Kalfarentzos F, Vagenas C, Michail A, Vasilakos P, Markoy S, Kordossis T, Androulakis J
Department of Surgery, School of Medicine, University of Patras, Greece.
Nutrition. 1991 Sep-Oct;7(5):347-9.
We examined the possible physiologic effects of intravenous (IV) amino acids (AAs) and long-chain triacylglycerols (LCTs) on gallbladder (GB) motility and release of cholecystokinin (CCK) on humans. GB contraction was studied in normal volunteers after administration of a fatty meal and IV infusion of AA and LCT. The GB contraction volume was calculated with ultrasound. Cholecystokinin-8 (CCK-8) and cholecystokinin-33/39 (CCK-33/39) were measured by radio-immunoassay. Administration of a fatty meal resulted in GB contraction by 60% of its basal volume and was accompanied by an increase in the serum levels of both CCK-8 and CCK-33/39. Administration of IV AA and LCT resulted in GB contraction by 17 and 37%, respectively, of its basal volume. The latter contractions were accompanied by increased levels of CCK-8 only. We conclude that IV administration of AA and LCT can result in human GB contraction and induce the release of only CCK-8. Continuous IV administration of AA and LCT for greater than 2h causes exhaustion of CCK-8 release, so that the GB returns to its initial volume.
我们研究了静脉输注氨基酸(AA)和长链三酰甘油(LCT)对人体胆囊(GB)运动及胆囊收缩素(CCK)释放可能产生的生理效应。在正常志愿者摄入脂肪餐以及静脉输注AA和LCT后,对GB收缩情况进行研究。通过超声计算GB收缩容积。采用放射免疫分析法测定胆囊收缩素-8(CCK-8)和胆囊收缩素-33/39(CCK-33/39)。摄入脂肪餐导致GB收缩至基础容积的60%,同时血清中CCK-8和CCK-33/39水平升高。静脉输注AA和LCT分别使GB收缩至基础容积的17%和37%。后一种收缩仅伴随CCK-8水平升高。我们得出结论,静脉输注AA和LCT可导致人体GB收缩且仅诱导CCK-8释放。持续静脉输注AA和LCT超过2小时会导致CCK-8释放耗竭,从而使GB恢复至初始容积。