Beglinger C
Division of Gastroenterology, University Hospital, Basel, Switzerland.
Digestion. 1999;60 Suppl 1:61-3. doi: 10.1159/000051456.
Evidence based on animal studies suggests that cholecystokinin (CCK) is involved in the induction and development of acute experimental pancreatitis. However, the results obtained with CCK or CCKA receptor antagonists in different species (rats, mice) and different models of acute pancreatitis (cerulein pancreatitis, hemorrhagic pancreatitis induced by choline-deficient, ethionine-supplemented diet, arginine-induced pancreatitis, sodium taurocholate-induced pancreatitis) produced variable results. The route of administration, the specificity and potency of compounds and the design of the study are predictive for the outcome. Based on the available information, CCK appears to play a contributory role in the development of acute experimental pancreatitis in mice and rats. No conclusions can be drawn from these results with respect to the human disease.
基于动物研究的证据表明，胆囊收缩素（CCK）参与急性实验性胰腺炎的诱导和发展。然而，在不同物种（大鼠、小鼠）以及不同急性胰腺炎模型（蛙皮素诱导的胰腺炎、胆碱缺乏-蛋氨酸补充饮食诱导的出血性胰腺炎、精氨酸诱导的胰腺炎、牛磺胆酸钠诱导的胰腺炎）中使用CCK或CCKA受体拮抗剂所获得的结果各不相同。给药途径、化合物的特异性和效力以及研究设计对结果具有预测性。根据现有信息，CCK似乎在小鼠和大鼠急性实验性胰腺炎的发展中起促成作用。关于人类疾病，这些结果无法得出结论。
