Simpson K W, Beechey-Newman N, Lamb C R, Smyth J B, Hughes G, Coombe K, Sumar N, Hermon-Taylor J
Department of Small Animal Medicine and Surgery, Royal Veterinary College, U.K.
Dig Dis Sci. 1995 Oct;40(10):2152-61. doi: 10.1007/BF02208999.
To study the early pathogenesis of acute edematous pancreatitis in dogs, we examined the relationship of pancreatic hyperstimulation with cholecystokinin-8 (10 micrograms/kg/hr intravenously for 6 hr) to alterations in circulating pancreatic enzymes and pancreatic morphology with special reference to trypsinogen activation. Cholecystokinin-8 infusion was associated with increases in plasma amylase, lipase, trypsin-like immunoreactivity, and plasma and urine trypsinogen activation peptide. Pancreatic parenchymal swelling and interlobular and subcapsular fluid accumulations were detected ultrasonographically within 2 hr of cholecystokinin-8. Circulating trypsin-like immunoreactivity and trypsinogen activation peptide in urine reached a peak at 2 and 4 hr, respectively, then declined despite progressive increases in circulating amylase and lipase and intrapancreatic fluid. No significant changes were observed in dogs receiving a saline infusion. This study illustrates that cholecystokinin-8 induces edematous pancreatitis in dogs that is associated with a short-lived burst of trypsinogen activation.
为研究犬急性水肿性胰腺炎的早期发病机制，我们特别参照胰蛋白酶原激活情况，研究了胆囊收缩素-8（静脉注射，10微克/千克/小时，持续6小时）引起的胰腺过度刺激与循环胰腺酶及胰腺形态改变之间的关系。输注胆囊收缩素-8与血浆淀粉酶、脂肪酶、类胰蛋白酶免疫反应性以及血浆和尿液中胰蛋白酶原激活肽水平升高有关。在输注胆囊收缩素-8后2小时内，超声检查发现胰腺实质肿胀以及小叶间和包膜下积液。尿液中循环类胰蛋白酶免疫反应性和胰蛋白酶原激活肽分别在2小时和4小时达到峰值，随后尽管循环淀粉酶、脂肪酶以及胰腺内液体持续增加，但二者水平下降。接受生理盐水输注的犬未观察到明显变化。本研究表明，胆囊收缩素-8可诱发犬的水肿性胰腺炎，且这与胰蛋白酶原的短暂激活爆发有关。
