Effect of Truncal Vagotomy on Cholecystokinin Release, Gallbladder Contraction, and Gallbladder Sensitivity to Cholecystokinin in Humans

Masclee, Ad; Jansen, J. B. M. J.; Driessen, W. M. M.; Geuskens, L.M.; Lamers, C. B. H. W.

doi:10.1016/0016-5085(90)90354-4

Cited by 54 publications

(22 citation statements)

References 26 publications

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“…Guzman et al [ 13] demonstrated that electric vagal stimula tion did not alter plasma CCK in dogs, where as Linden [14] reported CCK elevation under the same circumstances. Sham feeding aug mented CCK release in dogs [15], but not in man [16], According to some researchers, TV did not alter basal CCK release in men [11,17], whereas others reported elevated values [18]. In the present study we showed that although our surgical procedures did not af fect integrated CCK responses, they elevated the basal plasma CCK levels highly signifi cantly.…”

Section: Contraction In Vagotomized Patientssupporting

confidence: 46%

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Effect of Vagotomy on Cholecystokinin Release and Gallbladder Contraction in Patients with Complicated Duodenal Ulcer

Huang

Huang²,

McKay³

et al. 1994

Eur Surg Res

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In this prospective study, we investigated gallbladder (GB) contraction and plasma cholecystokinin (CCK) levels in response to food intake before and 1 month after vagotomy in 27 patients with complicated duodenal ulcer. Highly selective vagotomy (HSV) was carried out in 6 patients, truncal vagotomy and pyloroplasty (TVP) in 4, truncal vagotomy and antrectomy (TVA) in 7, selective vagotomy and pyloroplasty (SVP) in 5 and selective vagotomy and antrectomy (SVA) in another 5 patients with pyloric stenosis. The results of our studies indicated that (1) basal plasma CCK levels increased significantly after vagotomy, (2) none of the vagotomy operations altered the integrated CCK response, (3) unlike HSV, SVA and TVA, SVP and TVP decreased GB emptying and (4) antrectomy significantly enhanced CCK release after food intake. We concluded from these findings that the operative procedure of HSV, SVA or TVA to circumvent bile stasis-related postvagotomy cholelithiasis is superior to SVP or TVP in the surgical treatment of complicated duodenal ulcer.

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Section: Contraction In Vagotomized Patientssupporting

confidence: 46%

“…Oral cholecystography [3,9], intravenous cholangiography [10], infusion cholescintigraphy [11,12] and ultrasonography [5,8] have in the past been employed to study GB con tractility by measuring areas [3,8], volumes [5,9] or radioactivities [11,12] in humans. 368 Huang/Huang/McKay/Rayford CCK Release and Gallbladder…”

Section: Discussionmentioning

confidence: 99%

Effect of Vagotomy on Cholecystokinin Release and Gallbladder Contraction in Patients with Complicated Duodenal Ulcer

Huang

Huang²,

McKay³

et al. 1994

Eur Surg Res

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“…Numerous studies of the effects of vagotomy on gall-bladder responsiveness have indicated that CCK-induced contractions are lessened or delayed following vagotomy (Tinker & Cox, 1969;Isaza et al, 1971;Fried et al 1983;Pitt et al 1983;Masclee et al 1990). It is possible that CCK is acting on presynaptic CCK receptors that are located on vagal nerve terminals.…”

Section: Discussionmentioning

confidence: 99%

“…The CCK-induced contractile response of the gall-bladder has been reported to be unchanged following vagotomy in some studies (Shaffer, 1982;Pellegrini, Lewin, Patti, Thomas, Ryan & Way, 1985), and increased in others (Tinker & Cox, 1969;Isaza, Jones, Dragstedt & Woodward, 1971;Fried, Ogden, Greeley & Thompson, 1983;Pitt, Doty & DenBesten, 1983). In a more recent study, Masclee 90 G. M. MA WE CCK EFFECT IN GALL-BLADDER GANGLIA and colleagues (Masclee, Jansen, Riessen, Geuskens & Lamers, 1990) concluded that vagotomy changed the time course but not the magnitude of fat-stimulated gallbladder contraction. Results of studies showing a change in the CCK-induced gallbladder contraction could be interpreted as a vagotomy-induced decrease in responsiveness of the tissue to CCK.…”

Section: Introductionmentioning

confidence: 97%

The role of cholecystokinin in ganglionic transmission in the guinea‐pig gall‐bladder.

