Effects of low extracellular calcium on cytosolic calcium and ischemic contracture.
We have shown that myocardial cytosolic calcium [Cai] rises during ischemia. Simultaneously membrane bound stores are depleted. The [Cai] rise precedes the onset of irreversible ischemic contracture. We found that a low extracellular calcium [Cao] (100 microM) perfusate decreased peak contracture pressure and delayed the time to onset and to peak of ischemic contracture in the isolated retroperfused rabbit heart subjected to 37 degrees C ischemia. [Cai] was measured with the intracellular [Cai] fluorescent indicator Fura-2 AM (10 microM) in a separate group. In the group exposed to 2.45 mM Ca2+ there was a significant rise (P less than 0.05) in [Cai] to above 50% of preischemic value after 30 min of ischemia. The [Cai] in the low [Cao] perfused group at 30 min of ischemia was 30% below the preischemic value. The peak of the [Cai] rise in the low [Cao] perfusate group was markedly attenuated and delayed to 40 min. Taken together it appears that low calcium perfusate (100 microM) prior to ischemia attenuates the ischemia-induced [Cai] rise, delays the onset, and decreases the force of contracture with irreversible ischemic injury.
Department of Surgery, University of Illinois, Chicago.
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Jimenez
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del Nido
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Sarin
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Nakamura
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Feinberg
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Levitsky
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000008:administration & dosage* / Q000378:metabolism; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D003600:Cytosol / Q000378:metabolism*; D009200:Myocardial Contraction; D011817:Rabbits; D013050:Spectrometry, Fluorescence
D000255:Adenosine Triphosphate; D002118:Calcium