Cholecystokinin and gallbladder contraction: Effect of CCK infusion

Byrnes, D. J.; Borody, Thomas J.; Daskalopoulos, George; Boyle, M; Benn, I

doi:10.1016/0196-9781(81)90041-3

Cited by 51 publications

(14 citation statements)

References 8 publications

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“…We have recently shown that several molecular forms of CCK. both larger and smaller than CCK33, are released during infusion of bombesin in man [12], Studies using radioimmunoassay techniques employing gastrin antibodies with different degrees of cross-reactivity with CCK have suggested that a small molecular form of CCK, possibly CCK8, predominates in post prandial plasma [13][14][15], However, radioim munoassays using more specific CCK anti bodies or other separation techniques indi cate that considerable amounts of larger forms of CCK are released after feeding [16][17][18][19]. In this respect it is interesting to note that after feeding in dogs small CCK predom inates in portal blood, while large forms of CCK predominate in peripheral plasma [20], In another study by the same group it was shown that the different ratios between large and small forms of CCK in portal and pe ripheral plasma resulted from a preferential elimination of small forms by passage through the liver [21], In conclusion, administration of atropine delays, but does not inhibit the plasma CCK response to intraduodenal corn oil in man.…”

Section: Discussionmentioning

confidence: 99%

Effect of Atropine on the Plasma Cholecystokinin Response to Intraduodenal Fat in Man

Hopman

Jansen

Lamers³

1984

Digestion

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The present study was undertaken to determine whether atropine inhibits the plasma cholecystokinin (CCK) response to intraduodenal fat. Plasma CCK concentrations were measured by radioimmunoassay using two sequence-specific antibodies. Antibody 1703 bound to all COOH-terminal CCK peptides containing at least 14 amino acid residues, while antibody T204 was specific for the sulphated tyrosine region of CCK. Intraduodenal instillation of 60 ml corn oil in 6 normal subjects induced significant increases in plasma CCK. Intravenous administration of atropine (0.015 mg/kg as bolus followed by 0.005 mg/kg · h over 3 h) resulted in significant inhibition of plasma CCK concentrations at 10, 20 and 30 min (antibody 1703) and at 20 and 30 min (antibody T204) after instillation of fat. However, the peak increments in plasma CCK during atropine (8.6 ± 1.9 pmol/l, antibody 1703; 5.4 ± 1.1 pmol/l, antibody T204) were not different from those found without atropine (6.3 ± 0.8 pmol/l, antibody 1703; 3.9 ± 0.9 pmol/l, antibody T204). Similarly, the integrated plasma CCK secretion after intraduodenal fat was not significantly different when measured during atropine (461 ± 119 pmol/l·3 h, antibody 1703; 269 ± 97 pmol/l·3 h, antibody T204) and without atropine (428 ± 62 pmol/l·3 h, antibody 1703; 188 ± 66 pmol/l·3 h).It is concluded that administration of atropine delays but does not inhibit the CCK response to intraduodenal corn oil in man.

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Section: Discussionmentioning

confidence: 99%

Effect of Atropine on the Plasma Cholecystokinin Response to Intraduodenal Fat in Man

Hopman

Jansen

Lamers³

1984

Digestion

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“…Others employing radioimmunoassays have reported an inverse correlation between gallbladder volume and plasma CCK levels estimated after a fatty meal (50,51). However, it had not been established whether CCK alone infused under steadystate conditions and approximating physiologic concentrations could account for gallbladder contraction.…”

Section: Cck Infusion and Gallbladder Ultrasonographymentioning

confidence: 99%

Cholecystokinin bioactivity in human plasma. Molecular forms, responses to feeding, and relationship to gallbladder contraction.

Liddle¹,

Goldfine²,

Rosen³

et al. 1985

J. Clin. Invest.

678

345

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“…Lack of an easy-to-perform and reliable method to estimate gallbladder vol ume in man, and lack of a sensitive and spe cific technique to determine plasma chole cystokinin (CCK), which is generally ac cepted to play a crucial role in postprandial gallbladder emptying, have hampered prog ress in this field of investigation [3]. How ever, the development of sensitive and spe cific radioimmunoassays for CCK in plas ma, and the availability of ultrasonography and cholescintigraphy as easy-to-perform and accurate means for the assessment of gallbladder motility in man, enabled the elu cidation of the mechanisms that mediate gallbladder responses to meals [4][5][6][7][8][9][10][11][12][13][14][15]. The aims of this study were: (1) to determine the effect of cephalic stimulation on gallbladder volume and plasma CCK concentrations; (2) to determine the effect of atropine on gall bladder volume and plasma CCK in re sponse to cephalic stimulation, and (3) to compare the cephalic stimulation of gall bladder contraction with the postprandial gallbladder contraction.…”

Section: Introductionmentioning

confidence: 99%

Cephalic Stimulation of Gallbladder Contraction in Humans: Role of Cholecystokinin and the Cholinergic System

Hopman¹,

Jansen²,

Rosenbusch³

1987

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To determine the role of cholecystokinin and the cholinergic system in cephalic stimulation of gallbladder contraction and to compare the degree of gallbladder contraction by cephalic stimulation with postprandial gallbladder contraction, 8 healthy volunteers (4 males, 4 females, 20–65 years) underwent the following studies: sham feeding of an appetizing meal, sham feeding with intravenous atropine, and ingestion of the same meal. Gallbladder volume was measured by real-time ultrasonography and plasma cholecystokinin by a sensitive and specific radioimmunoassay using antibody T204. Gallbladder contraction in response to sham feeding, 30 ± 4% (p = 0.0001 vs. basal), amounted to half of that seen after real feeding, 69 ± 5% (p < 0.0001 vs. basal). Significant dissociation between gallbladder response to sham feeding and real feeding was seen from 40 min (p < 0.005-p = 0.0001). Atropine did not affect basal gallbladder volume but completely abolished gallbladder contraction in response to sham feeding. Neither sham feeding without nor sham feeding with atropine significantly affected plasma cholecystokinin levels. On the other hand, real feeding induced significant increases in plasma cholecystokinin from a basal level of 2.3 ± 0.1 pM to a peak value of 5.9 ± 0.4 pM at 40 min. It is concluded that an important cephalic phase of postprandial gallbladder contraction exists which is cholecystokinin-independent but dependent on a cholinergic mechanism.

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Cholecystokinin and gallbladder contraction: Effect of CCK infusion

Cited by 51 publications

References 8 publications

Effect of Atropine on the Plasma Cholecystokinin Response to Intraduodenal Fat in Man

Effect of Atropine on the Plasma Cholecystokinin Response to Intraduodenal Fat in Man

Cholecystokinin bioactivity in human plasma. Molecular forms, responses to feeding, and relationship to gallbladder contraction.

Cephalic Stimulation of Gallbladder Contraction in Humans: Role of Cholecystokinin and the Cholinergic System

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