Redistribution of myocardial calcium during ischemia. Relationship to onset of contracture.
Cytosolic calcium accumulation has been proposed as a mediator for the pathologic changes that occur during myocardial ischemia. Whether the rise in cytosolic calcium is a result of influx or redistribution from internal stores has not been elucidated. Isolated retroperfused rabbit hearts were subjected to ischemia at 37 degrees C. The distribution of calcium between cytosol and internal membrane stores and the relationship between cytosolic calcium and the onset of left ventricular contracture were investigated. One group of hearts was loaded with the fluorescent calcium probe Fura 2-AM to measure cytosolic calcium and a second group with chlortetracycline to indicate changes in membrane-bound calcium. After the onset of ischemia there is a rise in cytosolic calcium, at least in part attributable to redistribution of calcium from intraorganellar sites to cytosol. The release of membrane-bound calcium and rise in cytosolic calcium preceded the onset of irreversible ischemic injury, that is, contracture.
Department of Surgery, New England Deaconess Hospital, Boston, Mass.
E
E
Jimenez
P
P
del Nido
H
H
Feinberg
S
S
Levitsky
D000818:Animals; D002118:Calcium / Q000032:analysis / Q000378:metabolism*; D000252:Calcium-Transporting ATPases; D003600:Cytosol / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism*; D011817:Rabbits
D000252:Calcium-Transporting ATPases; D002118:Calcium