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Jan B.m.j. Jansen - One of the best experts on this subject based on the ideXlab platform.
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effect of circulating peptide yy on Gallbladder Motility in response to feeding in humans
Gastroenterology, 2001Co-Authors: Frank Hoentjen, Wim P.m. Hopman, Jan B.m.j. JansenAbstract:Background and aim. Peptide YY (PYY) is a gastrointestinal hormone which is localized in the distal small bowel, colon and rectum. It has been suggested that PYY plays an important role in the ileocolonic brake. The term ileocolonic brake refers to the phenomenon that the presence of unabsorbed nutrients in the distal gut induces slowing of gastric and pancreatic secretion and inhibits gastrointestinal Motility. Because the role of PYY in the regulation of postprandial Gallbladder Motility is relatively unknown, the effect of PYY on Gallbladder Motility in response to regular meal ingestion and during the cephalic phase of meal ~mulation was studied.In addition we have determined the effect of PYY on plasma cholecystoldnin (CCK) which is the principal mediator of the intestinal phase of Gallbladder contraction, and on plasma pancreatic polypeptide (PP) which is a gut peptide under strong vegat-chotinorgic control. Methods. After an overnight fast, Gallbladder volumes (ultrasonograpby) and plasma concentrations of CCK, PP and PYY were measured in response to modified sham feeding and to regular feeding during intravenous infusion of a physiological dose (30 pmol/kg.h) of PYY or during intravenous infusion of saline in eight healthy volunteers (3M, 5F; 19-24 yrs). Studies were performed in a randomized crossover design on two separate days. Results. PYY significantly reduced Gallbladder emptying in response to modified sham feeding from 410_+106 mL.90 min to -28_+99mL.90 min (P
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Effect of circulating peptide YY on Gallbladder Motility in response to feeding in humans
Gastroenterology, 2001Co-Authors: Frank Hoentjen, Wim P.m. Hopman, Jan B.m.j. JansenAbstract:Background and aim. Peptide YY (PYY) is a gastrointestinal hormone which is localized in the distal small bowel, colon and rectum. It has been suggested that PYY plays an important role in the ileocolonic brake. The term ileocolonic brake refers to the phenomenon that the presence of unabsorbed nutrients in the distal gut induces slowing of gastric and pancreatic secretion and inhibits gastrointestinal Motility. Because the role of PYY in the regulation of postprandial Gallbladder Motility is relatively unknown, the effect of PYY on Gallbladder Motility in response to regular meal ingestion and during the cephalic phase of meal ~mulation was studied.In addition we have determined the effect of PYY on plasma cholecystoldnin (CCK) which is the principal mediator of the intestinal phase of Gallbladder contraction, and on plasma pancreatic polypeptide (PP) which is a gut peptide under strong vegat-chotinorgic control. Methods. After an overnight fast, Gallbladder volumes (ultrasonograpby) and plasma concentrations of CCK, PP and PYY were measured in response to modified sham feeding and to regular feeding during intravenous infusion of a physiological dose (30 pmol/kg.h) of PYY or during intravenous infusion of saline in eight healthy volunteers (3M, 5F; 19-24 yrs). Studies were performed in a randomized crossover design on two separate days. Results. PYY significantly reduced Gallbladder emptying in response to modified sham feeding from 410_+106 mL.90 min to -28_+99mL.90 min (P
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Effect of cisapride on Gallbladder Motility after extracorporeal lithotripsy shock-wave
1995Co-Authors: Reto Brignoli, Florian Froehlich, Jan B.m.j. Jansen, Gian Dorta, André L. Blum, M. FriedAbstract:Backgrounrt/Aims: Altered Gallbladder Motility is regarded as one of the important factors involved in the formation and recurrence of gallstones. Previous studies have suggested that cisapride increases postprandial Gallbladder contraction and may therefore be theoretically useful in preventing stone recurrence. The aim of our study was therefore to investigate the effect of cisapride on Gallbladder Motility in stonefree patients after extracorporeal shock-wave lithotripsy, as compared to healthy volunteers pairmatched for age and sex. Methods: Each subject received cisapride or placebo in a double-blind, cross-over, random order. Gallbladder volumes were measured by ultrasonography in the fasting state and after intake of a standard liquid meal. Plasma cholecystokinin levels were determined by radioimmunoassay. Results: Fasting Gallbladder volumes were smaller in patients as compared to volunteers (20.721.3 ml vs. 46.029.2 ml; ~~0.05) but were not modified by cisapride (21.121.7 ml vs. X6+11.3 ml). The maximal postprandial decrease in Gallbladder volume was simi
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Effect of cisapride on Gallbladder Motility after extracorporeal shock-wave lithotripsy.
