Evaluation of prostacyclin production by human gallbladder
D. L. Kaminski, Y. G. Deshpande, S. Westfall and D. Herbold
Department of Surgery, St Louis University Medical Center 63104.
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.