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Mechanisms of impaired gallbladder contractile response in chronic acalculous cholecystitis
Authors:Anders R. Merg M.D.  Scott E. Kalinowski B.S.  Marilyn M. Hinkhouse B.S.  Frank A. Mitros M.D.  Kimberly S. Ephgrave M.D.  Joseph J. Cullen M.D.
Affiliation:(1) Department of Pathology, University of Iowa College of Medicine, Iowa City, Iowa;(2) Department of Surgery, University of Iowa College of Medicine, Iowa City, Iowa;(3) Veterans Administration Medical Center, Iowa City, Iowa;(4) 4622 JCP, University of Iowa Hospitals and Clinics, 52242 Iowa City, IA
Abstract:The mechanisms involved in the impaired gallbladder contractile response in chronic acalculous cholecystitis are unknown. To determine the mechanisms that may lead to impaired gallbladder emptying in chronic acalculous cholecystitis, gallbladder specimens removed during hepatic resection (controls) and after cholecystectomy for chronic acalculous cholecystitis were attached to force transducers and placed in tissue baths with oxygenated Krebs solution. Electrical field stimulation (EFS) (1 to 10 Hz, 0.1 msec, 70 V) or the contractile agonists, CCK-8 (10-9 to 10-5) or K+ (80 mmol/L), were placed separately in the tissue baths and changes in tension were determined. Patients with chronic acalculous cholecystitis had a mean gallbladder ejection fraction of 12% ± 4%. Pathologic examination of all gallbladders removed for chronic acalculous cholecystitis revealed chronic cholecystitis. Spontaneous contractile activity was present in gallbladder strips in 83% of control specimens but only 29% of gallbladder strips from patients with chronic acalculous cholecystitis (P < 0.05 vs. controls). CCK-8 contractions were decreased by 54% and EFS-stimulated contractions were decreased by 50% in the presence of chronic acalculous cholecystitis (P < 0.05 vs. controls). K+-induced contractions were similar between control and chronic acalculous cholecystitis gallbladder strips. The impaired gallbladder emptying in chronic acalculous cholecystitis appears to be due to diminished spontaneous contractile activity and decreased contractile responsiveness to both CCK and EFS. Presented at the Forty-Second Annual Meeting of The Society for Surgery of the Alimentary Tract, Atlanta, Georgia, May 20–23, 2001 (poster presentation). Supported by the Veterans Administration Research Service and National Institutes of Health training grant HLO 7485-19.
Keywords:Acalculous cholecystitis  motility  gallbladder
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