The role of prostacyclin and thromboxane in rat burn and freeze injuries

Abstract

Deep dermal injuries elicit discrete reaction patterns dependent on the type of injury sustained. Full thickness burn injuries produce an avascular focus of dead and dying tissue surrounded by a peripheral zone of secondary vascular dilation. In contrast, equivalent freeze injuries demonstrate vascular patency both centrally and peripherally. The basis for these differences are unknown. Because of their potent vasoactive and hematologic properties, the presence of two endogenously generated eicosanoids, thromboxane A 2 (Tx A 2) and prostacyclin (PGI 2), were examined in this process. Implanted stainless steel mesh chambers served as an in vivo interstitial collecting reservoir permitting repeated sampling of the wound fluid without tissue disruption. Standard burn and freeze injuries were administered to the skin covering the implanted chambers. The major metabolites of these eicosanoids: 6-keto PGF 1α and TxB 2 were measured in wound fluid during the first 24 hr following injury. Although both TxB 2 and 6-keto PGF 1α increased significantly following either injury, treatment with indomethacin did not alter the vascular sequelae despite evident cyclooxygenase inhibition. Latex infusion of whole rats confirmed the considerable difference between these two types of injury, with or without indomethacin. Thus, little evidence was found to support the importance of either TxA 2 or PGI 2 in the vascular alterations which follow burn or freeze injury.