Effects of hypoxia on the cellular electrical activity of adult and neonatal canine ventricular myocardium.

Standard microelectrode techniques were utilized to evaluate the effects of acute hypoxia on the cellular electrical activity of neonatal and adult ventricular myocardium. Control action potential parameters from adult and neonatal tissues were not significantly different. Thirty minutes of acute hypoxic superfusion significantly (p less than 0.05) reduced all adult action potential indices. In neonatal preparations, only action potential duration at 50% repolarization (-17%) and action potential duration at 90% repolarization (-12%) were reduced significantly. After 60 min of hypoxia, action potential amplitude, maximum diastolic potential, and phase 0 upstroke velocity from neonates were still not reduced significantly. The alteration in neonatal action potential parameters induced by 1 h of hypoxic superfusion (5.5 mM glucose) were all reversed by 16.5 mM glucose despite continued hypoxia. Exclusion of glucose from the hypoxic superfusate did not greatly affect the response of neonatal tissues to hypoxia. In adult action potentials, the degree of decrease for each action potential parameter was markedly greater compared to the hypoxic solution with normal (5.5 mM) glucose. Following hypoxic superfusion of neonatal preparations with 0 mM glucose, reoxygenation with 16.5 mM glucose resulted in action potential parameters with exceeded control values by 4 to 25%. Our data indicate a greater resistance of developing myocardium to the detrimental effects of hypoxia on cellular electrical activity. This seems to be related to a greater glycolytic activity of neonatal myocardium compared to adult hearts.