[Myocardial metabolism during the pre-ischemic administration of metabolic myocardial protection in coronary surgical patients].

Metabolic myocardial preservation by means of preischemic insulin administration (glucose-potassium-insulin, GPI; acute parenteral alimentation, APA) with the aim of a preischemic myocardial glycogen enrichment was performed in 20 consecutive CABG patients (12 in the APA group, 8 in the control group). Before and after 30 min of an infusion (APA or 0.9% NaCl solution), blood levels of potassium, glucose, NEFA (non-esterified fatty acids) and lactate were determined from arterial (a), central venous (cv) and coronary sinus (cs) blood. The cs potassium level in the APA group decreased from 4.06 to 3.56 mmol/l, whereas in the control group an increase from 3.78 to 4.36 mmol/l occurred. The difference between the two groups (interaction) was significant, p less than 0.002. The myocardial glucose extraction (a-cs difference) in the APA group increased from 3.83 to 10.08 mg/dl, whereas in the control group a change from 3.37 to 0.87 mg/dl occurred (p less than 0.0003). The myocardial NEFA (non-esterified fatty acids) extraction in the APA group decreased from 0.25 to -0.06 mmol/l, whereas in the control group no change (0.08 to 0.13 mmol/l) occurred (p less than 0.05). The myocardial lactate extraction in the APA group increased from 0.13 to 0.70 mmol/l, whereas in the control group no change occurred (0.47 to 0.51 mmol/l), interaction p less than 0.0001. It is concluded that a preischemic insulin administration (APA) for metabolic preservation leads to: (1) myocardial potassium extraction, obviously caused by intracellular potassium shifting; (2) increased myocardial glucose extraction; (3) decreased myocardial NEFA extraction, the last two obviously caused by a shift of the myocardial metabolism from predominant lipolysis to predominantly glycolysis; and (4) surprisingly, increased myocardial lactate extraction (decreased lactate production), obviously caused by the avoidance of a myocardial lactate accumulation by way of stimulated pyruvate oxidation. Increased anaerobically, available ATP without myocardial lactate production must be considered a metabolic contribution to myocardial protection against ischemic damage.