Document Detail


Does the heart fail in endotoxin shock?
MedLine Citation:
PMID:  2406036     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Evidence for a major participatory role of the myocardium in the hemodynamic response to endotoxemia and sepsis has been controversial. Early interpretations about in situ changes in cardiac performance during shock were confounded by the concomitant influence of uncontrolled pathophysiologic adjustments in cardioactive variables such as preload, afterload, sympathoadrenal discharge, left ventricular diastolic compliance (stiffness), and in some studies myocardial hypoperfusion/ischemia. Despite such complexities, many recent studies with intact subjects and isolated preparations consistently point toward a relatively early involvement of myocardial dysfunction in circulatory shock syndromes associated with gram-negative bacteria and sepsis. The cardiac dysfunction cannot be accounted for by a direct toxic effect of the endotoxin molecule itself on cardiac myocytes. Rather, evidence is compelling that endotoxin interacts first with other types of cellular or tissue elements. The latter evoke biologic reactions through some unknown pathway culminating in deleterious effects in the heart. Discovery of the casual mechanism(s) responsible for myocardial sequelae of endotoxemia and sepsis remains a key objective in experimental and clinical research in circulatory shock pathogenesis.
Authors:
F L Abel
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Circulatory shock     Volume:  30     ISSN:  0092-6213     ISO Abbreviation:  Circ. Shock     Publication Date:  1990 Jan 
Date Detail:
Created Date:  1990-03-19     Completed Date:  1990-03-19     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0414112     Medline TA:  Circ Shock     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  5-13     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of South Carolina School of Medicine, Columbia 29208.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiac Output, Low / etiology*,  physiopathology
Dogs
Endotoxins
Guinea Pigs
Heart / physiopathology*
Hemodynamics / physiology
Rabbits
Rats
Shock, Septic / complications*,  physiopathology
Swine
Chemical
Reg. No./Substance:
0/Endotoxins

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


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