MYOCARDIAL LOSS OF GLUTAMATE AFTER COLD CHEMICAL CARDIOPLEGIA AND STORAGE IN ISOLATED BLOOD-PERFUSED PIG HEARTS

Metabolic adaptation of the ischemic human heart includes release of l actate, augmented uptake of glucose and glutamate, together with incre ased release of citrate and alanine. In the present study exchanges of these metabolites were examined in relation to left ventricular funct ion (LVF) in pig hearts during reperfusion after hypothermic cardiople gic-induced global ischemia and storage.Three groups of pig hearts wer e studied. Group I consisted of 11 hearts subjected to 9 minutes of wa rm ischemia prior to cold chemical cardioplegia with Bretschneider's c ardioplegic solution (CCC), and hypothermic storage (HS), for a total of 180 minutes. Groups II and III, 8 hearts in each, were subjected to 90 and 180 minutes of CCC and HS, without precardioplegic warm ischem ia. All hearts were reperfused in an isolated blood-perfused Langendor ff model. Myocardial oxygen uptake and LVF were two-fold depressed in Group I compared to Groups II and III during the first 25 minutes of r eperfusion. An increased uptake of glucose (p < 0.05) and augmented re lease of lactate (p < 0.01) and citrate (p < 0.001) were found during the reperfusion period in the hearts subjected to precardioplegic warm ischemia, indicating an increased total ischemic burden compared to G roups II and III. No significant changes in LVF or myocardial metaboli sm were noted between Groups II and III during reperfusion. In all thr ee heart groups a substantial release or loss of glutamate was found a t start of reperfusion, although in the preischemic state prior to car dioplegia pig hearts were found to extract glutamate from the circulat ion to an extent similar to that of the human heart. The mechanism und erlying the documented loss of glutamate is unknown. Myocardial loss o f glutamate may be a major cause why glutamate-enrichment during reper fusion improves recovery of hearts subjected to cardioplegia.