ABSTRACT
Cholesterol cholelithiasis and cholecystitis are characterized by bile stasis which in turn could be due to altered contractility of gallbladder smooth muscle. The major hypothesis forming the basis for the above scheme is that cholesterol feeding will lead to an early decrease in gallbladder smooth muscle contractility. One piece of evidence available to indicate that a second substance is involved is that there is an influx of leukocytes into the gallbladders of cholesterol fed animals. Levels of certain prostaglandins were found to increase during cholesterol feeding, and aspirin administration was found to prevent stones from forming in animals fed cholesterol diet. Results from studies over the last several years have suggested that mild inflammation, lithogenic bile and biliary stasis are prominent features of gallstone disease in the cholesterol-fed prairie dog model. Compared to strips from animals fed the control diet, strips from animals fed cholesterol diet showed a biphasic response.
