De Boer S Y, Masclee A A, Lam W F, Jansen J B, Lamers C B
Department of Gastroenterology, University Hospital Leiden, The Netherlands.
Dig Dis Sci. 1994 Feb;39(2):268-74. doi: 10.1007/BF02090196.
The present study was undertaken to investigate the effect of acute hyperglycemia on the gallbladder contraction induced by intravenous administration of high doses of amino acids (Vamin 18, 250 mg protein/kg/hr). Six healthy volunteers were studied in random order on two occasions during normoglycemia and hyperglycemia with blood glucose levels stabilized at 15 mmol/liter. Gallbladder volumes, measured with ultrasonography, were studied for 60 min before and for 120 min during intravenous infusion of amino acids (IVAA). Administration of IVAA resulted in a significant reduction (P < 0.05) in gallbladder volume from 32 +/- 5 cm3 to 17 +/- 2 cm3 during normoglycemia. During hyperglycemia no significant changes in gallbladder volume were observed in response to IVAA. No significant changes in plasma CCK concentration, the major hormonal stimulus for gallbladder contraction, occurred in response to IVAA. During hyperglycemia, pancreatic polypeptide (PP) secretion, as an indirect measure of vagal cholinergic tone, in response to IVAA was significantly (P < 0.05) reduced compared to normoglycemia. It is concluded that: (1) administration of high doses of IVAA results in significant gallbladder contraction, (2) high doses of IVAA do not stimulate CCK secretion, (3) acute hyperglycemia inhibits IVAA-induced gallbladder contraction, and (4) acute hyperglycemia inhibits basal and stimulated plasma PP secretion, suggesting impaired vagal-cholinergic tone during hyperglycemia.
本研究旨在探讨急性高血糖对静脉注射高剂量氨基酸(凡命18,250毫克蛋白质/千克/小时)诱导的胆囊收缩的影响。六名健康志愿者在血糖正常和高血糖状态下分两次随机接受研究,血糖水平稳定在15毫摩尔/升。在静脉输注氨基酸(IVAA)前60分钟和输注期间120分钟,用超声测量胆囊体积。在血糖正常时,静脉输注氨基酸导致胆囊体积从32±5立方厘米显著减少(P<0.05)至17±2立方厘米。在高血糖期间,静脉输注氨基酸后未观察到胆囊体积有显著变化。静脉输注氨基酸后,胆囊收缩的主要激素刺激物血浆CCK浓度未发生显著变化。在高血糖期间,作为迷走神经胆碱能张力间接指标的胰多肽(PP)分泌,与血糖正常时相比,对静脉输注氨基酸的反应显著降低(P<0.05)。研究得出以下结论:(1)静脉输注高剂量氨基酸导致胆囊显著收缩;(2)高剂量静脉输注氨基酸不刺激CCK分泌;(3)急性高血糖抑制静脉输注氨基酸诱导的胆囊收缩;(4)急性高血糖抑制基础和刺激状态下的血浆PP分泌,提示高血糖期间迷走神经胆碱能张力受损。