Hopman W P, Jansen J B, Rosenbusch G, Lamers C B
Department of Gastroenterology, University Hospital Nijmegen, The Netherlands.
Hepatology. 1990 Feb;11(2):261-5. doi: 10.1002/hep.1840110216.
To determine the role of cholecystokinin and the cholinergic system in intestinal stimulation of gallbladder contraction, we studied the effects of atropine on plasma cholecystokinin and gallbladder contraction in six healthy volunteers (four men and two women aged 20 to 27 yr). Effects were noted after intraduodenal fat instillation and after dosage with exogenous cholecystokinin inducing plasma cholecystokinin concentrations similar to those after intraduodenal fat instillation. At regular intervals before and after administration of each stimulus, plasma cholecystokinin concentrations and gallbladder volumes were measured by radioimmunoassay and real-time ultrasonography, respectively. Intraduodenal infusion of 250 ml 20% Intralipid induced a peak plasma cholecystokinin increment of 10.2 +/- 1.6 pmol/L compared with 10.7 +/- 0.7 pmol/L during infusion of 1 Ivy dog unit per kilogram per hour of cholecystokinin. The increases in plasma cholecystokinin after fat and exogenous cholecystokinin administration were accompanied by similar decreases in gallbladder volume. Integrated gallbladder contraction after fat instillation was 3,939% +/- 288%.min compared with 3,301% +/- 359%.min during cholecystokinin infusion (NS). Atropine (0.015 mg/kg as bolus followed by 0.005 mg/kg/hr) did not change plasma cholecystokinin concentrations but induced similar inhibition of gallbladder contraction to 2,296% +/- 511%.min (p less than 0.05) after intraduodenal fat instillation and to 1,756% +/- 456%.min (p less than 0.05) during cholecystokinin infusion. We conclude that cholecystokinin is of major importance in intestinal stimulation of gallbladder contraction. Atropine inhibits the gallbladder response to intraduodenal fat. This inhibition is not due to a reduction in cholecystokinin secretion but to a diminished gallbladder response to cholecystokinin.
为确定胆囊收缩素和胆碱能系统在肠道刺激胆囊收缩中的作用,我们研究了阿托品对6名健康志愿者(4名男性和2名女性,年龄20至27岁)血浆胆囊收缩素和胆囊收缩的影响。在十二指肠内注入脂肪后以及给予外源性胆囊收缩素使血浆胆囊收缩素浓度达到与十二指肠内注入脂肪后相似水平后,观察了相关效应。在每次刺激给药前后的固定时间间隔,分别通过放射免疫测定法和实时超声检查来测量血浆胆囊收缩素浓度和胆囊体积。十二指肠内输注250 ml 20%英脱利匹特(Intralipid)导致血浆胆囊收缩素峰值增加10.2±1.6 pmol/L,而每小时每千克输注1个艾维氏(Ivy)犬单位胆囊收缩素时,该峰值增加为10.7±0.7 pmol/L。给予脂肪和外源性胆囊收缩素后血浆胆囊收缩素的增加伴随着胆囊体积的类似减小。注入脂肪后胆囊的整体收缩为3939%±288%.min,而输注胆囊收缩素期间为3301%±359%.min(无显著性差异)。阿托品(0.015 mg/kg静脉推注,随后0.005 mg/kg/hr)并未改变血浆胆囊收缩素浓度,但在十二指肠内注入脂肪后对胆囊收缩产生了类似的抑制作用,抑制率为2296%±511%.min(p<0.05),在输注胆囊收缩素期间抑制率为1756%±456%.min(p<0.05)。我们得出结论,胆囊收缩素在肠道刺激胆囊收缩中起主要作用。阿托品抑制胆囊对十二指肠内脂肪的反应。这种抑制并非由于胆囊收缩素分泌减少,而是由于胆囊对胆囊收缩素的反应减弱。