用。方法：采用束缚应激模型和胆胰管出口阻断法闭合十二指肠环模型。评估应激后、AP前麻醉剂阻断自主弧反射(AAR)的效果。考虑迷走神经和交感神经通路的参与以及CCK-A受体的参与。通过生化和组织病理学分析评估其严重程度。结果：应激后AP的诱发较无应激时更为严重。腺泡和脂肪坏死、出血和中性粒细胞浸润灶均匀分布，应激后大小和数目明显增大。AP触发后，胃溃疡演变为溃疡、出血、胃壁坏死。应激后AP大鼠血清淀粉酶、脂肪酶、C反应蛋白、IL-6、IL-10、血浆HSP72及胰腺和肺组织髓过氧化物酶均显著升高，而胰腺淀粉酶和脂肪酶显著降低。阻断AAR可改善应激后AP。结论：应激加重胰腺病理，AP加重胃病理，麻醉治疗对两者均有利。在其他动物模型中的约束对于研究压力在其他疾病进化中的影响是有用的。版权所有(C)2004 S.Karger AG，巴塞尔和IAP。
Background and Aims: In the general adaptation syndrome, gastric lesions are the first manifestation of stress. We hypothesized that acute pancreatitis (AP), an inflammatory acute disease, will be exacerbated if unchained following stress. Visceral hypersensitivity will be enhanced due to catecholaminergic discharges leading to an over-induction of the intrapancreatic cholinergic tone with increased response of the pancreocyte to cholecystokinin (CCK). Our aim was to investigate the influence of stress before AP on the later AP, and the effect of AP on underlying diseases such as gastric ulceration. Methods: The model of stress induced by restraint was followed by the bilio-pancreatic duct outlet exclusion closed duodenal loops model. The effect of autonomous arc reflex (AAR) interruption by anesthetics after stress but before AP was assessed. The participation of the vagal and sympathetic pathways and involvement of CCK-A receptors were considered. The degree of severity was evaluated using biochemical and histopathological analyses. Results: Induction of AP after stress was more severe than in its absence. Acinar and fat necrosis, hemorrhage and neutrophil infiltrate foci were evenly distributed, being significantly greater in size and number after stress. Gastric ulceration evolved to ulcer, hemorrhage and gastric necrosis after AP triggering. Serum amylase, lipase, C-reactive protein, IL-6, IL-10 and plasmatic hsp72 as well as pancreatic and lung myeloperoxidase were significantly elevated in AP after stress while pancreatic amylase and lipase were significantly reduced. AAR blockage ameliorated AP after stress. Conclusions: Stress aggravates pancreatic pathology while AP deteriorates gastric pathology, and anesthetic treatment was beneficial for both. Restraint in other animal models can be useful to study the influence of stress in the evolution of other diseases. Copyright (C) 2004 S. Karger AG, Basel and IAP.