Document Detail


A burning issue: do sepsis and systemic inflammatory response syndrome (SIRS) directly contribute to cardiac dysfunction?
MedLine Citation:
PMID:  16146710     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Heart disease is among the leading causes of death in all populations. Cardiac dysfunctions are major complications in patients with advanced viral or bacterial infection, severe trauma and burns accompanied with multiple organ failure - collectively known as systemic inflammatory response syndrome (SIRS). SIRS, which is often subsequent to sepsis, is clinically featured by hypotension, tachypnea, hypo- or hyperthermia, leukocytosis and myocardial dysfunction. The striking association between inflammation and cardiac dysfunction not only prognoses likelihood of survival in patients with SIRS but also prompts the necessity of understanding the pathophysiology of cardiac dysfunction in SIRS, so that effective therapeutic regimen may be identified. Compelling evidence has shown significant and independent link among inflammation, sepsis, insulin resistance and cardiac dysfunction. Several cytokine signaling molecules have been speculated to play important roles in the onset of cardiac dysfunction under SIRS including endothelin-1 and toll-like receptor. Involvement of these pathways in cardiac dysfunction has been convincingly validated with transgenic studies. Nevertheless, the precise mechanism of action underscoring inflammation-induced cardiac contractile dysfunction is far from being clear. Given the substantial impact of inflammation and SIRS on health care, ecosystems and national economy, it is imperative to understand the cellular mechanisms responsible for cardiac contractile dysfunction under inflammation and sepsis so that new and effective therapeutic strategy against such devastating heart problems may be developed.
Authors:
Jun Ren; Shan Wu
Publication Detail:
Type:  Journal Article; Review     Date:  2006-01-01
Journal Detail:
Title:  Frontiers in bioscience : a journal and virtual library     Volume:  11     ISSN:  1093-4715     ISO Abbreviation:  Front. Biosci.     Publication Date:  2006  
Date Detail:
Created Date:  2005-09-08     Completed Date:  2006-06-02     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9709506     Medline TA:  Front Biosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  15-22     Citation Subset:  IM    
Affiliation:
Division of Pharmaceutical Sciences, Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY 82071, USA. jren@uwyo.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Biopterin / analogs & derivatives,  metabolism
Cytokines / metabolism
Diabetes Mellitus / metabolism
Endothelin-1 / metabolism
Heart Diseases / pathology
Humans
Inflammation / complications*,  pathology*
Insulin Resistance*
Myocardium / pathology*
Nitric Oxide / chemistry
Sepsis / complications*,  pathology*
Shock, Septic
Systemic Inflammatory Response Syndrome / metabolism,  pathology*
Toll-Like Receptors / metabolism
Chemical
Reg. No./Substance:
0/Cytokines; 0/Endothelin-1; 0/Toll-Like Receptors; 10102-43-9/Nitric Oxide; 17528-72-2/5,6,7,8-tetrahydrobiopterin; 22150-76-1/Biopterin

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


Previous Document:  Immunotherapy as part of a multidisciplinary approach to melanoma treatment.
Next Document:  Sepsis-induced myocardial dysfunction and myocardial protection from ischemia/reperfusion injury.