Niederau C, Grendell J H
St. Josef-Hospital, Academic Teaching Hospital, Department of Internal Medicine, Oberhausen, Germany.
Digestion. 1999;60 Suppl 1:69-74. doi: 10.1159/000051458.
This presentation reviews the role of cholecystokinin (CCK) as a contributory factor for the development and progression of acute pancreatitis (AP) and the perspective of CCK receptor antagonists for treatment of AP. High, supraphysiological concentrations of CCK induce AP in various species including man. There is also evidence that physiological increases in plasma CCK deteriorates AP in several animal models. The latter findings support the hypothesis that CCK plays a contributory or permissive role for the development of AP. The majorities of experimental studies show that the prophylactic and therapeutic use of CCK antagonists ameliorates AP. The latter effects were clearly shown for models of biliary AP in which plasma CCK is increased due to a feedback mechanism. However, CCK antagonists also had beneficial effects in models in which plasma CCK is not increased. In animal strains which do not have a CCK-A-receptor due to a genetic abnormality AP induced by a certain noxious factor does not develop to the same severity when compared to animals with a normal CCK-A-receptor. Thus, CCK acts as a permissive or contributory factor for the development and progression of AP. There is also evidence that CCK antagonists have a potential therapeutic benefit. Clinical studies will evaluate their therapeutic potential for patients with AP.
本报告综述了胆囊收缩素（CCK）作为急性胰腺炎（AP）发生和发展的一个促成因素的作用，以及CCK受体拮抗剂治疗AP的前景。高浓度、超生理浓度的CCK可在包括人类在内的多种物种中诱发AP。也有证据表明，在几种动物模型中，血浆CCK的生理性升高会使AP恶化。后一项发现支持了CCK在AP发生中起促成或允许作用的假说。大多数实验研究表明，CCK拮抗剂的预防性和治疗性应用可改善AP。对于胆汁性AP模型，这种后一种效应很明显，在该模型中，由于反馈机制，血浆CCK会升高。然而，CCK拮抗剂在血浆CCK未升高的模型中也有有益作用。在因基因异常而没有CCK-A受体的动物品系中，与具有正常CCK-A受体的动物相比，由某种有害因素诱发的AP发展到的严重程度不同。因此，CCK在AP的发生和发展中起允许或促成作用。也有证据表明CCK拮抗剂具有潜在的治疗益处。临床研究将评估它们对AP患者的治疗潜力。
