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.