Forty years have passed since classical experiments in lambs documented that, during the transition from fetal to neonatal life, disturbances in pulmonary vascular tone and reactivity could lead to systemic hypoxemia.1 Shortly after that, James and Rowe demonstrated that hypoxia caused a precipitous fall in arterial saturation in human infants with evidence of incomplete postnatal adjustment to extrauterine respiration.2 Their finding of elevations in pulmonary vascular pressure and hypoxemia was interpreted as evidence for the "re-establishment of the fetal pattern of circulation." Additional, more detailed, observations of transitional changes in the central circulation of normal and abnormal infants were reported in the late 1950s.3-5

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