EFFECT OF PROSTAGLANDINS ON THE DERMAL MICROCIRCULATION AFTER BURNING, AND THE INHIBITION OF THE EFFECT BY SPECIFIC PHARMACOLOGICAL AGENTS

In all skin burns, there exists a zone of stasis which is not immediately coagulated but which shows a progressive compromise in microvascu- lar circulation, with a complete cessation of dermal perfusion by 24 hours. This progressive dermal ischemia has been previously demonstrated to be prevented by the topical application of methylprednisolone acetate. One property of this steroid-its antiprostaglandin effect-was chosen for further study. Three additional substances, all thought to be antiprostaglandins, were evaluated for their ability to prevent dermal ischemia in standardized partial-thickness burns in guinea pigs. Treatment with indomethacin or acetylsalicylic acid preserved dermal perfusion about as much as did methylprednisolone acetate. These 3 agents are known to be inhibitors of specific steps in the synthesis of prostaglandins. The third substance, nicotinic acid, had no demonstrable effect on the dermal ischemia and skin sections from animals treated with it were identical to sections from the untreated controls. However, nicotinic acid has not been demonstrated to be a specific inhibitor of prostaglandin synthesis. It appears from these studies that prostaglandins have a role in the progressive dermal ischemia after burning, and that specific antiprostaglandins may be effective in preventing these progressive changes and in improving dermal perfusion. This could lead, in turn, to lessening the depth and amount of skin necrosis after a burn. © 1979 American Society of Plastic Surgeons.