Reversal of myocardial ischemic contracture and the relationship to functional recovery and tissue calcium.

We subjected isolated rat hearts to normothermic ischemia until contracture developed, then reperfused them for 30 min. Recovery of developed pressure, rate of change in left ventricular pressure (dP/dt), and changes in end-diastolic pressure measured after 30 min of reperfusion were compared with preischemic values for each heart. Values after untreated ischemic arrest were compared with those after potassium arrest, potassium reperfusion (both oxygenated and deoxygenated), and combined potassium arrest and potassium reperfusion. Potassium arrest lengthened the time to the onset of contracture and thus lengthened the total ischemic time. Functional recovery was not improved over that in the untreated hearts, most likely due to this additional ischemic time. The use of buffer with a high potassium content for the first 5 min of reperfusion, however, significantly improved functional recovery if the perfusate was oxygenated, but did not improve functional recovery if the perfusate was deliberately deoxygenated. Combined potassium arrest and reperfusion delayed the onset of contracture and thus increased total ischemic time, yet improved recovery. Tissue calcium was elevated in all hearts undergoing contracture and reperfusion. Our results suggest that contracture can be reversed and that functional recovery can be improved in spite of increased tissue calcium.