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.