Pathogenesis of early cardiac myocyte damage after severe burns

Background: The importance of early cardiac myocyte damage during postburn trauma has been emphasized in recent years. However, its pathogenesis, prev ention, and treatment have not been fully clarified, The aim of this study is to define its pathogenesis. Methods: Rats with 30% third-degree burns were used. Cardiac biochemical ma rkers reflecting cardiac myocyte damage including troponin T, cardiac myosi n light chain I, creatinine kinase and its cardiac-specific isoenzyme compo und, as web as inflammatory mediators such as tumor necrosis factor, endoth elin/nitric oxide ratio, malondialdehyde, and superoxide dismutase, were de termined. Results: Cardiac biochemical markers reflecting cardiac myocyte damage, inc luding troponin T, cardiac myosin light chain 1, cardiac-specific isoenzyme compound, were all significantly elevated between 3 hours and 24 hours aft er burn. Changes in tumor necrosis factor, endothelin/nitric oxide ratio, a nd malondialdehyde were similar to those of cardiac biochemical markers. In contrast, levels of superoxide dismutase declined markedly after burn. Conclusion: The findings of this study shelved that considerable amounts of myocardial constructive protein degradation and release due to destruction of cardiac myocytes occurred early after severe burns. The inflammatory me diators released after burn injury may be involved in the pathogenesis of m yocardial destruction.