Plasma hypoxanthine reacts more abruptly to changes in oxygenation than base deficit and uric acid in newborn piglets

Previously, high postmortem concentrations of hypoxanthine have been found in vitreous humor of children dying from sudden infant death syndrome (SIDS). We wanted to investigate further the accumulation of hypoxanthine in vitreous humor during hypoxia. Twenty-four piglets aged 9-15 days were exposed to continuous hypoxemia (180 min 11% O2, n = 6), long interval intermittent hypoxemia (60 min 11% O2, 20 min room air, n = 7) or short interval intermittent hypoxemia (10 min 9% O2, 10 min room air with (n = 6) or without (n = 5) superimposed ligation of both carotid arteries). The increase in vitreous humor Hyp was four-fold higher (p < 0.01) with ligation of the carotid arteries (14 +/- 2.4 to 38 +/- 8.9 mumol/l) than without ligation (15 +/- 2.8 to 21 +/- 5.9 mumol/l). During continuous hypoxemia, plasma Hyp (r = 0.85), Xa (r = 0.89) uric acid (UA) (r = 0.85), and base deficit (BD) (r = 0.78) increased almost linearly (p < 0.001). Plasma Hyp responded more abruptly to changes in oxygenation than base deficit (BD) and UA. Ligation of the carotid arteries had a strong impact on Hyp accumulation in vitreous humor, suggesting that vitreous humor Hyp is not merely a filtration product of plasma Hyp, but reflects local hypoxia/ischemia in the eye.