Recent reports suggest that cholecystectomy provides relief of symptoms in 75-90% of patients with CAC (JSLS 3:221, 1999). Decreased gallbladder ejection fraction, determined by cholecystokinin (CCK) cholescintigraphy, has a high predictive value for the diagnosis of chronic acalculous cholecystitis (CAC). However, the mechanisms involved in the impaired gallbladder contractile response in CAC are unknown.
AIM: To determine the mechanisms that may lead to impaired gallbladder emptying in CAC.
METHODS: Six patients (3 males, 3 females) underwent laparoscopic cholecystectomy for the diagnosis of CAC. All patients had ultrasonography and cholescintigraphy with calculation of gallbladder ejection fraction as part of their workup. Gallbladder specimens removed during hepatic resection (controls) and following cholecystectomy for CAC were attached to force transducers and placed in tissue baths oxygenated with Krebs solution. Electrical field stimulation (EFS) (1-10 Hz, 0.1-msec, 70 V) or the contractile agonists, CCK-8 (10-910-5), bethanechol (10-4), or K+ (80 mM), were placed separately in the tissue baths and changes in tension were determined.
RESULTS: Patients with CAC had a mean gallbladder ejection fraction of 12 ± 4%. Pathological examination of all gallbladders removed for CAC revealed chronic cholecystitis. Spontaneous contractile activity was present in gallbladder strips in 80% of controls but only 33% of gallbladder strips from patients with CAC (P < 0.05 vs controls). CCK-8 contractions were decreased by 49% with CAC (P < 0.05 vs controls), while EFS-stimulated contractions were decreased by 45% (P < 0.05 vs controls). However, Bethanechol- and K+-induced contractions were similar between controls and CAC gallbladders.
CONCLUSIONS: The impaired gallbladder emptying in CAC appears to be due to diminished spontaneous contractile activity and decreased contractile responsiveness to both CCK and EFS.