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

Huang, Yaw-Bin; Huang, Tiao‐Lai; McKay, Dana; Rayford, Ph.L.

doi:10.1159/000129357

Cited by 4 publications

(3 citation statements)

References 14 publications

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“…Gallbladder contraction is principally governed by the interaction between the parasympathetic motor function of the vagus nerve and cholecystokinin (CCK). Although the precise physiologic mechanism remains unclear, in postvagotomy states, including truncal vagotomy and pyloroplasty, an increase in the basal plasma CCK level occurs 1 and is accompanied by the augmented sensitivity of gallbladder contractile response to CCK. 2 The subsequent impairment in gallbladder motility as a result of sustained contraction potentiates hydrophobic bile salt cholestasis and cholecystitis.…”

Section: Answer To Image 4 (Page 46): Chronic Cholecystitis Resultingmentioning

confidence: 99%

A Woman With Chronic Postprandial Abdominal Pain and Vomiting

2016

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Question: A 35-year-old woman presented with a 3-month history of postprandial abdominal discomfort and vomiting. The patient's history included left jugular foramen schwannoma with involvement of the vagus and spinal accessory nerves (cranial nerves X and XI) treated with left level II/III neck dissection 4 months before presentation; intraoperatively, electromyography (EMG) monitoring confirmed transection of both nerves in the process of tumor resection. Physical examination yielded a soft, nondistended abdomen with bowel sounds present; no guarding, rebound, or bruits were found. The only laboratory abnormality included a mildly elevated leukocyte count of 11.7 Â 10 9 /L (normal range, 3.5-10.5 Â 10 9 /L). Abdominal computed tomographic imaging demonstrated pronounced gallbladder contraction (Figure A [transverse plane] and Figure B [coronal plane]; arrows) without additional intra-abdominal pathology. Subsequent abdominal ultrasound performed in the fasting state also demonstrated gallbladder contraction (Figure C). The patient proceeded to cholecystectomy for diagnostic and therapeutic intent. Postoperative surgical pathology revealed chronic inflammation and thickened muscularis mucosa of the gallbladder (Figure D; star indicates thickened muscularis mucosa). After cholecystectomy, the patient reported complete symptomatic resolution. What are the diagnosis and the likely etiology? Look on page 47 for the answer and see the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.

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Section: Answer To Image 4 (Page 46): Chronic Cholecystitis Resultingmentioning

confidence: 99%

A Woman With Chronic Postprandial Abdominal Pain and Vomiting

2016

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“…Similar results were observed in patients after truncal vagotomy with or without antrectomy. 10 In truncal vagotomy patients, fasting gall‐bladder emptying in relation to stimulation with erythromycin showed a significantly higher gall‐bladder emptying rate compared with normal subjects. 11 This might be explained by the denervation theory, resulting in a higher sensitivity of the gall‐bladder to prokinetic substances.…”

Section: Surgical Procedures and Gall‐bladder Motilitymentioning

confidence: 90%

“…Impaired post‐prandial gall‐bladder emptying has been demonstrated in patients where a pyleroplastic has been added either to a truncal vagotomy or selective gastric vagotomy. 10 This was explained by changes in gastric emptying. However, there is no information available on the relationship between post‐prandial gall‐bladder emptying and gastric emptying in these patients.…”

Section: Surgical Procedures and Gall‐bladder Motilitymentioning

confidence: 99%

Review article: gall‐bladder motility after intestinal surgery

Qvist

2000

Aliment Pharmacol Ther

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Summary There is a close relationship in humans between gall‐bladder motility and gastrointestinal motility during the fasting state, as well as in the post‐prandial period. Only a minority of publications take this relationship into account in the description of biliary dysmotility after various surgical procedures. Most publications deal with post‐prandial gall‐bladder motility or with stimulation of gall‐bladder contraction from various prokinetic drugs or gastrointestinal hormones. Impaired gall‐bladder motility has been demonstrated after Billroth II gastric resection, pyloroplasty and colectomy, but the epidemiological data on the risk of gallstone formation in these patients are too scarce and equivocal to recommend prophylactic cholecystectomy. Future studies on gall‐bladder motility after surgical procedures should include measurements of gall‐bladder motility during the fasting state, as well as in the post‐prandial period. The measurements should be related to the migrating motor complexes, and this necessitates a simultaneous recording of gastrointestinal motility.

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