Garcia-Montero A C, Manso M A, Rodriguez A I, De Dios I
Department of Physiology and Pharmacology, Faculty of Biology, University of Salamanca, Spain.
Pancreas. 1994 May;9(3):309-15. doi: 10.1097/00006676-199405000-00005.
The prophylactic and therapeutic effects of a potent cholecystokinin (CCK) receptor antagonist, L-364,718, on acute pancreatitis induced by caerulein were evaluated, analyzing morphologic and functional pancreatic parameters jointly. Edematous pancreatitis was induced by four subcutaneous injections of caerulein (20 micrograms/kg) in rats at 1-h intervals. Prophylactic administration of L-364,718 (0.1 mg/kg) prevented rise in serum amylase levels, interstitial edema, vacuolization, and impairment of pancreatic enzyme secretion that accompany caerulein-induced acute pancreatitis. After 7 days, a spontaneous regression of the morphologic alterations caused by caerulein-induced acute pancreatitis occurs; however, recovery of the secretory function of the pancreas was only reached after this period of time when L-364,718 was administered therapeutically (0.1 mg/kg/day). Prophylactically or therapeutically administered, L-364,718 exerts a beneficial effect on caerulein-induced acute pancreatitis, indicating that CCK (exogenous or endogenous) plays an important role in the development of this pathology.
评估了一种强效胆囊收缩素（CCK）受体拮抗剂L-364,718对由蛙皮素诱导的急性胰腺炎的预防和治疗作用，联合分析胰腺的形态学和功能参数。通过给大鼠每隔1小时皮下注射4次蛙皮素（20微克/千克）诱导水肿性胰腺炎。预防性给予L-364,718（0.1毫克/千克）可防止血清淀粉酶水平升高、间质水肿、空泡化以及伴随蛙皮素诱导的急性胰腺炎出现的胰腺酶分泌受损。7天后，由蛙皮素诱导的急性胰腺炎引起的形态学改变会自发消退；然而，仅在这段时间之后，当进行治疗性给予L-364,718（0.1毫克/千克/天）时，胰腺的分泌功能才得以恢复。无论是预防性还是治疗性给予，L-364,718对蛙皮素诱导的急性胰腺炎均发挥有益作用，表明CCK（外源性或内源性）在这种病理过程的发展中起重要作用。
