Endogenous nickel release as a possible cause of coronary vasoconstriction and myocardial injury in acute burn of rats.
The aim of the present study was to test the hypothesis that endogenous nickel release may play a role in myocardial depression in the acute phase of burn shock in rats. Serum nickel concentration (Se-Ni) measured by atomic absorption spectrophotometry, the sensitivity of isolated perfused hearts to exogenous nickel chloride (0.01 mumol/l), and ultrastructural myocardial alterations, as well as subcellular localization of endogenous Ni by the dimethylglyoxim method, were analyzed in the first week after standardized third-degree full thickness skin thermal burn covering 20-25% of the body surface. In the first 2 days after burn a significant fivefold increase of Se-Ni concentration was observed which leveled off by the end of the first postburn week. The coronary vascular resistance increasing effect of exogenous NiCl2 grew significantly in the first 3 h after burn, decreased to control in the 2nd postburn day, and increased again in the second half of the week after burn. Both ultrastructural damages and nickel containing reaction products could be observed in the myocardium 7 days after burn. The experimental results suggest that endogenous nickel release may play a role in coronary vasospasm and consequent myocardial depression in the acute phase of burn shock in the rat.
D000208:Acute Disease; D000818:Animals; D002056:Burns / Q000150:complications*; D009202:Cardiomyopathies / Q000209:etiology; D003329:Coronary Vasospasm / Q000209:etiology*; D005260:Female; D006321:Heart / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000648:ultrastructure; D009532:Nickel / Q000009:adverse effects* / Q000097:blood / Q000378:metabolism*; D051381:Rats; D012774:Shock, Traumatic / Q000150:complications*
D009532:Nickel