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ARTICLES

Correlation between cytosolic free calcium, contracture, ATP, and irreversible ischemic injury in perfused rat heart.

C Steenbergen, E Murphy, J A Watts, R E London
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https://doi.org/10.1161/01.RES.66.1.135
Circulation Research. 1990;66:135-146
Originally published January 1, 1990
C Steenbergen
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E Murphy
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J A Watts
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R E London
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Abstract

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.

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Circulation Research
January 1, 1990, Volume 66, Issue 1
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    Correlation between cytosolic free calcium, contracture, ATP, and irreversible ischemic injury in perfused rat heart.
    C Steenbergen, E Murphy, J A Watts and R E London
    Circulation Research. 1990;66:135-146, originally published January 1, 1990
    https://doi.org/10.1161/01.RES.66.1.135

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    Correlation between cytosolic free calcium, contracture, ATP, and irreversible ischemic injury in perfused rat heart.
    C Steenbergen, E Murphy, J A Watts and R E London
    Circulation Research. 1990;66:135-146, originally published January 1, 1990
    https://doi.org/10.1161/01.RES.66.1.135
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