Journal of hepatology, 1995Co-Authors: Joël Thorens, Reto Brignoli, Florian Froehlich, Jan B.m.j. Jansen, Gian Dorta, André L. Blum, Jean F. Schnegg, M. FriedAbstract:Abstract Background/Aims: Altered Gallbladder Motility is regarded as one of the important factors involved in the formation and recurrence of gallstones. Previous studies have suggested that cisapride increases post-prandial Gallbladder contraction and may therefore be theoretically useful in preventing stone recurrence. The aim of our study was therefore to investigate the effect of cisapride on Gallbladder Motility in stone-free patients after extracorporeal shock-wave lithotripsy, as compared to healthy volunteers pair-matched for age and sex. Methods: Each subject received cisapride or placebo in a double-blind, cross-over, random order. Gallbladder volumes were measured by ultrasomography in the fasting state and after intake of a standard liquid meal. Plasma cholecystokinin levels were determined by radioimmunoassay. Results: Fasting Gallbladder volumes were smaller in patients as compared to volunteers (20.7±1.3 ml vs. 46.0±9.2 ml; p p p Conclusions: The results of this study suggest that cisapride does not alter postprandial Gallbladder contraction but accelerates Gallbladder refilling in patients free from gallstones after extracorporeal shock-wave lithotripsy. This effect of cisapride is probably due to an acceleration of gastric emptying also causing a secondary enhanced cholecystokinin release.
Susanne Holmgren - One of the best experts on this subject based on the ideXlab platform.
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Intraduodenal Fat and Amino Acids Activate Gallbladder Motility in the Rainbow Trout, Oncorhynchus mykiss
General and comparative endocrinology, 1995Co-Authors: Göran Aldman, Susanne HolmgrenAbstract:Abstract The effects on gall bladder Motility of intraduodenal injections of fat (cod liver oil) and amino acids were investigated in rainbow trout, Onchorhynchus mykiss, in vivo. Fat (1 ml/kg. 15 min) increased basic tonus of the Gallbladder by 79% and frequency of contractions by 53%; both effects were antagonized by pretreatment with atropine (1.2 mg/kg). The amino acid mixture similarly increased tonus and frequency of contractions of the Gallbladder smooth muscle by 63 and 109%, respectively. The effects were mimicked by intraarterial infusion of cholecystokinin (100 pmol-1 nmol/kg-hr). It is concluded that the presence of oil and amino acids in the duodenum stimulates rainbow trout Gallbladder Motility and tension, possibly by a release of cholecystokinin, and that the effect of oil, as for cholecystokinin, involves a cholinergic pathway.
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Duodenal acidification and intra-arterial injection of CCK8 increase Gallbladder Motility in the rainbow trout, Oncorhynchus mykiss.
General and comparative endocrinology, 1992Co-Authors: G. Aldman, D. Grove, Susanne HolmgrenAbstract:A sensitive method for in vivo measurement of intra-Gallbladder pressure in free swimming rainbow trout (Oncorhynchus mykiss) is described. The method gives information on changes in Gallbladder pressure after either instillation of liquids into the duodenum or infusion/injection of agents into the circulatory system. Blood samples can also be taken. Duodenal acidification is a potent initiating factor for Gallbladder Motility in the rainbow trout. Intra-arterially injected sulfated octapeptide of cholecystokinin is also a potent excitatory agent for activating the Gallbladder. Acidification of the upper intestine causes release of cholecystokinin, which affects Gallbladder Motility in trout as in mammals.
