Publication Date:
1980-08-15
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boykin, J V Jr -- Eriksson, E -- Sholley, M M -- Pittman, R N -- New York, N.Y. -- Science. 1980 Aug 15;209(4458):815-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6157189" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Burns/complications/physiopathology/*therapy
;
Cell Membrane Permeability
;
Cimetidine/*pharmacology
;
*Cold Temperature
;
Edema/etiology/physiopathology
;
Guanidines/*pharmacology
;
Histamine Release/*drug effects
;
Indomethacin/pharmacology
;
Male
;
Mice
;
Receptors, Histamine H2/physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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