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.