Pathogenesis of platelet-activating factor-induced gastric mucosal damage in rats.

Platelet-activating factor (PAF), given intravenously, induced erosions and hyperemia to the rats stomachs. Gastric mucosal blood flow was decreased and thiobarbituric acid (TBA) reactants (an index of lipid peroxidation) in the gastric mucosa were increased 10 min after PAF injection. Superoxide dismutase plus catalase reduced the gastric mucosal lesions and TBA reactants, but had no influence on gastric mucosal blood flow. A reduction in the number of circulating polymorphonuclear leukocytes (PMN) reduced the gastric mucosal damage and TBA reactants, and inhibited the decrease in gastric mucosal blood flow, as observed 30 and 60 min after PAF injection. PAF induced superoxide production by rat PMN and enhanced that stimulated by opsonized zymosan or phorbol myristate acetate. These results suggest that microcirculatory disturbance and oxygen-derived free radicals generated by PMN play important roles in gastric mucosal lesions induced by PAF.