Histamine-mediated delayed permeability response after scald burn inhibited by cimetidine or cold-water treatment.
Scald injury to one ear of the hairless mouse induced significant (P < .05) delayed edema formation in remote, uninjured skin. This remote edema formation was completely inhibited by immediate cold-water treatment of the scalded ear. Cold-water treatment significantly reduced histamine loss from the scalded ear, and the edema-inhibiting effect of the treatment could be mimicked by treating the animal prior to injury with the H2-histamine receptor antagonist cimetidine or a drug that causes histamine depletion. These observations suggest (i) that a histamine-mediated, delayed permeability response occurs after thermal injury that causes remote edema formation and (ii) that one mechanism of remote edema inhibition by cold-water treatment is the prevention of histamine release from thermally injured tissues.
D000818:Animals; D002056:Burns / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D002463:Cell Membrane Permeability; D002927:Cimetidine / Q000494:pharmacology*; D003080:Cold Temperature; D004487:Edema / Q000209:etiology / Q000503:physiopathology; D006146:Guanidines / Q000494:pharmacology*; D006636:Histamine Release / Q000187:drug effects*; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D051379:Mice; D011970:Receptors, Histamine H2 / Q000502:physiology
D006146:Guanidines; D011970:Receptors, Histamine H2; D002927:Cimetidine; D007213:Indomethacin