Effect of cimetidine, hydrocortisone superoxide dismutase and catalase on the development of oedema after thermal injury.
A new hypothesis for the pathophysiological mechanism underlying the development of oedema after a thermal injury has been tested in an experimental burn model. Support was given to the suggestion that oxygen-derived free radicals produced by invading leucocytes which upon activation release the superoxide radical (O2-), may be partly responsible for the increase in microvascular permeability seen after thermal injury. By removal of oxygen-derived free radicals with radical scavengers (superoxide dismutase and catalases) it was possible to reduce significantly the post-burn oedema formation. For comparison, one series of rats was pretreated with hydrocortisone and another with the histamine H2-blocker cimetidine. Hydrocortisone reduced the very early post-burn oedema formation which might partly be due to its membrane-stabilizing influence and partly to a direct effect on the microvasculature, causing a reduction of the vasodilatation observed post-burn. The inhibition of post-burn oedema formation by cimetidine, earlier demonstrated in animal burn models, was confirmed in the present study. The mean arterial blood pressure (MAP) in the cimetidine-treated rats decreased, however, after treatment. It is therefore difficult to determine to what extent the concentration of oedema is attributable to histamine H2-receptor blockade and to what extent to the reduced blood pressure. The influence of MAP on post-burn odema formation was further illustrated in two series of rats anaesthetized with Inactin an Hypnorm/Valium respectively. The results underline the importance of using the same anaesthetic throughout the experimental series.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002056:Burns / Q000150:complications*; D002199:Capillary Permeability / Q000187:drug effects; D002374:Catalase / Q000494:pharmacology*; D002927:Cimetidine / Q000494:pharmacology*; D004487:Edema / Q000201:enzymology / Q000209:etiology / Q000503:physiopathology*; D006146:Guanidines / Q000494:pharmacology*; D006854:Hydrocortisone / Q000494:pharmacology*; D008297:Male; D009504:Neutrophils / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D013482:Superoxide Dismutase / Q000494:pharmacology*
D006146:Guanidines; D002927:Cimetidine; D002374:Catalase; D013482:Superoxide Dismutase; D006854:Hydrocortisone