Twenty-five dogs underwent 45 minutes of normothermic ischemic arrest. Fifteen minutes after unclamping, no heart could support the systemic circulation. In all dogs, we prolonged bypass for 30 minutes in the beating empty state. In 15 dogs, we reclamped the aorta for 10 minutes and further lowered oxygen demands by the continuous infusion of a 37° C blood cardioplegic solution (K + 30 mEq/L, pH 7.6, Ca ++ I mEq/L). In 10 of these dogs, we added L-glutamate (0.026M) to the blood cardioplegic solution. Coronary blood flow (microspheres), metabolism (oxygen content plus ATP), left ventricular compliance (intraventricular balloon), and left ventricular performance (balloon and Starling curves) were measured during control and at 15 and 45 minutes after unclamping. During rearrest, postischemic hearts treated with L-glutamate showed the highest oxygen uptake (2.25 cc/100 gm/min)* and the best recovery of adenosine triphosphate (ATF) (75%).* In the working state, 45 minutes after unclamping, the hearts receiving L-glutamate were better able to augment left ventricular subendocardial flow (85% versus 47%)* and oxygen uptake (108% versus 83%).* Consequently, they had greater recovery of the rate of contraction, +dP/dt (83% versus 72%),* and relaxation, —dP/dt (83% versus 71%),* and the highest stroke work index (1.20 versus 0.74 gm-m/kg).* Rearresting the postischemic heart with a blood cardioplegic solution containing L-glutamate results in nearly complete reversal of ischemic damage. We suspect that L-glutamate increases postischemic ATP production by stimulating oxidative metabolism through replenishment of Kreb cycle intermediates lost during ischemia.