Within 24 hours after a full-thickness
burn injury, predictable alterations occur in the dermal vasculature. At the immediate site of injury, vessels lose patency. In the periphery, vasodilation and increased permeability become widespread. A variety of interventions were employed to prevent these vascular sequelae. While systemic treatment, immediately after
burn trauma, with
hydrocortisone or the non-steroidal anti-inflammatory compound
indomethacin, was ineffective in preventing vascular alteration, treatments with other NSAI agents such as
ibuprofen and
imidazole were effective in preventing microvascular occlusion. In addition, utilizing standard radioimmunoassay techniques, the concentrations of the metabolites of two potent
eicosanoids,
thromboxane and
prostacyclin, were measured from fluid collected in the implanted
wound chambers. Following full-thickness
burns, the synthesis and release of
thromboxane were inhibited by
indomethacin, imidazole, and
ibuprofen. Furthermore,
indomethacin and
ibuprofen, but not
imidazole, blocked the synthesis and release of
prostacyclin into
wound fluid. Significantly,
ibuprofen was effective in preserving the dermal vasculature, even when administration was delayed as long
as 6 hours after
burn trauma.
Pharmacologic actions not associated with the production of
thromboxane or
prostacyclin appear responsible for the protective effects of
ibuprofen during
burn injury. Such findings do not support an important role for either
thromboxane or
prostacyclin in the development of vascular alterations following
burn injury.