Document Detail

Correlation between cytosolic free calcium, contracture, ATP, and irreversible ischemic injury in perfused rat heart.
MedLine Citation:
PMID:  2295135     Owner:  NLM     Status:  MEDLINE    
The relations between ATP depletion, increased cytosolic free calcium concentration [( Cai]), contracture development, and lethal myocardial ischemic injury, as evaluated by enzyme release, were examined using 19F nuclear magnetic resonance to measure [Cai] in 1,2-bis(2-amino-5-fluorophenoxy)ethane-N,N,N',N'-tetraacetic acid (5F-BAPTA)-loaded perfused rat hearts. Total ischemia at 37 degrees C was induced in beating hearts, potassium-arrested hearts, magnesium-arrested hearts, and hearts pretreated with 0.9 microM diltiazem to reduce but not abolish contractility. In the beating hearts, time-averaged [Cai], which is intermediate between the systolic and the basal [Cai], was 544 +/- 74 nM. In contrast, in the potassium- and magnesium-arrested hearts, the time-averaged values are lower than in beating hearts (352 +/- 88 nM for potassium arrest, 143 +/- 22 nM for magnesium arrest). During ischemia, ATP depletion, contracture, and a rise in [Cai] are delayed by cardiac arrest, but all occur more rapidly in the potassium-arrested hearts than in the magnesium-arrested hearts. The diltiazem-treated hearts were generally similar to the magnesium-arrested hearts in their response to ischemia. Under all conditions, contracture development was initiated after tissue ATP had fallen to less than 50% of control; invariably, there was a progressive rise in [Cai] during and following contracture development. Reperfusion with oxygenated perfusate shortly after peak contracture development resulted in a return of [Cai] to its preischemic level, resynthesis of creatine phosphate, no significant enzyme release, and no substantial loss of 5F-BAPTA from the heart. The data demonstrate that an increase in [Cai] precedes lethal myocardial ischemic injury. This rise in [Cai] may accelerate the depletion of cellular ATP and may directly contribute to the development of lethal ischemic cell injury.
C Steenbergen; E Murphy; J A Watts; R E London
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation research     Volume:  66     ISSN:  0009-7330     ISO Abbreviation:  Circ. Res.     Publication Date:  1990 Jan 
Date Detail:
Created Date:  1990-02-15     Completed Date:  1990-02-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  135-46     Citation Subset:  IM    
Department of Pathology, Duke University Medical Center, Durham, North Carolina.
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MeSH Terms
Adenosine Triphosphate / analysis*
Calcium / analysis*
Coronary Disease / metabolism*
Cytosol / analysis*
Heart Arrest, Induced
Magnetic Resonance Spectroscopy
Models, Cardiovascular
Myocardial Contraction*
Myocardial Reperfusion
Grant Support
Reg. No./Substance:
56-65-5/Adenosine Triphosphate; 7440-70-2/Calcium

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