• M Choi and H P Ehrlich.
• Wound Healing Laboratory, Shriners Burns Institute, Massachusetts General Hospital, Harvard Medical School, Boston 02142.
• Am. J. Pathol. 1993 Feb 1;142(2):519-28.

AbstractThermal energy causes an immediate, irreversible injury at the burn site, followed by a delayed, reversible tissue loss in the area surrounding the burn site due to progressive ischemia. We investigated the role of lipid peroxidation in the pathogenesis of progressive ischemia in a rat burn model. The burn model consisted of a row of four 10 x 20 mm burns separated by three unburned 5 x 20 mm skin bridges (interspaces). The interspaces became ischemic and necrotic by 24 hours, producing a single wound with the merger of the burn sites. U75412E, a lipid peroxidation inhibitor, preserved vascular patency, restored blood flow, prevented a rise in tissue conjugated dienes, and maintained tissue viability in the interspaces. Four separate burn wounds healed between three viable strips of hair-bearing interspaces. The treatment was effective, when given systemically during the period between 2 hours before and 1 hour after the burn. U75412E prevented progressive burn ischemia and the expansion of tissue loss.

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