Roles of ischemia and hypoxia and the molecular pathogenesis of post-burn cardiac shock

Objective: To evaluate the roles of ischemia and hypoxia in the development of post-burn cardiac shock and its molecular pathogenesis. Methods: One hundred and fifty healthy adult Wistar rats were divided into the control group and burn group inflicted with 30% total body surface area third degree burn. Groups were processed at 1, 3, 6, 12 and 24 h post-burn. Myocardial contractile function, myocardial microvascular permeability, volume of regional myocardial blood flow, levels of myocardial myosin light chain 1 (CM-LC1), myocardial NF-κB (nuclear factor kappa B) activity, MPO (myeloperoxidase), TNFα (tumor necrosis factor α) mRNA expression and levels of myocardial TNFα were measured. Main results: Myocardial microvascular permeability began to rise at 1 h post-burn and was still rising at 24 h (2.1 times as high as that of the control group); the volume of regional myocardial blood flow fell significantly and remained at a level markedly lower than that in the control group; CM-LC1 also rose significantly and reached a level 18.6 times as high as that in the control group; myocardial NF-κB activity and TNFα mRNA expression were significantly promoted; elevation of levels of myocardial TNFα and MPO activity occurred; cardiac mechanic parameters including LVSP, ±dp/dt max significantly decreased while LVEDP increased. Conclusion: The findings of the present study suggest severe myocardial damage due to ischemia and hypoxia following burns; promotion of myocardial NF-κB activity and TNFα mRNA expression in myocardium may be an important factor in the development of post-burn cardiac shock.