A new explanation for the progressive tissue loss in electrical injuries.
A reproducible electrical injury to the hind limb was produced in rats, an injury characterized by progressive tissue necrosis. Serial histochemical examinations of cross sections with a peroxidase-antiperoxidase method revealed increased production of arachidonic acid metabolites, especially thromboxane, at distal sites near the entrance wound and in periosseous tissues more proximally. Levels of these vasoactive substances remained elevated during the time of progressive necrosis and demarcation of seemingly normal, uninjured tissue. Treatment with agents capable of blocking thromboxane production allowed tissue salvage, as evidenced by a decreased autoamputation rate and an increased total surviving length. From this study it appears that an electrical injury is thermal trauma, producing elevated levels of arachidonic acid metabolites in areas of greatest heat production. Prolonged thromboxane excess, with resultant vasoconstriction and thrombosis in the microcirculation, is seen to play a key role in the progressive tissue loss characteristic of the injury. The use of antithromboxane agents may be of benefit in halting this progression and salvaging tissue in these devastating injuries.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D002058:Burns, Electric / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D015237:Dinoprost; D015232:Dinoprostone; D007093:Imidazoles / Q000627:therapeutic use; D008297:Male; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013929:Thromboxane B2 / Q000378:metabolism
D001095:Arachidonic Acids; D007093:Imidazoles; D011458:Prostaglandins E; D011460:Prostaglandins F; D016718:Arachidonic Acid; D013929:Thromboxane B2; C029899:imidazole; D015237:Dinoprost; D015232:Dinoprostone