Abstract
The role of platelet-activating factor (PAF) as a mediator of gastric damage associated with burn injury was examined in the rat. Gastric mucosal hemodynamics was recorded continuously by means of laser-Doppler flowmetry and reflectance spectrophotometry. Burn injury induced prolonged hypotension and rapid-onset and long-lasting gastric mucosal hemodynamic derangement—that is, ischemia with congestion. This hemodynamic disturbance was significantly inhibited by CV-6209, a specific PAF antagonist. Elevated tissue levels of thiobarbituric acid reactants and pathologic changes in the gastric mucosa subsequent to burn injury were also significantly alleviated by the preadministration of CV-6209. These results strongly suggest a role of PAF as an important mediator of gastric damage after burn injury through its potent vasoactive effect on gastric microcirculation.