Cardioplegia and ischemia in the canine heart evaluated by P-31 magnetic resonance spectroscopy

Background. Warm continuous blood cardioplegia provides excellent protectio n, but must be interrupted by ischemic intervals to aid visualization. We h ypothesized that (1) as ischemia is prolonged, the reduced metabolic rate o ffered by cooling gives the advantage to hypothermic cardioplegia; and (2) prior cardioplegia mitigates the deleterious effects of normothermic ischem ia. Methods. Isolated cross-perfused canine hearts underwent cardioplegic arres t followed by 45 minutes of global ischemia at 10 degrees C or 37 degrees C , or 45 minutes of normothermic ischemia without prior cardioplegia. Left v entricular function was measured at baseline and during 2 hours of recovery . Metabolism was continuously evaluated by phosphorus-31 magnetic resonance spectroscopy. Results. Adenosine triphosphate was 71% +/- 4%, 71% +/- 7%, and 38% +/- 5% of baseline at 30 minutes, and 71% +/- 4%, 48% +/- 5%, and 39% +/- 6% at 42 minutes of ischemia in the cold ischemia, warm ischemia, and normothermic ischemia without prior cardioplegia groups, respectively. Left ventricular systolic function, left ventricular relaxation, and high-energy phosphate l evels recovered fully after cold cardioplegia and ischemia. Prior cardiople gia delayed the decline in intracellular pH during normothermic ischemia in itially by 9 minutes, and better preserved left ventricular relaxation duri ng recovery, but did not ameliorate the severe postischemic impairment of l eft ventricular systolic function, marked adenosine triphosphate depletion, and creatine phosphate increase. Left ventricular distensibility decreased in all groups. Conclusions. When cardioplegia is followed by prolonged ischemia, better pr otection is provided by hypothermia than by normothermia. Prior cardioplegi a confers little advantage on recovery after prolonged normothermic ischemi a but delays initial ischemic metabolic deterioration, which would contribu te to the safety of brief interruptions of warm cardioplegia. (Ann Thorac S urg 2000;70:197-205) (C) 2000 by The Society of Thoracic Surgeons.