M. Fried - One of the best experts on this subject based on the ideXlab platform.
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Effect of cisapride on Gallbladder Motility after extracorporeal lithotripsy shock-wave
1995Co-Authors: Reto Brignoli, Florian Froehlich, Jan B.m.j. Jansen, Gian Dorta, André L. Blum, M. FriedAbstract:Backgrounrt/Aims: Altered Gallbladder Motility is regarded as one of the important factors involved in the formation and recurrence of gallstones. Previous studies have suggested that cisapride increases postprandial Gallbladder contraction and may therefore be theoretically useful in preventing stone recurrence. The aim of our study was therefore to investigate the effect of cisapride on Gallbladder Motility in stonefree patients after extracorporeal shock-wave lithotripsy, as compared to healthy volunteers pairmatched for age and sex. Methods: Each subject received cisapride or placebo in a double-blind, cross-over, random order. Gallbladder volumes were measured by ultrasonography in the fasting state and after intake of a standard liquid meal. Plasma cholecystokinin levels were determined by radioimmunoassay. Results: Fasting Gallbladder volumes were smaller in patients as compared to volunteers (20.721.3 ml vs. 46.029.2 ml; ~~0.05) but were not modified by cisapride (21.121.7 ml vs. X6+11.3 ml). The maximal postprandial decrease in Gallbladder volume was simi
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Effect of cisapride on Gallbladder Motility after extracorporeal shock-wave lithotripsy.
Journal of hepatology, 1995Co-Authors: Joël Thorens, Reto Brignoli, Florian Froehlich, Jan B.m.j. Jansen, Gian Dorta, André L. Blum, Jean F. Schnegg, M. FriedAbstract:Abstract Background/Aims: Altered Gallbladder Motility is regarded as one of the important factors involved in the formation and recurrence of gallstones. Previous studies have suggested that cisapride increases post-prandial Gallbladder contraction and may therefore be theoretically useful in preventing stone recurrence. The aim of our study was therefore to investigate the effect of cisapride on Gallbladder Motility in stone-free patients after extracorporeal shock-wave lithotripsy, as compared to healthy volunteers pair-matched for age and sex. Methods: Each subject received cisapride or placebo in a double-blind, cross-over, random order. Gallbladder volumes were measured by ultrasomography in the fasting state and after intake of a standard liquid meal. Plasma cholecystokinin levels were determined by radioimmunoassay. Results: Fasting Gallbladder volumes were smaller in patients as compared to volunteers (20.7±1.3 ml vs. 46.0±9.2 ml; p p p Conclusions: The results of this study suggest that cisapride does not alter postprandial Gallbladder contraction but accelerates Gallbladder refilling in patients free from gallstones after extracorporeal shock-wave lithotripsy. This effect of cisapride is probably due to an acceleration of gastric emptying also causing a secondary enhanced cholecystokinin release.
Jing Zhang Liu - One of the best experts on this subject based on the ideXlab platform.
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Nucleus raphe obscurus participates in regulation of Gallbladder Motility through vagus and sympathetic nerves in rabbits
2015Co-Authors: Yu-feng Xie, Chuanyong Liu, Jing Zhang LiuAbstract:The aim of the present study is to investigate if the nucleus raphe obscurus (NRO) participate in regulating the Gallbladder Motility in rabbits. Rabbits were fasted for about 20-24 hours. After anesthetization with urethane, an incision was made at the middle of the abdomen and the Gallbladder was exposed. A frog bladder connected with force transducer was inserted into the Gallbladder through a small incision at the funds to record Gallbladder Motility (tonic contraction and phasic contraction). Glutamate and other chemicals were microinjected into NRO through a vitreous tube attached to a microsyringe. We found both the tonic contraction and phasic contraction of the Gallbladder were enhanced after the glutamate was injected into NRO. GABA inhibited Gallbladder Motility if administrated in the same way. Microinjection of ketamine, NMDA (N-methyl-D-aspartate) receptor antagonist, into NRO inhibited the phasic contraction of Gallbladder. Administration of CNQX (6-cyano-7-nitroquinoxaline-2, 3-dione), a non-NMDA receptor antagonist, enhanced the Gallbladder tonic contraction. Pretreatment of ketamine into NRO attenuated the effect of glutamate, while pretreatment of CQNX had no effect on it. Intravenous injection of atropine or vagotomy completely abolished the effect of glutamate on Gallbladder phasic contraction, while intravenous injection of phentolamine o
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Oxytocin microinjected into dorsal motor nucleus of the vagus excites Gallbladder Motility via NMDA receptor-NO-cGMP pathway.
