In a canine model, prostaglandin F2alpha release from platelets mediates pulmonary changes during platelet aggregation, an effect that can be inhibited by acetylsalicylic acid.
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Acetylsalicylic acid may blunt platelet-driven pulmonary pressure rises in canines; leaves open any role in human lung injury or hypertension.
Increases in pulmonary arterial pressure, tracheal insufflation pressure, and blood levels of the prostaglandin F2alpha metabolite, 15-keto-13, 14-dihydro F2alpha, were observed after protamine chloride or thrombin-induced platelet aggregation and release reaction in dogs. These effects were largely eliminated after administration of acetylsalicylic acid, an inhibitor of prostaglandin synthesis. The platelet aggregation was not noticeably affected. It is suggested that release of prostaglandin F2alpha from platelets is an important factor for the pulmonary changes during induced platelet aggregation. The necessity of measuring metabolite levels, rather than prostaglandin F2alpha levels, in blood during in vivo conditions is demonstrated.
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Rådegran et al. (1977) studied this question.
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