Endogenous nickel release in injured patients: a possible cause of myocardial damage.
Atom absorption spectrophotometry was used for the study of serum nickel levels in 58 injured patients. From 27 autopsies an electron cytochemical examination of the myocardium was performed in 19 patients. In patients with severe burns and cerebral injury, the serum nickel content showed a significant increase in the early period after injury. In these cases direct traumatic or toxic damage to the central nervous system and, in cases of early death, cerebral oedema, were present. The ECG tracings revealed disturbances in repolarization in a large majority. Nickel-dimethylglyoxim complex precipitates were found in the myocardium of all patients who died. In addition to disorientation, increased serum nickel levels and abnormal ECG records were observed in septicaemia. On the basis of these observations and the experimental data, we suggest that one of the causes of posttraumatic myocardial damage may be endogenous nickel release as part of the homeostatic disequilibrium arising as a direct or indirect effect of the injury.
D000293:Adolescent; D000328:Adult; D000368:Aged; D001930:Brain Injuries / Q000097:blood*; D002056:Burns / Q000097:blood*; D009202:Cardiomyopathies / Q000209:etiology*; D004562:Electrocardiography; D006651:Histocytochemistry; D006801:Humans; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D009532:Nickel / Q000097:blood*; D010091:Oximes / Q000378:metabolism; D013997:Time Factors
D010091:Oximes; C013501:dimethylglyoxime; D009532:Nickel