Brain research, 2005Co-Authors: Chuanyong Liu, Dong-ping Xie, Ke Jing Liu, Yu Qin Zhou, Jing Zhang LiuAbstract:Our recent study indicated that, in the dorsal motor nucleus of the vagus (DMV), the N-methyl-D-aspartic acid (NMDA) receptor-nitric oxide (NO)-cGMP pathway participated in the regulation of Gallbladder Motility in rabbits. Oxytocin (OT) is involved as a neurotransmitter in autonomic regulation. The aim of the present experiments is to investigate the effect of OT microinjected into DMV on the Gallbladder Motility and the involvement of NMDA receptor-NO-cGMP pathway. A frog bladder connected with transducer was inserted into the Gallbladder to record the Gallbladder pressure. Microinjection of OT (10-50 nmol/L, 100 nl) dose dependently increased the strength of Gallbladder phasic contraction. The excitatory effect of OT (10 nmol/L, 100 nl) was completely abolished by atosiban (10 mmol/L, 100 nl), the specific OT receptor antagonist, but was not influenced by [deamino-Pen(1), O-Me-Tyr(2),Arg(8)]-vasopressin (10 mmol/L, 100 nl), the V(1) receptor antagonist. Pretreatment of ketamine (10 mmol/L, 100 nl), the NMDA receptor antagonist, suppressed the Gallbladder motor response to OT; but pretreatment of 6-Cyaon-7-Nitroquinoxaline-2,3-(1H,4H)-Dione (CNQX; 10 mmol/L, 100 nl), the non-NMDA receptor antagonist, did not affect it. Pretreatment of L-NAME (10 mmol/L, 100 nl), the nitric oxide synthase (NOS) inhibitor, or methyl blue (10 mmol/L, 100 nl), the guanylyl cyclase inhibitor, inhibited the excitatory effect of OT on Gallbladder Motility. Hence, we deduced that the microinjection of OT into the DMV enhanced the Gallbladder Motility through binding specific OT receptors and activating the NMDA receptor-NO-cGMP pathway.
