Document Detail


Roles of ischemia and hypoxia and the molecular pathogenesis of post-burn cardiac shock.
MedLine Citation:
PMID:  14636759     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Yuesheng Huang; Zhiqing Li; Zongcheng Yang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Burns : journal of the International Society for Burn Injuries     Volume:  29     ISSN:  0305-4179     ISO Abbreviation:  Burns     Publication Date:  2003 Dec 
Date Detail:
Created Date:  2003-11-25     Completed Date:  2004-03-25     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8913178     Medline TA:  Burns     Country:  England    
Other Details:
Languages:  eng     Pagination:  828-33     Citation Subset:  IM    
Affiliation:
Institute of Burn Research, Southwestern Hospital, Third Military Medical University, 400038, Chongqing, PR China. yshuang@public.cta.cq.cn
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / complications*,  metabolism,  physiopathology
Burns / complications*,  metabolism,  physiopathology
Capillary Permeability
Coronary Circulation
Myocardial Contraction
Myocardial Ischemia / complications*,  metabolism,  physiopathology
Myocardium / metabolism
Myosin Light Chains / analysis
NF-kappa B / analysis
Peroxidase / analysis
RNA, Messenger / analysis
Rats
Rats, Wistar
Regional Blood Flow
Shock, Cardiogenic / etiology*,  metabolism,  physiopathology
Time Factors
Tumor Necrosis Factor-alpha / analysis,  genetics
Chemical
Reg. No./Substance:
0/Myosin Light Chains; 0/NF-kappa B; 0/RNA, Messenger; 0/Tumor Necrosis Factor-alpha; EC 1.11.1.7/Peroxidase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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