The Annals of thoracic surgery · 2000
Effects of hyperoxia on neonatal myocardial energy status and response to global ischemia.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wittnich C, Torrance S M, Carlyle C E
Аннотация
BACKGROUND: This study examines the effect of neonatal exposure to clinically 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 hours, n = 11), mild hyperoxia (250 mm Hg, 2 hours, n = 9), or severe hyperoxia (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 early ischemia, hearts exposed to severe hyperoxia had better ATP and glycogen preservation (p < 0.003). These hearts exhibited almost complete (92%) creatine phosphate depletion, in contrast to incomplete creatine phosphate use in all other neonatal hearts, even in the face of 30% ATP reductions. However, hearts exposed to severe hyperoxia also had a higher incidence of fibrillation during ischemia, which accelerated ATP and glycogen degradation.
CONCLUSIONS: Although severe hyperoxia provided an energy-sparing effect during early ischemia, it also increased the incidence of ventricular fibrillation, which negated this beneficial effect.
METHODS: Three-day-old pigs were ventilated to normoxia (80 mm Hg, 2 or 5 hours, n = 11), mild hyperoxia (250 mm Hg, 2 hours, n = 9), or severe hyperoxia (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 early ischemia, hearts exposed to severe hyperoxia had better ATP and glycogen preservation (p < 0.003). These hearts exhibited almost complete (92%) creatine phosphate depletion, in contrast to incomplete creatine phosphate use in all other neonatal hearts, even in the face of 30% ATP reductions. However, hearts exposed to severe hyperoxia also had a higher incidence of fibrillation during ischemia, which accelerated ATP and glycogen degradation.
CONCLUSIONS: Although severe hyperoxia provided an energy-sparing effect during early ischemia, it also increased the incidence of ventricular fibrillation, which negated this beneficial effect.