Effect of hypoxia and reoxygenation on mitochondrial function in neonatal myocardium.

The effect of hypoxia and reoxygenation on mitochondrial function was studied in the newborn and adult rabbit hearts. In control muscle, mitochondrial state 3 respiration (state 3 QO2), respiratory control index (RCI), energy-dependent calcium uptake, ATP content, and adenine nucleotide translocase in the newborn were significantly greater than in the adult. After 60 min hypoxia, both the newborn and adult showed significant decrease in 1) tissue glycogen, adenine nucleotides, and creatine phosphates and 2) mitochondrial adenine nucleotides, adenine nucleotide translocase, and glutamate-supported state 3 respiration. In the adult, reoxygenation following 60 min hypoxia was not associated with significant recovery in any of the variables described above, and there was significant decrease in the rate of calcium uptake. In the newborn, the values of all variables returned to control except for tissue glycogen and adenine nucleotide translocase. The data suggest that the effect of hypoxia on mitochondrial function in the newborn is less than in the adult. This occurs because of 1) the lower energy demand in the newborn, 2) higher tissue glycogen and higher rates of glycolysis in the newborn, 3) increased degradation and/or efflux of ATP and ADP in the adult, and 4) possibly a difference in the sarcolemmal resistance to hypoxia in the two age groups.