Document Detail

The role of accumulation of sodium and calcium on contractile failure of the hypoxic/reoxygenated heart.
MedLine Citation:
PMID:  8632618     Owner:  NLM     Status:  MEDLINE    
The present study was undertaken to determine whether myocardial energy or ion levels are related to oxygen-replenishment-induced recovery of cardiac contractile force after hypoxia. Isolated rat hearts were perfused for 3 to 40 min under hypoxic conditions, followed by 45 min of reoxygenation. Hypoxia induced a cessation of cardiac contractile force, a rise in resting tension, a decrease in high energy phosphates, and an increase in lactate. Myocardial ATP, creatine phosphate (CP) and lactate reached steady-state levels after 15, 10 and 5 min of hypoxia, respectively. Hypoxic conditions in the present study also caused an increase in sodium content and a decrease in potassium content, but not changes in calcium content, along with a prolonged hypoxic period. When the hearts were perfused for more than 25 min under hypoxic conditions, no recovery of contractile force was observed following 45-min of reoxygenation. Hypoxic perfusion for more than 25 min induced an accumulation of tissue sodium content approximately 3 fold higher than the pre-hypoxic value at the end of hypoxia, and also induced a marked increase in myocardial calcium content upon reoxygenation. When tissue sodium content accumulated by less than 300% of the pre-hypoxic value, cardiac contractile function was partially reversed by reoxygenation and calcium-overload was not observed. The recovery of post-hypoxic cardiac contractility correlated with tissue sodium content during hypoxia rather than with myocardial high energy phosphate content at the end of hypoxia. These results suggest that accumulation of tissue sodium content in the hypoxic myocardium and calcium content in the reoxygenated myocardium may be indicative of hypoxia/reoxygenation-induced cardiac contractile failure.
K Tanonaka; T Niwa; S Takeo
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Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Japanese heart journal     Volume:  37     ISSN:  0021-4868     ISO Abbreviation:  Jpn Heart J     Publication Date:  1996 Jan 
Date Detail:
Created Date:  1996-06-28     Completed Date:  1996-06-28     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0401175     Medline TA:  Jpn Heart J     Country:  JAPAN    
Other Details:
Languages:  eng     Pagination:  105-17     Citation Subset:  IM    
Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Japan.
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MeSH Terms
Adenosine Triphosphate / metabolism
Anoxia / metabolism*
Calcium / metabolism*
Cell Membrane Permeability
Energy Metabolism
Ion Channels / metabolism
Lactates / metabolism
Lactic Acid
Myocardial Contraction / physiology*
Myocardium / metabolism*
Phosphates / metabolism
Phosphocreatine / metabolism
Rats, Wistar
Sodium / metabolism*
Reg. No./Substance:
0/Ion Channels; 0/Lactates; 0/Phosphates; 50-21-5/Lactic Acid; 56-65-5/Adenosine Triphosphate; 67-07-2/Phosphocreatine; 7440-23-5/Sodium; 7440-70-2/Calcium

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

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