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Research report Oxytocin microinjected into dorsal motor nucleus of the vagus excites Gallbladder Motility via NMDA receptor-NO-cGMP pathway
2005Co-Authors: Chuanyong Liu, Dong-ping Xie, Ke Jing Liu, Yu Qin Zhou, Jing Zhang LiuAbstract:Our recent study indicated that, in the dorsal motor nucleus of the vagus (DMV), the N-methyl-d-aspartic acid (NMDA) receptor–nitric oxide (NO)–cGMP pathway participated in the regulation of Gallbladder Motility in rabbits. Oxytocin (OT) is involved as a neurotransmitter in autonomic regulation. The aim of the present experiments is to investigate the effect of OT microinjected into DMVon the Gallbladder Motility and the involvement of NMDA receptor–NO–cGMP pathway. A frog bladder connected with transducer was inserted into the Gallbladder to record the Gallbladder pressure. Microinjection of OT (10–50 nmol/L, 100 nl) dose dependently increased the strength of Gallbladder phasic contraction. The excitatory effect of OT (10 nmol/L, 100 nl) was completely abolished by atosiban (10 mmol/L, 100 nl), the specific OT receptor antagonist, but was not influenced by [deamino-Pen 1 , O-Me-Tyr 2 ,Arg 8 ]-vasopressin (10 mmol/L, 100 nl), the V1 receptor antagonist. Pretreatment of ketamine (10 mmol/L, 100 nl), the NMDA receptor antagonist, suppressed the Gallbladder motor response to OT; but pretreatment of 6-Cyaon-7-Nitroquinoxaline-2,3-(1H,4H)-Dione (CNQX; 10 mmol/L, 100 nl), the non-NMDA receptor antagonist, did not affect it. Pretreatment of l-NAME (10 mmol/L, 100 nl), the nitric oxide synthase (NOS) inhibitor, or methyl blue (10 mmol/L, 100 nl), the guanylyl cyclase inhibitor, inhibited the excitatory effect of OTon Gallbladder Motility. Hence, we deduced that the microinjection of OT into the DMVenhanced the Gallbladder Motility through binding specific OT receptors and activating the NMDA receptor–NO–cGMP pathway. D 2004 Elsevier B.V. All rights reserved. Theme: Neurotransmitters, modulators, transporters, and receptors Topic: Interactions between neurotransmitters
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microinjection of glutamate into dorsal motor nucleus of the vagus excites Gallbladder Motility through nmda receptor nitric oxide cgmp pathway
Neurogastroenterology and Motility, 2004Co-Authors: C. Y. Liu, Dong-ping Xie, Jing Zhang LiuAbstract:We have reported that both glutamate and nitric oxide (NO) participated in the regulation of Gallbladder Motility in dorsal motor nucleus of the vagus (DMV). The aim of this study is to investigate the type of receptor in DMV that mediates the excitatory effect of glutamate on Gallbladder Motility and the correlation between the glutamate and NO. A frog bladder connected with a force transducer was inserted into the Gallbladder to record the change of Gallbladder pressure. Glutamate (65 mmol L(-1), 100 nL) microinjected into DMV significantly increased the strength of Gallbladder phasic contraction. This effect was abolished by ketamine (180 mmol L(-1), 100 nL), the specific N-methyl-d-aspartic acid (NMDA) receptor antagonist, but was not influenced by 6-cyaon-7-nitroquinoxaline-2,3-(1H,4H)-dione (CNQX) (180 mmol L(-1), 100 nL), the non-NMDA ionotropic receptor antagonist. N(G)-nitro-l-arginine-emthyl (l-NAME) (1 mol L(-1), 100 nL), the nitric oxide synthase (NOS) inhibitor, reversed the excitatory effect of glutamate on Gallbladder Motility. Microinjection of sodium nitroprusside (SNP), the NO donor, into DMV enhanced the Gallbladder Motility, and this effect was not modulated by ketamine. Microinjection of NMDA (5 mmol L(-1), 100 nL) increased the strength of Gallbladder phasic contraction, and this effect was attenuated by methylene blue (100 mmol L(-1), 100 nL), the soluble guanylate cyclase inhibitor. These results suggest that glutamate regulate the Gallbladder Motility through the NMDA receptor - NO - cGMP pathway in DMV.
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Participation of caudal ventrolateral medulla in the regulation of Gallbladder Motility in rabbits.
The Chinese journal of physiology, 2004Co-Authors: Feng-yu Liu, Chuanyong Liu, Jing Zhang Liu, Dong-ping XieAbstract:To investigate whether the caudal ventrolateral medulla (CVLM) participates in the regulation of Gallbladder Motility, we studied the effects of microinjection of L-glutamate and other agents into the CVLM on Gallbladder pressure (GP) in anesthetized rabbits. A frog bladder connected with a force transducer was inserted into the Gallbladder to record the change of GP. Microinjection of L-glutamate into the CVLM decreased GP, While micnoinjection of γ-amino-butyric acid (GABA) increased GP. Microinjection of ketamine, a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, into CVLM increased GP, while microinjection of 6-cyano-7-nitroquinoxaline-2, 3-(1H, 4H)-dione (CNQX), a competitive (±)-a-amino-3-hydroxy-5- methylisoxazole-4-propionic acid (AMPA)/kainate receptor antagonist, had no significant effect on GP. The effects of L-glutamate was abolished by ketainine, but not by CNQX. Intravenous injection of phentolamine or transection of the spinal cord eliminated the effects of L-glutamate on GP. These results indicate that [1] CVLM participated in the regulation of Gallbladder Motility; [2] endogenous L-glutamate in CVLM is involved in the regulation mediated by NMDA receptors, the output of which is sent through sympathetic nerve and x-adrenergic receptors.
