Abstract
Although proquazone is less ulcerogenic than indomethacin in rat and man, it inhibits more effectively than indomethacin gastric mucosal synthesis of 6-keto-prostaglandin (PG) F1α in both species during incubationin vitro. The more pronounced inhibitory activity of proquazone can be observed on formation of 6-keto-PGF1α from endogenous substrate by fragments of gastric mucosa as well as on conversion of exogenous arachidonic acid by a microsomal fraction of mucosal homogenates indicating high affinity of proquazone for gastric mucosal cyclo-oxygenase. After oral administration, however, both drugs exhibit equal inhibitory potency on gastric formation of 6-keto-PGF1α in the rat. These findings indicate that pharmacokinetic properties of non-steroidal anti-inflammatory drugs (NSAID) contribute significantly to their inhibitory action on gastric PG formationin vivo. The comparable reduction of gastric 6-keto-PGF1α synthesis observed after oral administration of proquazone and indomethacin in the rat suggests that the ulcerogenic effects of NSAID result not only from inhibition of the gastric PG system. Effects on other processes and other enzyme systems, e.g. the lipoxygenase pathway of arachidonic acid metabolism, may modulate drug-induced ulcerogenicity and deserve further investigation.
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