EFFECT OF MAGNESIUM IN CARDIOPLEGIC SOLUTION UPON HYPOTHERMIC ISCHEMIC MYOCARDIAL MITOCHONDRIA

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Twelve anesthetized mongrel dogs were subjected to systemic hypothermia and potassium-induced cardioplegia for 60 minutes with or without magnesium-1-aspartate. The effect of magnesium was assessed by indices of mitochondrial oxidative phosphorylation. Cardiac arrest was induced by potassium (20 mEq per liter) (6 dogs) or potassium (20 mEq per liter)-magnesium (8 mM per liter). The heart was reperfused for ten minutes following arrest. Dogs were supported by standard cardiopulmonary bypass with hypothermia at 20°C of myocardial temperature. Mitochondria were isolated from the endocardium, the epicardium of the left ventricle and the ventricular septum. ADP : 0 ratio state 3 respiration were well maintained in both groups following 60 minutes of ischemic arrest and 10 minutes of reperfusion. Magnesium suppressed the non-phosphorylated oxygen consumption of mitochondria, therefore, respiratory control index was significantly enhanced in the group of potassium-magnesium-1-aspartate cardioplegia. These data suggest that magnesium protects functional capacity of mitochondrial phosphorylation in the myocardium from ischemia.