Cornelis B.h.w. Lamers - One of the best experts on this subject based on the ideXlab platform.
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Effect of intragastric or intraduodenal administration of a polymeric diet on Gallbladder Motility, small-bowel transit time, and hormone release
The American journal of gastroenterology, 1998Co-Authors: M. Ledeboer, Izak Biemond, Ad A.m. Masclee, Cornelis B.h.w. LamersAbstract:Effect of intragastric or intraduodenal administration of a polymeric diet on Gallbladder Motility, small-bowel transit time, and hormone release
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Effect of insulin on basal and cholecystokinin-stimulated Gallbladder Motility in humans
Journal of hepatology, 1998Co-Authors: H. A. J. Gielkens, Cornelis B.h.w. Lamers, W. F. Lam, Minneke J. Coenraad, Marijke Frölich, Jacques A. Van Oostayen, Ad A.m. MascleeAbstract:Abstract Background/Aims: Acute hyperglycemia inhibits Gallbladder contraction. In non-diabetic subjects this inhibitory effect may result from endogenous hyperinsulinemia. Therefore we investigated the effects of acute hyperglycemia and euglycemic hyperinsulinemia on basal and cholecystokinin-stimulated Gallbladder Motility. Methods: Gallbladder volume (ultrasonography) and duodenal bilirubin output were studied simultaneously in nine healthy volunteers (age 20–52 years) on 3 separate occasions in random order during: (a) saline infusion (control), (b) hyperglycemic hyperinsulinemic clamping (HG; plasma glucose at 15 mmol/l), and (c) euglycemic hyperinsulinemic clamping (HI; plasma insulin at 150 mU/l, glucose at 4–5 mmol/l). After a 2-h basal clamp period, cholecystokinin was infused intravenously for 60 min at 0.25 IDU · kg −1 · h −1 , followed by another 60 min at 0.5 IDU · kg −1 · h −1 . Results: HI and HG significantly ( p p p p Conclusions: In healthy subjects acute hyperglycemia and euglycemic hyperinsulinemia reduce basal duodenal bilirubin output and inhibit Gallbladder emptying stimulated by low dose cholecystokinin. These results suggest that insulin is involved in the inhibitory effect of hyperglycemia on basal and cholecystokinin-stimulted Gallbladder Motility.
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Gallbladder Motility and cholecystokinin secretion during continuous enteral nutrition.
The American journal of gastroenterology, 1997Co-Authors: M. Ledeboer, A.a.m. Masclee, Izak Biemond, Cornelis B.h.w. LamersAbstract:OBJECTIVES During total parenteral nutrition, Gallbladder Motility is impaired, resulting in sludge and stone formation. Little is known about Gallbladder Motility during prolonged enteral nutrition. METHODS We studied Gallbladder Motility during continuous enteral nutrition (CEN) in nine hospitalized patients with active inflammatory bowel disease. The patients received a polymeric diet (2000 kcal/24 h) by CEN through a nasogastric tube for a prolonged period. Gallbladder volumes were obtained daily by ultrasonography, starting from day 0 (before CEN) and on 7 consecutive days during CEN. At days 0, 1, 4, and 7, the Gallbladder response to i.v. cholecystokinin (CCK-33; 0.5 Ivy Dog unit/kg/h) was studied. Plasma CCK levels were determined at regular intervals by radioimmunoassay. RESULTS No significant differences were observed on day 0 between patients and a group of nine healthy control subjects in fasting Gallbladder volumes (19.4 +/- 2.3 and 19.6 +/- 2.4 cm3, respectively) and Gallbladder contraction during CCK infusion (56 +/- 14% and 69 +/- 7%, respectively). During CEN, from day 1 to day 7, mean Gallbladder volume remained significantly (p < 0.05) reduced compared with fasting Gallbladder volume, and mean plasma CCK levels remained significantly (p < 0.05) increased compared with fasting levels. Although Gallbladder volume was significantly reduced during CEN, the Gallbladder contractile response to CCK was not affected; at days 1, 4, and 7, Gallbladder contraction was 36-57%. CONCLUSIONS During CEN, 1) Gallbladder volume is significantly reduced and plasma CCK levels are significantly increased, 2) these effects are sustained over time (7 days), and 3) the Gallbladder remains responsive to exogenous CCK. These results indicate that Gallbladder contractility and Gallbladder responsiveness to CCK are preserved during prolonged CEN in patients with inflammatory bowel disease.
