Document Detail


The effect of hyperdynamic sepsis on myocardial performance.
MedLine Citation:
PMID:  3995694     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The reviewed studies support the contention that during the high flow or hyperdynamic phase of gram-negative septicemia, cardiac reserve is compromised because of intrinsic myocardial dysfunction. The latter is not referable to coronary hypoperfusion or peripheral pooling or decreased venous return. Although, under resting, nonstressed conditions, indices of myocardial function may appear normal or even elevated, a decreased reserve is evident when additional stress is imposed on the myocardium. Hearts removed from septic rats during the hyperdynamic stage and perfused in vitro (using the isolated perfused working heart preparation) showed a rightward and downward shift in work function curves, indicating a severe depression in cardiac function. Possible mechanisms for the observed dysfunction are discussed. No significant alterations in high energy phosphate production or substrate utilization were observed, indicating that altered myocardial metabolism is not likely to be a significant contributor to the dysfunction. Our results suggest that cardiac dysfunction is partially due to an elevation in the cytosolic calcium concentration which may slow the rate of ventricular relaxation. These studies emphasize that intrinsic cardiac function is depressed early during the course of the septic episode at a time that precedes the onset of circulatory shock.
Authors:
K H McDonough; C H Lang; J J Spitzer
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulatory shock     Volume:  15     ISSN:  0092-6213     ISO Abbreviation:  Circ. Shock     Publication Date:  1985  
Date Detail:
Created Date:  1985-07-12     Completed Date:  1985-07-12     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0414112     Medline TA:  Circ Shock     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  247-59     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / metabolism
Cardiac Output
Contractile Proteins / metabolism
Coronary Circulation*
Energy Metabolism
Heart Ventricles / physiopathology
Hemodynamics*
Homeostasis
Myocardial Contraction*
Myocardium / metabolism
Rats
Shock, Septic / physiopathology*
Grant Support
ID/Acronym/Agency:
HL07098/HL/NHLBI NIH HHS; HL23157/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Contractile Proteins; 7440-70-2/Calcium

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


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