title: Gallbladder muscle dysfunction in patients with chronic acalculous disease.
abstract: OBJECTIVE
  The mechanisms responsible for the abnormalities of gallbladder emptying in patients with chronic acalculous gallbladder disease (AGD) have not been elucidated. This study was designed to determine whether a muscle defect could explain this gallbladder dysfunction.
  
  
  METHODS
  Gallbladder contraction induced by a continuous intravenous cholecystokinin octapeptide (CCK-8) infusion was determined by ultrasonography in control subjects, patients with AGD, pigment stones, and cholesterol stones. Muscle cells were obtained by enzymatic digestion. (125)I-CCK-8 binding and [(35)S]guanosine triphosphate gamma S (GTP gamma S) binding studies were performed.
  
  
  RESULTS
  In vivo gallbladder contraction induced by CCK-8 was significantly lower in AGD (29.4%) and cholesterol stones (28.8%) than in pigment stones (59.8%) and normal controls (57.8%; P < 0.01). In vitro muscle cell contraction induced by CCK-8 was also lower in AGD than in pigment stones. It remained impaired in AGD after stimulation with the G-protein activators GTP gamma S and AlF(4) and with the second messenger 1,2-dioctanoyl-sn-glycerol. However, GTP gamma S binding induced by CCK-8 and vasoactive intestinal polypeptide and the binding capacity of CCK receptors were not different between AGD and pigment stones.
  
  
  CONCLUSIONS
  These findings suggest that there is a good correlation between in vivo and in vitro gallbladder response to CCK-8 in patients with AGD. Unlike those found in cholesterol stones, the muscle defects in AGD appear to reside in the contractile apparatus.
authors.affiliation: Department of Surgery, Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island, USA.
authors.forename: J
authors.initials: J
authors.lastname: Amaral
authors.forename: Z L
authors.initials: ZL
authors.lastname: Xiao
authors.forename: Q
authors.initials: Q
authors.lastname: Chen
authors.forename: P
authors.initials: P
authors.lastname: Yu
authors.forename: P
authors.initials: P
authors.lastname: Biancani
authors.forename: J
authors.initials: J
authors.lastname: Behar
mesh_terms: D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D002769:Cholelithiasis / Q000000981:diagnostic imaging / Q000503:physiopathology; D002784:Cholesterol; D002908:Chronic Disease; D003085:Colic / Q000000981:diagnostic imaging / Q000503:physiopathology; D004075:Diglycerides / Q000494:pharmacology; D005704:Gallbladder / Q000503:physiopathology*; D005705:Gallbladder Diseases / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016473:Gallbladder Emptying / Q000187:drug effects / Q000502:physiology*; D016244:Guanosine 5'-O-(3-Thiotriphosphate) / Q000378:metabolism / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D007457:Iodine Radioisotopes; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D009130:Muscle, Smooth / Q000503:physiopathology; D011949:Receptors, Cholecystokinin / Q000378:metabolism; D012844:Sincalide / Q000008:administration & dosage / Q000378:metabolism; D013462:Sulfur Radioisotopes; D014463:Ultrasonography; D014660:Vasoactive Intestinal Peptide / Q000378:metabolism / Q000494:pharmacology
chemical_list: D004075:Diglycerides; D007457:Iodine Radioisotopes; D011949:Receptors, Cholecystokinin; D013462:Sulfur Radioisotopes; D014660:Vasoactive Intestinal Peptide; D016244:Guanosine 5'-O-(3-Thiotriphosphate); D002784:Cholesterol; D012844:Sincalide