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Gallbladder Motility and cholecystokinin secretion in chronic pancreatitis: relationship with exocrine pancreatic function
Journal of hepatology, 1997Co-Authors: H. A. J. Gielkens, Cornelis B.h.w. Lamers, Eric-hans Eddes, Juda Vecht, Jaques A. Van Oostayen, Ad A.m. MascleeAbstract:Abstract Background/Aims: Postprandial Gallbladder Motility is regulated mainly by the hormone cholecystokinin (CCK). Since CCK secretion may be reduced in patients with pancreatic insufficiency (PI), we studied postprandial Gallbladder Motility in these patients. Methods: Fifteen patients with PI due to chronic pancreatitis and 17 healthy control subjects were studied. Gallbladder volumes (ultrasonography) and plasma CCK concentrations (RIA) were determined at regular intervals for 120 min after meal ingestion. Urinary PABA and faecal fat excretion were measured to determine pancreatic exocrine function. Results: Patients with PI had larger fasting Gallbladder volumes than controls (48±6 cm 3 versus 29±2 cm 3 ; p 3 ) and controls (20±2 cm 3 ). However, the percentage postprandial Gallbladder emptying in patients with PI was significantly reduced compared to controls (at 120 min; 29±8% versus 68±3%; p 3 versus 9±1 cm 3 ; p p r =0.81; p Conclusions: In patients with pancreatic insufficiency due to chronic pancreatitis: 1) fasting and residual postprandial Gallbladder volumes are significantly increased; 2) postprandial CCK secretion and percentage Gallbladder contraction are significantly reduced; 3) percentage postprandial Gallbladder emptying is related to the degree of pancreatic exocrine insufficiency.
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Effect of intravenous fat on cholecystokinin secretion and Gallbladder Motility in man.
JPEN. Journal of parenteral and enteral nutrition, 1992Co-Authors: S. Y. De Boer, A.a.m. Masclee, J. Schipper, J. B. M. J. Jansen, M. C. W. Jebbink, Cornelis B.h.w. LamersAbstract:During total parenteral nutrition (TPN) Gallbladder bile stasis and hypoMotility have been well documented. Little is known, however, about the effect of the separate components of TPN on Gallbladder motor function. Inasmuch as fat, administered intraduodenally, is a potent stimulus of cholecystokinin (CCK) secretion and Gallbladder contraction we have investigated whether intravenous (IV) fat affects Gallbladder Motility. Six healthy volunteers were studied on two separate occasions, during infusion of Intralipid 10%, 200 mL/h or saline infusion (control) for 3 hours, to evaluate the effect of IV infusion of fat on (1) plasma CCK concentration and Gallbladder volume and (2) CCK-induced Gallbladder emptying. Intravenous infusion of Intralipid resulted in significant increases in serum triglycerides from 0.9 ± 0.1 to 5.1 ± 1.3 mmol/L (at 90 min). During fat infusion no significant changes in plasma CCK and Gallbladder volume were noted when compared with basal values or to the control experiment. During IV...
