Effect of magnesium in cardioplegic solution upon hypothermic ischemic myocardial mitochondria.

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Abstract
Twelve anesthetized mongrel dogs were subjected to systemic hypothermia and K-induced cardioplegia for 60 min with or without magnesium-1-aspartate. The effect of Mg was assessed by indices of mitochondrial oxidative phosphorylation. Cardiac arrest was induced by K (20 meq/l) (6 dogs) or K (20 meq/l)-Mg (8 mM/l). The heart was reperfused for 10 min following arrest. Dogs were supported by standard cardiopulmonary bypass with hypothermia at 20.degree. C of myocardial temperature. Mitochondria were isolated from the endocardium, the epicardium of the left ventricle and the ventricular septum. ADP:0 ratio and state 3 respiration were well maintained in both groups following 60 min of ischemic arrest and 10 min of reperfusion. Mg suppressed the non-phosphorylated O2 consumption of mitochondria; respiratory control index was significantly enhanced in the group of potassium-magnesium-1-aspartate cardioplegia. Mg apparently protects functional capacity of mitochondrial phosphorylation in the myocardium from ischemia.