Effect of magnesium in cardioplegic solution upon hypothermic ischemic myocardial mitochondria.
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 degrees 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 minutes of ischemic arrest and 10 minutes of reperfusion. Magnesium suppressed the non-phosphorylated oxygen consumption of mitochondria, therefore, respiratory control index was signficantly 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.
D000818:Animals; D002315:Cardiopulmonary Bypass; D003326:Coronary Circulation; D004285:Dogs; D006324:Heart Arrest, Induced; D007036:Hypothermia, Induced; D008274:Magnesium / Q000494:pharmacology*; D008929:Mitochondria, Heart / Q000187:drug effects / Q000502:physiology*; D010085:Oxidative Phosphorylation; D011188:Potassium / Q000008:administration & dosage
D008274:Magnesium; D011188:Potassium