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

Abstract

To evaluate the roles of ischemia and hypoxia in the development of post-burn cardiac shock and its molecular pathogenesis. 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 24h 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-kappaB (nuclear factor kappa B) activity, MPO (myeloperoxidase), TNFalpha (tumor necrosis factor alpha) mRNA expression and levels of myocardial TNFalpha were measured. Myocardial microvascular permeability began to rise at 1h post-burn and was still rising at 24h (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-kappaB activity and TNFalpha mRNA expression were significantly promoted; elevation of levels of myocardial TNFalpha and MPO activity occurred; cardiac mechanic parameters including LVSP, +/-dp/dt max significantly decreased while LVEDP increased. The findings of the present study suggest severe myocardial damage due to ischemia and hypoxia following burns; promotion of myocardial NF-kappaB activity and TNFalpha mRNA expression in myocardium may be an important factor in the development of post-burn cardiac shock.