Comparison of hepatic elimination of different forms of cholecystokinin in dogs. Bioassay and radioimmunoassay comparisons of cholecystokinin-8-sulfate and -33-sulfate.
Comparison of hepatic elimination of different forms of cholecystokinin in dogs. Bioassay and radioimmunoassay comparisons of cholecystokinin-8-sulfate and -33-sulfate.
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狗不同形式胆囊收缩素的肝脏消除比较。
DOI：
10.1172/jci111686
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Thompson,JC
中科院分区：
文献类型：
--
作者：
Sakamoto,T;Fujimura,M;Newman,J;Zhu,XG;GreeleyJr,GH;Thompson,JC
在5只有胰瘘和胆囊瘘的清醒狗和完全性门腔静脉转位的狗中，评价了肝转运对外源性胆囊收缩素-8-硫酸盐和-33-硫酸盐（分别为CCK-8和CCK-33）刺激胆囊收缩和胰腺外分泌的能力，以及对每种药物外周血浆浓度的影响。门静脉注射CCK-8（0.125、0.25、0.50和1.0 μ g/kg/h，持续5 min）后，胆囊压力增量分别比全身注射相同剂量CCK-8时降低36%、45%、39%和25%（P <0.05）。在随后的实验中，与CCK-8全身给药的结果相比，CCK-8（0.10 μ g/kg/h）30分钟输注门静脉系统期间，综合胰液体积、碳酸氢盐和蛋白质分泌分别减少了22%、32%和48%（P <0.05）。与此相反，胆囊压力和胰腺外分泌反应门静脉注射CCK-33没有显着差异（P> 0.05）与CCK-33全身给药的结果。血浆CCK-8放射免疫测定结果表明，门静脉给药时CCK-8积分值显著低于全身给药时（P <0.05）。然而，CCK-33的结果没有变化，无论是通过全身还是门静脉途径给药（P> 0.05）。因此，本研究表明，CCK-8是部分失活的肝脏，而CCK-33不是，这表明CCK-3在循环中可能发挥重要作用，在生理调节胆囊和胰腺外分泌。
The influence of hepatic transit on the ability of exogenous cholecystokinin-8-sulfate and -33-sulfate (CCK-8 and CCK-33, respectively) to stimulate gallbladder contraction and exocrine pancreatic secretion, as well as on the peripheral plasma concentration of each agent, was evaluated in five conscious dogs with pancreatic and gallbladder fistulas and complete portacaval transposition. The gallbladder pressure increments after portal administration of CCK-8 (0.125, 0.25, 0.50, and 1.0 microgram/kg per h for 5 min) were diminished by 36, 45, 39 and 25%, respectively, in comparison with those obtained with systemic administration of identical doses of CCK-8 (P less than 0.05). In a subsequent experiment, the integrated pancreatic juice volume, bicarbonate, and protein secretion were diminished by 22, 32, and 48%, respectively, during a 30-min infusion of CCK-8 (0.10 micrograms/kg per h) into the portal venous system, in comparison with the results obtained with systemic administration of CCK-8 (P less than 0.05). In contrast, the gallbladder pressure and pancreatic exocrine secretory responses to portal administration of CCK-33 did not differ significantly (P greater than 0.05) from the results obtained with systemic administration of CCK-33. Radioimmunoassay for CCK-8 in plasma showed that the integrated CCK-8 value during portal administration was significantly lower (P less than 0.05) than it was during systemic administration. The results for CCK-33, however, did not vary, whether it was given by a systemic or portal route (P greater than 0.05). Thus, the present study demonstrates that CCK-8 is partially inactivated by the liver whereas CCK-33 is not, which suggests that CCK-3 in the circulation may play a significant role in the physiologic regulation of the gallbladder and exocrine pancreas.