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[Gallbladder function and CCK after gastrectomy].

N Hanyu1, T Aoki, Y Ohira

  • 1Second Department of Surgery, Jikei University School of Medicine, Tokyo, Japan.

Nihon Geka Gakkai Zasshi
|September 1, 1991
PubMed
Summary
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Following gastrectomy, gallbladder dysfunction may occur due to altered cholecystokinin (CCK) release and loss of the gastro-cholecystic reflex. This impacts gallbladder contraction and may contribute to gallstone formation.

Area of Science:

  • Gastroenterology
  • Endocrinology
  • Biliary System Physiology

Background:

  • Postgastrectomy cholelithiasis (gallstones) is a clinical concern.
  • Biliary tract dyskinesia is a potential contributing factor.
  • Cholecystokinin (CCK) is a key hormone regulating gallbladder function.

Purpose of the Study:

  • To investigate postgastrectomy gallbladder function.
  • To examine cholecystokinin (CCK) levels after gastrectomy.
  • To elucidate the mechanisms of altered gallbladder contraction.

Main Methods:

  • Experimental study design.
  • Measurement of postprandial gallbladder contraction.
  • Assessment of endogenous cholecystokinin (CCK) levels.
  • Analysis of gastro-cholecystic reflex.

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Main Results:

  • Postprandial gallbladder contraction is primarily mediated by endogenous CCK, with a contribution from the gastro-cholecystic reflex.
  • Gastrectomy leads to a decrease in gallbladder contraction, attributed to the loss of the gastro-cholecystic reflex.
  • Altered food passage after total gastrectomy and Roux-en-Y reconstruction changes CCK secretion dynamics, influencing gallbladder response.

Conclusions:

  • The gastro-cholecystic reflex plays a significant role in postprandial gallbladder contraction.
  • Loss of this reflex post-gastrectomy contributes to impaired gallbladder function.
  • Modified CCK secretion dynamics post-Roux-en-Y reconstruction impact gallbladder contractility, potentially increasing gallstone risk.