An experimental study on the role of gallbladder mucosal fluid secretion and intraluminal pressure in cholecystitis.

The cystic duct was ligated and gallstones were implanted into the gallbladder in cats. Five to eighteen weeks later the hydrostatic pressure in the gallbladder lumen was measured after laparotomy, and fluid transport across the gallbladder epithelium was studied and compared to the microscopic gallbladder morphology. Instead of the normal absorption many of these gallbladders continuously secreted fluid to the lumen and had raised intraluminal hydrostatic pressure (61 +/- 8 SEM, mmHg). Morphological signs of acute gallbladder inflammation were common (47%) in gallbladders with mucosal fluid secretion, but were never seen in those that absorbed fluid (p less than 0.05). Gallbladder mucosal fluid transport correlated with a histological score of the inflammation (r = +0.68, p less than 0.01). Gallbladder fluid secretion decreased when the intraluminal pressure was experimentally raised to the initially observed level, demonstrating mechanisms counteracting the secretion in this situation. An increased intraluminal pressure is suggested to be involved in the pathophysiology of acute cholecystitis.