prostaglandin-f1 and Cholecystitis

The etiologic role of crystalline material in inflammatory arthritis is well established. The role of crystals in cholecystitis is unclear. We hypothesized that crystalline cholesterol monohydrate stimulates guinea pig gallbladder inflammation in vivo.. Crystalline cholesterol monohydrate, lipopolysaccharide (LPS), lysolecithin, polystyrene latex spheres (noninflammatory particles), and saline were instilled into guinea pig gallbladders for 24 to 72 hours after cystic duct ligation. Water transport across gallbladder mucosa was measured. Gallbladder tissue was analyzed for mucus layer thickness, myeloperoxidase, prostaglandin E2 (PGE2) prostaglandin F-1 alpha (PGF-1 alpha), and interleukin-1. Luminal fluid was also examined for PGE2 and PGF-1 alpha. Values for each test were compared with saline controls by using Student's test (p < 0.05).. Crystalline cholesterol, LPS, and lysolecithin caused significant reduction in mucus layer thickness, reversed water absorption to secretion across the gallbladder mucosa, caused significant increases in myeloperoxidase and interleukin-1 in gallbladder tissue, and caused significant increases in PGE2 and PGF-1 alpha in luminal fluid. These effects were generally dose- but not time-dependent. Polystyrene latex particles caused no difference in outcomes compared with saline controls.. Crystalline cholesterol monohydrate has dose-dependent inflammatory effects in the guinea pig gallbladder in vivo that are not simply-due to mechanical irritation of the gallbladder wall by crystalline particles. Crystals in the gallbladder may have an etiologic role in cholecystitis.

Topics: Animals; Cholecystitis; Cholesterol; Crystallography; Dinoprostone; Dose-Response Relationship, Drug; Gallbladder; Guinea Pigs; Peroxidase; Prostaglandins F; Water-Electrolyte Balance

The prostanoids have been demonstrated to be involved in gallbladder physiology and disease. In previous reports, prostaglandin E (PGE) compounds were found to be increased in inflamed human gallbladders. Prostaglandin synthetase inhibition decreased PGE formation by human gallbladders; however, the relief of symptoms of cholecystitis did not correlate well with the decrease in PGE formation. This suggested that other prostanoids may be involved in cholecystitis. The purpose of this study was to evaluate the production of the proinflammatory arachidonic acid metabolite prostacyclin by gallbladders from patients with calculous cholecystitis. The formation of PGE and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), the stable metabolite of prostacyclin, in normal human gallbladder mucosal cells and muscle tissue was compared with that produced by diseased mucosal cells and muscle tissue. Normal human gallbladders produced small amounts of 6-keto-PGF1 alpha, and no differences in formation rates were evident when muscle tissue was compared with mucosal cells. Diseased gallbladders produced significantly greater amounts of 6-keto-PGF1 alpha than did normal gallbladders, and diseased gallbladder muscle produced approximately four times greater amounts of 6-keto-PGF1 alpha than did diseased gallbladder mucosa. Prostacyclin formation is increased in diseased human gallbladders and may be an important mediator of the inflammatory changes of cholecystitis.

Topics: Acute Disease; Cholecystitis; Cholelithiasis; Chronic Disease; Epoprostenol; Female; Gallbladder; Glucuronidase; Humans; Male; Middle Aged; Mucous Membrane; Prostaglandins F; Reference Values