Document Detail


The effect of hypodynamic endotoxin shock on myocardial high energy phosphates in the rat.
MedLine Citation:
PMID:  2686834     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
High energy phosphate concentrations were determined in the isolated perfused (in vitro) and intact (in situ) heart preparations in the rat during a control period and at various time intervals (1,2,4,8 or 16 h) following the intraperitoneal injection of 4 mg.kg-1 E coli endotoxin. Arterial glucose and lactate concentrations were determined just prior to excising the hearts. Following the induction of endotoxin shock, myocardial ATP and creatine phosphate decreased in both the in situ and in vitro preparations, while AMP increased only in the in situ group. There was no significant alteration in ADP in either group throughout the 16 h experimental period. Myocardial energy charge decreased at 1 h following endotoxin shock and remained depressed throughout the 16 h study period. Total heart weights as well as the wet/dry ratio were unaltered throughout the experiment. The reductions in ATP and creatine phosphate during endotoxin shock were a direct result of the shock state and not due to the loss of myocardial mass or the presence of oedema. One hour following the induction of endotoxin shock plasma glucose increased then returned to the control value by 2 h and remained at the pre-endotoxin level throughout the experimental protocol. Arterial lactate concentration increased following endotoxin administration and remained elevated until 16 h, where it was not different from the control value. Data from the present study clearly indicate a myocardial energy deficit during acute hypodynamic endotoxin shock in the rat and may provide a mechanism for the cardiac dysfunction normally associated with this shock paradigm.
Authors:
R M Raymond; J Gordey
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cardiovascular research     Volume:  23     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  1989 Mar 
Date Detail:
Created Date:  1990-01-17     Completed Date:  1990-01-17     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  200-4     Citation Subset:  IM    
Affiliation:
Department of Surgery, Loyola University, Stritch School of Medicine, Maywood, Illinois.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Monophosphate / metabolism
Adenosine Triphosphate / metabolism
Animals
Endotoxins / pharmacology
Escherichia coli*
Heart / drug effects
Myocardium / metabolism*
Perfusion
Phosphates / metabolism*
Phosphocreatine / metabolism
Rats
Rats, Inbred Strains
Shock, Septic / metabolism*
Grant Support
ID/Acronym/Agency:
HL-31163/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Endotoxins; 0/Phosphates; 56-65-5/Adenosine Triphosphate; 61-19-8/Adenosine Monophosphate; 67-07-2/Phosphocreatine

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


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