Yuesheng Huang1, Zhiqing Li, Zongcheng Yang. 1. Institute of Burn Research, Southwestern Hospital, Third Military Medical University, 400038, Chongqing, PR China. yshuang@public.cta.cq.cn
Abstract
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 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. MAIN RESULTS: 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. CONCLUSION: 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.
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 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. MAIN RESULTS: 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. CONCLUSION: 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.
Authors: Wenjing Xu; Tomasa Barrientos; Lan Mao; Howard A Rockman; Anthony A Sauve; Nancy C Andrews Journal: Cell Rep Date: 2015-10-08 Impact factor: 9.423