Document Detail


Myocardial function in sepsis and endotoxin shock.
MedLine Citation:
PMID:  2690645     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Myocardial function in sepsis and endotoxin shock is reviewed. Clinical, whole animal, and isolated tissue studies are compared to answer the question whether sepsis and/or endotoxin directly damage the myocardium. Myocardial performance is considered relative to control of preload, afterload, and heart rate. Despite the fact that these vary widely in different studies, there is overwhelming evidence that myocardial performance is depressed in both sepsis and endotoxin shock. The depression is dose related, occurs early after large doses of endotoxin but may follow a hyperdynamic phase in sepsis or after low doses of endotoxin. Endotoxin itself does not appear to be the depressant factor; the final depressant substance(s) is unknown. Calcium transport by the sarcoplasmic reticulum is depressed. This defect is more prominent in the endocardium than in the epicardium. Myocardial adenosinetriphosphatase (ATPase) and norepinephrine stores may be depleted. The septic myocardium has an increased dependence on sympathetic nerve stimulation. There is little evidence that the cause of the myocardial depression is an inadequate coronary blood flow.
Authors:
F L Abel
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  The American journal of physiology     Volume:  257     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1989 Dec 
Date Detail:
Created Date:  1990-02-02     Completed Date:  1990-02-02     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  R1265-81     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
Heart / physiopathology*
Hemodynamics
Humans
Shock, Septic / physiopathology*

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