Toriumi Y, Samuel I, Wilcockson D P, Turkelson C M, Solomon T E, Joehl R J
Surgical and Research Services, Veterans Affairs Lakeside Medical Center, Chicago, IL 60611.
J Lab Clin Med. 1993 Oct;122(4):450-4.
Obstruction-induced acute pancreatitis in rats is associated with increased plasma cholecystokinin (CCK) levels. Duodenal replacement of bile reduces severity of pancreatitis and limits CCK increase. We investigated the role of CCK in the pathogenesis of obstruction-induced acute pancreatitis by pretreating rats with the somatostatin analog octreotide and the CCK antagonist L-364,718. Octreotide inhibits duodenal CCK release, and L-364,718 competitively blocks CCK receptors. We studied 31 rats after (1) sham operation (n = 7), (2) bile and pancreatic duct obstruction (BPDO) (n = 12), (3) BPDO plus octreotide (20 micrograms/kg IP and then 5 micrograms/kg/hr IV) (n = 6), and (4) BPDO plus L-364,718 (1 mg/kg IP and then 0.25 mg/kg/hr IV) (n = 6). Rats were killed after 18 hours. Pancreas weight, acute pancreatitis histology score, and plasma amylase and CCK levels were determined. Octreotide and L-364,718 limited the increase in pancreas weight. Octreotide also limited the rise in plasma CCK levels. These findings suggest that CCK may play a role in the pathogenesis of obstruction-induced acute pancreatitis.
大鼠梗阻性急性胰腺炎与血浆胆囊收缩素（CCK）水平升高有关。十二指肠胆汁替代可减轻胰腺炎的严重程度并限制CCK升高。我们通过用生长抑素类似物奥曲肽和CCK拮抗剂L-364,718预处理大鼠，研究了CCK在梗阻性急性胰腺炎发病机制中的作用。奥曲肽抑制十二指肠CCK释放，而L-364,718竞争性阻断CCK受体。我们研究了31只大鼠，分别进行（1）假手术（n = 7），（2）胆管和胰管梗阻（BPDO）（n = 12），（3）BPDO加奥曲肽（20微克/千克腹腔注射，然后5微克/千克/小时静脉注射）（n = 6），以及（4）BPDO加L-364,718（1毫克/千克腹腔注射，然后0.25毫克/千克/小时静脉注射）（n = 6）。18小时后处死大鼠。测定胰腺重量、急性胰腺炎组织学评分以及血浆淀粉酶和CCK水平。奥曲肽和L-364,718限制了胰腺重量的增加。奥曲肽还限制了血浆CCK水平的升高。这些发现表明CCK可能在梗阻性急性胰腺炎的发病机制中起作用。
