Eysselein V E, Böttcher W, Kauffman G L, Walsh J H
Regul Pept. 1984 Oct;9(3):173-85. doi: 10.1016/0167-0115(84)90070-3.
The release of molecular forms of cholecystokinin (CCK) into the portal and peripheral blood in response to an intraduodenal perfusion of sodium oleate (9 mmol X h-1) was studied in six conscious dogs with chronic portal vein catheters. Immunoreactive CCK as concentrated from 20 ml plasma by C18 SEP PAK cartridges and the pattern of molecular forms of CCK were studied by G50 gel filtration. CCK-like immunoreactivity (CCK-LI) was measured in the column eluates with antibody 5135, which measures gastrin and CCK equally and requires the intact carboxyl-terminus for full recognition. Gastrin was measured specifically with antibody 1611. Intraduodenal perfusion with oleate did not alter basal gastrin release. Release of CCK-LI by intraduodenal oleate was calculated by the increments of the integrated CCK-LI peaks over basal. Total CCK-like immunoreactivity (CCK-LI), calculated by integration of all CCK-LI peaks in gel filtration eluates, increased over basal by 12 fmol/ml in the portal and by 6 fmol/ml in the peripheral plasma after intraduodenal perfusion with sodium oleate. The main molecular forms eluted on gel filtration in positions of CCK33,39 and of CCK8. The pattern of CCK in the peripheral plasma was similar to that in the portal plasma except that in the peripheral plasma large molecular forms were more abundant than small forms. This finding was confirmed when CCK39 and CCK8 were infused either into the portal vein or into the peripheral vein and peripheral plasma CCK levels were measured. Elimination of CCK8 after portal vein infusion compared to peripheral vein infusion was about 3 times higher than that of CCK39. The abundance of large molecular forms of CCK in the circulating blood which are similar in potency to small forms, underlines their role in the physiology of CCK.
在6只植入慢性门静脉导管的清醒犬中，研究了十二指肠内灌注油酸钠（9 mmol·h⁻¹）后胆囊收缩素（CCK）分子形式释放至门静脉血和外周血中的情况。用C18 SEP PAK柱从20 ml血浆中浓缩免疫反应性CCK，并通过G50凝胶过滤研究CCK的分子形式模式。用抗体5135测定柱洗脱液中的CCK样免疫反应性（CCK-LI），该抗体对胃泌素和CCK的检测能力相同，且需要完整的羧基末端才能完全识别。用抗体1611特异性测定胃泌素。十二指肠内灌注油酸钠未改变基础胃泌素释放。十二指肠内油酸钠引起的CCK-LI释放通过CCK-LI积分峰相对于基础值的增加来计算。通过对凝胶过滤洗脱液中所有CCK-LI峰进行积分计算得到的总CCK样免疫反应性（CCK-LI），在十二指肠内灌注油酸钠后，门静脉血中比基础值增加了12 fmol/ml，外周血中增加了6 fmol/ml。凝胶过滤洗脱时，主要的分子形式在CCK33、39和CCK8的位置洗脱。外周血中CCK的模式与门静脉血中的相似，只是在外周血中大分子形式比小分子形式更丰富。当将CCK39和CCK8注入门静脉或外周静脉并测量外周血CCK水平时，这一发现得到了证实。与外周静脉注射相比，门静脉注射后CCK8的消除率比CCK39高约3倍。循环血液中与小分子形式效力相似的CCK大分子形式的丰富性，突出了它们在CCK生理学中的作用。