Mawe

1991

The Journal of Physiology

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SUMMARY1. The effects of cholecystokinin (CCK) on intact guinea-pig gall-bladder ganglia were investigated with intracellular, single-electrode current-and voltage-clamp recording techniques.2. Cholecystokinin octapeptide (CCK-8; 0 01-100 nM) increased the amplitude of the fast excitatory postsynaptic potential (EPSP) that was evoked by stimulation of interganglionic fibre tracts. In most cases, neurones that exhibited subthreshold EPSPs in normal Krebs solution fired action potentials in the presence of CCK-8. In a low Ca2+/high Mg2" solution, CCK-8 caused a 3-fold increase in the amplitude of fast EPSPs.3. The amplitude of the evoked excitatory postsynaptic current (EPSC) was increased by CCK-8 (0 01-100 nM) in a concentration-dependent manner. The effect was maximal at 10 nM.4. Cholecystokinin octapeptide caused a 3-fold increase in the quantal content of the EPSP in a low Ca2+/high Mg2+ solution, but had no effect on the quantal size.5. The specific CCK-A receptor antagonist, MK-329 (formerly L-364,718; l0 nM), reversibly blocked the facilitatory effect of CCK-8 on ganglionic transmission. However, the specific CCK-B receptor antagonist, L-365,260 (10 nM), did not alter the presynaptic facilitatory effect of CCK-8. 6. The response of gall-bladder neurones to exogenously applied ACh was hot modified by CCK-8.7. Application of CCK-8, by superfusion (0 001-100 nM) or by pressure microejection (100 /am), had no effect on the membrane potential, membrane conductance, action potential, or threshold of gall-bladder neurones.8. Immunohistochemistry was employed to determine whether the actions of CCK could be elicited by release of the peptide from nerve terminals within the ganglionated plexus of the gall-bladder. Immunoreactivity for CCK was not detected in the ganglionated plexuses of the gall-bladder, but CCK immunoreactivity was plentiful in control preparations of intestinal myenteric and submucosal plexuses.9. These results show that CCK has a presynaptic facilitatory effect on fast synaptic transmission in guinea-pig gall-bladder ganglia, and that this effect is mediated by presynaptic CCK-A receptors. Furthermore, it appears that such an MS 8804 effect would normally occur in response to hormonal CCK, rather than CCK that is released from nerve terminals.

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“…Some authors have reported reduced gallbladder emptying after truncal vagotomy, [23][24][25][26] whereas others have found normal values. 27,28 We believe these discrepancies may arise from differences in the timing of investigation after operation and in the different methods used for estimating gallbladder function. There was modest increase in fasting volume in our patients who had undergone truncal vagotomy, compared with healthy volunteers (Fig.…”

Section: Manipulation Of Gallbladder Emptyingmentioning

confidence: 99%

Regulation and responses of gallbladder muscle activity in health and disease

Johnson

2003

ann r coll surg engl

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A complex relationship links biliary symptoms with the mechanisms of gallbladder emptying and the presence of gallstones. This relationship has been investigated by clinical studies of symptoms associated with gallstones, by investigation of gallbladder emptying and cholecystokinin (CCK) release in patients with gallstones, and after cholecystectomy, or truncal vagotomy, and in the irritable bowel syndrome (IBS). Laboratory studies examined receptor density on bovine gallbladder, and contractility of human gallbladder in response to a variety of stimuli was studied in vitro . A set of six symptoms associated with the presence of gallstones was identified; IBS appeared to be present in two-fifths of patients before cholecystectomy but only one-third of these patients had persistent IBS symptoms one year after operation. Gallbladder emptying studies confirmed the poor contraction of stone-bearing gallbladders; abnormal patterns of emptying were also found in patients with IBS. Gallbladder emptying and filling appear to be largely neurally regulated. CCK receptor density was very low in gallbladder tissue, suggesting that receptors on nerve cells might mediate the action of CCK. Relaxation of gallbladder muscle was mediated by adrenergic and nitrergic nerves. The inflammatory mediator bradykinin, however, had a strong direct action on muscle cells to cause gallbladder contraction. The work reported here gives an overview of the symptoms and mechanisms of disease associated with the presence of stones in the gallbladder.

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Effect of Truncal Vagotomy on Cholecystokinin Release, Gallbladder Contraction, and Gallbladder Sensitivity to Cholecystokinin in Humans

Cited by 54 publications

References 26 publications

Effect of Vagotomy on Cholecystokinin Release and Gallbladder Contraction in Patients with Complicated Duodenal Ulcer

Effect of Vagotomy on Cholecystokinin Release and Gallbladder Contraction in Patients with Complicated Duodenal Ulcer

The role of cholecystokinin in ganglionic transmission in the guinea‐pig gall‐bladder.

Regulation and responses of gallbladder muscle activity in health and disease

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