Cold-water treatment of scald injury and inhibition of histamine-mediated burn edema

Abstract

Using the hairless mouse ear burn model we have studied the effects of immediate short-term cold-water treatment (CWT) of a moderate scald injury (54°C water for 20 sec) to intact skin using 8–10°C water for 5 min. CWT following scald injury caused brief periods of arteriolar vasomotion and shortened the duration of postburn venular dilation by about 50% as compared to untreated burns. CWT significantly ( P < 0.05) reduced edema formation of the burned ear for only the first 2 hr after injury as compared to untreated burns. Significant delayed remote edema formation normally observed in abdominal and unburned (contralateral) ear skin after untreated ear scald injury was abolished after CWT to the burned ear. Chemical inhibition of remote burn edema, comparable to that achieved with CWT, was produced by cimetidine pretreatment or histamine depletion prior to injury. CWT also significantly decreased tissue histamine loss of the burned ear after scald injury Ultrastructural demonstration of increased vacuole formations in capillary and venular endothelial cells in edematous, unburned ear skin 2 hr after untreated scald injury suggested the presence of histamine-mediated remote burn edema formation. Predominant pathophysiologic mechanisms of CWT in local and remote burn edema inhibition and perhaps burn shock protection were suggested as: (1) decreased vascular response with a shortened duration of postburn venular dilation, and, most importantly, (2) the inhibition of local and systemic histamine release from thermally injured tissues.