Decreasing progressive dermal ischemia after burning could theoretically limit the amount of skin necrosis to the zone of coagulation. Methylprednisolone, aspirin, indomethacin, imidazole, dipyridamole, and methimazole have been shown to prevent dermal ischemia, suggesting that prostaglandins and/or thromboxanes may play a role in its pathogenesis. Specific antiprostaglandin antibodies (anti-PgE2, PgF2 alpha, PgI2, and TxA2) were reacted with tissue biopsies of burned guinea pig skin at various time intervals postburn. An immunoperoxidase technique with goat anti-rabbit immunoglobulin and horseradish peroxidase demonstrated the presence of the specific arachidonic acid metabolites. The burned tissue showed high levels of PgE2 and TxA2. The effects of three thromboxane inhibitors, imidazole, methimazole, and dipyridamole, on dermal ischemia were studied. Xenon133 washout studies were performed in burned and unburned areas. Tissue half-life of Xenon was prolonged in burned, untreated areas but this rapidly decreased in antithromboxane-treated burns. Repeated antiprostaglandin and antithromboxane antibody-immunoperoxidase studies on tissue from the thromboxane inhibitor-treated animals showed that PgE2, PgF2 alpha, and PgI2 were at the same levels as in untreated animals, but thromboxane (TxA2) was essentially absent, suggesting that thromboxane may be responsible for the progressive dermal ischemia after burning and that decreasing its production can increase dermal perfusion.