Background. This study examines the effect of neonatal exposure to clinical
ly relevant hyperoxia levels on both in vivo myocardial metabolism and the
subsequent metabolic response to global ischemia.
Methods. Three-day-old pigs were ventilated to normoxia (80 mm Hg, 2 or 5 h
ours, n = 11), mild hyperoxia (250 mm Hg, 2 hours, n = 9), or severe hypero
xia (500 mm Hg, 5 hours, n = 14). Ventricular biopsies obtained at the end
of the ventilation period, and at early and late ischemia were analyzed for
ATP, ADP, AMP, creatine phosphate, glycogen, and lactate.
Results. Hyperoxia did not significantly alter in vivo metabolism. During e
arly ischemia, hearts exposed to severe hyperoxia had better ATP and glycog
en preservation (p < 0.003). These hearts exhibited almost complete (92%) c
reatine phosphate depletion, in contrast to incomplete creatine phosphate u
se in all other neonatal hearts, even in the face of 30% ATP reductions. Ho
wever, hearts exposed to severe hyperoxia also had a higher incidence of fi
brillation during ischemia, which accelerated ATP and glycogen degradation.
Conclusions. Although severe hyperoxia provided an energy-sparing effect du
ring early ischemia, it also increased the incidence of ventricular fibrill
ation, which negated this beneficial effect. (Ann Thorac Surg 2000;70:2125-
31) (C) 2000 by The Society of Thoracic Surgeons.