Contractile activity and reperfusion-induced calcium gain after ischemia in the isolated rat heart.

Reperfusion of cardiac muscle after an ischemic episode results in the cells becoming overloaded with Ca2+. Gross ultrastructural changes, including the formation of contraction bands, also occur. The present study investigates the relationship, if any, between contractile activity during reperfusion and Ca2+ gain. Contractile activity was inhibited with 2,3-butanedione monoxime (BDM). Isolated perfused rat hearts were subjected to 30 minutes ischemia before reperfusion in the presence or absence of BDM. BDM (10 MIN) significantly reduced the Ca2+ gained during reperfusion. It also enhanced the ATP and creatine phosphate supplies. Ultrastructural examination of cells from hearts reperfused in the presence of BDM for 30 minutes revealed cells with relaxed myofibrils, some glycogen and intact sarcolemmal membranes, compared with cells from hearts reperfused in the absence of BDM which showed contraction bands, sarcolemmal discontinuities and swollen mitochondria. The 'protection' afforded by BDM did not result in a restoration of the cells to their normal state. Removal of BDM and continued reperfusion with Krebs-Henseleit buffer resulted in a gain in Ca2+ and ultrastructural damage, including contraction band formation. These findings suggest a role for contractile activity in the Ca2+ gain. However, preventing the damage which occurs as a result of contractile activity is not sufficient to restore the cells to their preischemic state. This suggests that the damage caused as a result of contractile activity is secondary to some other primary deleterious event.