Haciahmetoglu Tufan, Ertekin Cemalettin, Dolay Kemal, Yanar Fatih, Yanar Hakan, Kapran Yersu
General Surgery, Istanbul Faculty of Medicine, Millet Cad, Istanbul, Turkey.
Langenbecks Arch Surg. 2008 May;393(3):367-72. doi: 10.1007/s00423-007-0214-1. Epub 2007 Aug 3.
Although there are various experimental pancreatic models in animals, only a few studies have evaluated how intraductal pressure and contrast agent affect the development of pancreatitis after endoscopic retrograde cholangiopancreatograpy (ERCP).
The rats were randomly divided into seven groups (n = 8/group). The rats in all groups underwent laparotomy and their biliopancreatic ducts were cannulated transduodenally using a 24G catheter. In the control group, group 1, the biliopancreatic ducts of the rats were not infused with any fluid. The biliopancreatic ducts of the rats in groups 2, 3, and 4 were infused with 0.5 ml isotonic NaCl solution at 10, 2, and 50 mmHg, respectively. Groups 5, 6, and 7 were given 0.5 ml of 50% diluted contrast agent at 10, 25, and 50 mmHg, respectively. The serum amylase, aspartate aminotransferase (AST), lactic dehydrogenase (LDH), and C-reactive protein (CRP) were measured 24 h after the procedure. Pancreatic tissue was also evaluated histopathologically.
Pancreatitis due to the contrast agent was noted when comparing the low pressure isotonic NaCl group and the low pressure contrast group (p < 0.05). Based on serum amylase and CRP values, there was a positive correlation between the severity and frequency of acute pancreatitis and pressure (p < 0.01). AST and LDH levels increased in all of the groups that underwent the procedure; however, no correlation was detected with increasing pressure or with the use of contrast agent (p > 0.05). Both pancreatic edema and the inflammatory cell infiltration score were elevated in isotonic NaCl and contrast group (p < 0.05); however, necrosis was not significantly changed (p > 0.05).
The results of this study suggest that the main mechanism for preventing pancreatitis after ERCP is to minimize trauma to the pancreatic canal, to cannulate the pancreas only when it is necessary, and to give contrast agent under low pressure when it is needed.
尽管动物中有多种实验性胰腺模型，但仅有少数研究评估了内镜逆行胰胆管造影术（ERCP）后胰管内压力和造影剂如何影响胰腺炎的发生发展。
将大鼠随机分为七组（每组n = 8）。所有组的大鼠均接受剖腹手术，并使用24G导管经十二指肠插管至其胆胰管。在对照组（第1组）中，大鼠的胆胰管未注入任何液体。第2、3和4组大鼠的胆胰管分别以10、2和50 mmHg的压力注入0.5 ml等渗氯化钠溶液。第5、6和7组分别以10、25和50 mmHg的压力给予0.5 ml 50%稀释造影剂。术后24小时测量血清淀粉酶、天冬氨酸转氨酶（AST）、乳酸脱氢酶（LDH）和C反应蛋白（CRP）。还对胰腺组织进行了组织病理学评估。
比较低压力等渗氯化钠组和低压力造影剂组时，发现造影剂导致了胰腺炎（p < 0.05）。根据血清淀粉酶和CRP值，急性胰腺炎的严重程度和发生率与压力之间存在正相关（p < 0.01）。所有接受该操作的组中AST和LDH水平均升高；然而，未检测到与压力增加或造影剂使用之间的相关性（p > 0.05）。等渗氯化钠组和造影剂组的胰腺水肿和炎症细胞浸润评分均升高（p < 0.05）；然而，坏死情况无明显变化（p > 0.05）。
本研究结果表明，预防ERCP术后胰腺炎的主要机制是尽量减少对胰管的损伤，仅在必要时插管至胰腺，并在需要时低压给予造影剂。
