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用具备胃瘘和胆瘘的豚鼠于人工维持胆汁酸池恒定的条件下,观察促胰液素(SEC)和胆囊收缩素(CCK)族激素[包括雨蛙肽(CAE)、五肽胃泌素(G5)和内源性CCK]对肝胆汁分泌的影响及其相互作用。结果表明:静脉灌注SEC、CAE或肠内灌注左旋苯丙氨酸(L-PHE,促内源性CCK释放剂)后,胆汁流量、胆汁HCO_3~-和Cl~-排出量均显著增多,并呈量-效关系,但静脉注射G5则无利胆效应。在恒速灌注SEC的背景下,CAE或CCK对胆汁HCO3_3~-排出的效应分别大于它们单独给予时的效应(P<0.05或P<0.01)。这些激素对胆汁酸的排出量均无影响。上述结果表明,SEC、CAE和内源性CCK均有利胆作用,所刺激的肝胆汁属于不依赖胆汁酸部分。G5无利胆效应。在胆汁中HCO_3~-的排出方面,SEC与CAE或内源性CCK共同作用时有相互加强作用。
Guinea pigs with gastric fistula and biliary fistula were treated with SEC and cholecystokinin (CCK) hormones including CAE, pentagastrin G5) and endogenous CCK] on hepatobiliary secretion and their interactions. The results showed that bile flow, bile HCO_3 ~ - and Cl ~ - evidently increased after intravenous injection of SEC, CAE or intestinal L-PHE (endogenous CCK releasing agent) The dose-response relationship, but intravenous injection of G5 no gallstone effect. In the context of constant perfusion of SEC, the effect of CAE or CCK on bile HCO3_3 - efflux was greater than that when they were administered alone (P <0.05 or P <0.01). These hormones had no effect on bile acid excretion. The above results indicate that both SEC, CAE and endogenous CCK have the cholera effect, and the stimulated liver bile belongs to the bile acid-independent fraction. G5 no gall bladder effect. In the excretion of HCO 3 - in bile, SEC interacts with CAE or endogenous CCK to reinforce each other.