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1997 Abstract: 10 Role of cyclooxygenase-II for fluid secretion by the inflamed gallbladder mucosa.

Abstracts
1997 Digestive Disease Week

Role of cyclooxygenase-II for fluid secretion by the inflamed gallbladder mucosa.

B Nilsson[1], D Delbro[1], L Hedin[2], S Friman[1], S Andius[1], M Nilsson[3], J Svanvik[4]. Departments of Surgery[1] and Physiology[2], Anatomy[3], Sahlgrenska University Hospital, Goteborg, and Department of Surgery, University Hospital, Linkoping[4], Sweden.


The inflammatory fluid secretion by the gallbladder mucosa in experimental cholecystitis is induced by an activation of cyclooxygenase (COX), leading to an increase in prostaglandin formation. This, in turn, activates intrinsic, non-adrenergic non-cholinergic (NANC) secreto-motonerves to the mucosa (Jivegard et al., Dig Dis Sci 1987;32;1389-1394). COX exists as a constitutive (COX-I), and an inducible (COX-II) isoform. In the present study, we investigated a role of COX-II for the inflammatory fluid secretion of the feline gallbladder.

Methods: Experiments were performed 10 weeks after a surgical procedure in which chronic cholecystitis was induced in cats (n=11) by ligation of the cystic duct and the implantation of (human) gallstones in the gallbladder. Six previously unoperated animals served as controls. Gallbladder fluid transport was continuously monitored via a perfusion system after the i.v. administration of guanethidine and atropine.

Results: In inflamed gallbladders, there was steady fluid secretion that was reversed to absorption by the i.v. injection of the selective COX-II blocker, NS 398. This agent did not affect the absorptive process of the gallbladder in the controls. Increased levels of COX-II in inflamed, but not normal gallbladders were shown by immunoblotting.

Transport of fluid (ml/h; mean ± SEM) in experiments
on cats with inflamed or normal gallbladder

                             Basal (ml/h)        NS 398 (ml/h)
 Inflamed gallbladders       +0.28±0.07          -1.19±0.15***
 Normal gallbladders         -1.63±0.09          -1.61±0.10
***=p<0.001; ANOVA. + denotes secretion and - denotes absorption.

Conclusions: Increased levels of the inducible COX-II was shown in inflamed gallbladders. Selective pharmacological blockade of COX-II abolished the inflammatory fluid secretion. COX-II may be important in the regulation of the gallbladder mucosal fluid transport in cholecystitis. Moreover, a COX-II antagonist could be beneficial in human cholecystitis, with less side effects compared to unselective blockers.



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