In prior studies from this laboratory to determine the mechanisms whereby hypertrophied myocardium is more sensitive to ischemic injury than normal myocardium, it was demonstrated that hypertrophied rat hearts have lower basal high-energy phosphate levels and develop ischemic contracture sooner than normal myocardium. The purposes of this study were (1) to determine if the decrease in myocardial adenosine triphosphate (ATP) was associated with the increased rate of ischemic contracture and (2) to determine if arrest and perfusion of hypertrophied myocardium prior to the ischemic interval would allow recovery of high-energy phosphate stores and improve tolerance to ischemia. ATP levels were measured in isolated normal and hypertrophied rat hearts during (1) control nonworking Langendorff perfusion, (2)2 minutes of potassium chloride-arrested perfusion (30 mEq/L), or (3) 15 minutes of potassium chloride-arrested perfusion (30 mEq/L). Both groups were then made globally ischemic (37 degrees C) and the time to ischemic contracture recorded. Hypertrophied hearts were produced by permanent banding of the ascending aorta and confirmed by left ventricular (mg) body weight (gm) ratios (normal, 1.95 wet, p less than 0.05). After 2 minutes of mechanical arrest the time to ischemic contracture was increased 75% +/- 10% in normal and 44% +/- 4% in hypertrophied hearts. After 15 minutes of mechanical arrest with perfusion, hypertrophied myocardium re-established normal ATP levels and increased its time to ischemic contracture by 130% +/- 7%. These studies suggest that during potassium chloride arrest, additional preischemic metabolic recovery is possible by hypertrophied myocardium and leads to increased tolerance to ischemia beyond that accomplished by cessation of mechanical activity alone. This effect is seen only to a minor degree in normal myocardium.