The relationship between ischemic contracture and no-reflow phenomenon was studied in 59 isolated rat hearts during global ischemia. The contracture was measured by a water-filled balloon catheter placed in the left ventricular lumen. The time of onset of contracture was changed by preischemic infusion with buffer containing 0.5 mmoles/l iodoacetate (IAA) in order to get early contracture, and by hypothermia which delayed the development of contracture. The first signs of contracture were noticed in normothermia (37 degrees C) at 11 minutes, in hypothermia (26 degrees C) at 25 minutes, and in the IAA-infused group at 3 minutes. The completion of contracture occurred in these groups at 25, 90 and 11 minutes, respectively. The myocardial perfusability was tested at the pre- and postcontracture state by infusing 0.1% fluorescein in isotonic saline into the cannulated aortic root. The myocardial area perfused with fluorescein was quantified in colour photographs taken under ultraviolet light of frozen whole-heart sections. The myocardial perfusion - expressed ad percent of myocardial area - was 99% at the precontracture state in normothermia, 95% in hypothermia and 100% in the IAA-infused group. At the postcontracture state, the myocardial perfusion in these groups was 80, 56 and 18%, respectively. It was concluded that the no-reflow phenomenon in isolated rat heart is closely associated with the development of myocardial contracture during global ischemia.