de Jong A J, Klamer M, Jansen J B, Hopman W P, Lamers C B
Pancreas. 1987;2(3):339-43. doi: 10.1097/00006676-198705000-00014.
Since bombesin is a potent stimulus of the release of cholecystokinin (CCK), it has been suggested that the stimulatory effect of bombesin on pancreatic enzyme secretion is mediated by CCK. The present study was undertaken to determine the role of CCK in the bombesin-induced stimulation of plasma immunoreactive trypsin. Plasma CCK was measured by radioimmunoassay using the antibody T204, which binds to all biologically active sulfated COOH-terminal CCK-peptides. Plasma trypsin was also measured by radioimmunoassay. Infusion of 5 ng/kg/min bombesin in 6 healthy volunteers increased plasma CCK from 1.2 +/- 0.2-8.9 +/- 0.7 pM (p less than 0.0001). The peak increment in plasma CCK during bombesin (9.3 +/- 0.6 pM) was accompanied by a significant rise in plasma trypsin from 206 +/- 21-334 +/- 44 ng/ml (p less than 0.01). However, when similar increases in plasma CCK were achieved by infusion of 0.018 CU/kg/min CCK-33 (9.9 +/- 0.8 pM) or by intraduodenal instillation of 250 ml 20% Intralipid (9.7 +/- 1.9 pM), no significant changes in plasma trypsin were observed. It is therefore concluded that the stimulatory effect of bombesin on plasma immunoreactive trypsin is not mediated by CCK.
由于蛙皮素是胆囊收缩素(CCK)释放的有效刺激物,有人提出蛙皮素对胰腺酶分泌的刺激作用是由CCK介导的。本研究旨在确定CCK在蛙皮素诱导的血浆免疫反应性胰蛋白酶刺激中的作用。使用与所有具有生物活性的硫酸化COOH末端CCK肽结合的抗体T204,通过放射免疫测定法测量血浆CCK。血浆胰蛋白酶也通过放射免疫测定法测量。在6名健康志愿者中以5 ng/kg/分钟的速度输注蛙皮素,使血浆CCK从1.2±0.2 pM增加到8.9±0.7 pM(p<0.0001)。蛙皮素输注期间血浆CCK的峰值增加(9.3±0.6 pM)伴随着血浆胰蛋白酶从206±21 ng/ml显著升高至334±44 ng/ml(p<0.01)。然而,当通过以0.018 CU/kg/分钟的速度输注CCK-33(9.9±0.8 pM)或通过十二指肠内滴注250 ml 20%脂肪乳剂(9.7±1.9 pM)使血浆CCK达到类似增加时,未观察到血浆胰蛋白酶有显著变化。因此得出结论,蛙皮素对血浆免疫反应性胰蛋白酶的刺激作用不是由CCK介导的。