Document Detail


Hemorrhage activates myocardial NFkappaB and increases TNF-alpha in the heart.
MedLine Citation:
PMID:  9344778     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The heart is a tumor necrosis factor (TNFalpha) producing organ. Locally (v systemically)-produced TNFalpha likely contributes to myocardial dysfunction via direct suppression of myocardial contractile function, the induction of myocardial apoptosis, and the genesis of cardiac hypertrophy. Although recent studies have demonstrated increased myocardial TNFalpha following endotoxemia, it remains unknown whether shock, in the absence of sepsis, activates myocardial nuclear factor kappa B (NFkappaB, a TNFalpha transcription factor) and/or increases TNFalpha in the heart. To study this, rats were hemorrhaged and resuscitated, after which hearts were harvested and analysed for evidence of NFkappaB activation (electrophoretic mobility shift assay) and assayed for TNFalpha levels. Hemorrhage and resuscitation activated NFkappaB and resulted in a dramatic increase in myocardial TNFalpha. This study constitutes the initial demonstration that hemorrhagic shock activates the signaling mechanisms which culminate in increased myocardial TNFalpha. Indeed, this may have important clinical implications, since hemorrhage is a frequent complication of both iatrogenic and accidental trauma, as well as a potent instigator of multiple organ failure.
Authors:
D R Meldrum; R Shenkar; B C Sheridan; B S Cain; E Abraham; A H Harken
Related Documents :
17215988 - Iatrogenic cardiac herniation and torsion after surgery for a penetrating cardiac injury.
18256728 - Molecular events in the cardiomyopathy of sepsis.
7595968 - Transient severe myocardial ischemia during septic shock in a young woman with aids.
5101778 - Left ventricular function in acute myocardial infarction.
9468068 - Benefit of early sustained reperfusion in patients with prior myocardial infarction (th...
21679198 - Twelve hours of sustained ventricular fibrillation supported by a continuous-flow left ...
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  29     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1997 Oct 
Date Detail:
Created Date:  1998-02-03     Completed Date:  1998-02-03     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  2849-54     Citation Subset:  IM    
Copyright Information:
Copyright 1997 Academic Press Limited.
Affiliation:
Department of Surgery, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Heart
Hemorrhage / metabolism*
Male
Myocardium / metabolism*
NF-kappa B / metabolism*
Rats
Rats, Sprague-Dawley
Tumor Necrosis Factor-alpha / metabolism*
Grant Support
ID/Acronym/Agency:
GM-08315/GM/NIGMS NIH HHS; HL-43696/HL/NHLBI NIH HHS; HL-44186/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/NF-kappa B; 0/Tumor Necrosis Factor-alpha

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


Previous Document:  Hypertrophy decreases cardiac KATP channel responsiveness to exogenous and locally generated (glycol...
Next Document:  Myocardial oxygen tension in isolated erythrocyte-perfused rat hearts and comparison with crystalloi...