Obstructive sleep apnea (OSA), characterized by events of hypoxia-reoxygenation, is highly prevalent in pregnancy, negatively affecting the gestation process and particularly the fetus. Whether the consequences of OSA for the fetus and offspring are mainly caused by systemic alterations in the mother or by a direct effect of intermittent hypoxia in the fetus is unknown. In fact, how apnea-induced hypoxemic swings in OSA are transmitted across the placenta remains to be investigated. The aim of this study was to test the hypothesis, based on a theoretical background on the damping effect of oxygen transfer in the placenta, that oxygen partial pressure (Po2) swings resulting from obstructive apneas mimicking OSA are mitigated in the fetal circulation. To this end, four anesthetized ewes close to term pregnancy were subjected to obstructive apneas consisting of 25-s airway obstructions. Real-time Po2 was measured in the maternal carotid artery and in the umbilical vein with fast-response fiber-optic oxygen sensors. The amplitudes of Po2 swings in the umbilical vein were considerably smaller [3.1 ± 1.0 vs. 21.0 ± 6.1 mmHg (mean ± SE); P < 0.05]. Corresponding estimated swings in fetal and maternal oxyhemoglobin saturation tracked Po2 swings. This study provides novel insights into fetal oxygenation in a model of gestational OSA and highlights the importance of further understanding the impact of sleep-disordered breathing on fetal and offspring development. NEW & NOTEWORTHY This study in an airway obstruction sheep model of gestational sleep apnea provides novel data on how swings in oxygen partial pressure (Po2) translate from maternal to fetal blood. Real-time simultaneous measurement of Po2 in maternal artery and in umbilical vein shows that placenta transfer attenuates the magnitude of oxygenation swings. These data prompt further investigation of the extent to which maternal apneas could induce similar direct oxidative stress in fetal and maternal tissues.

AIM: Obstructive sleep apnea (OSA), characterized by events of hypoxiareoxygenation, is highly prevalent in pregnancy, negatively affecting the gestation process and particularly the fetus. Whether the consequences of OSA on the fetus and offspring are mainly caused by systemic alterations in the mother or by direct effect of intermittent hypoxia in the fetus is unknown. In fact, how apnea-induced hypoxemic swings in OSA are transmitted across the placenta remains to be investigated. The aim of this study was to test the hypothesis, based on a theoretical background on the dampening effect of oxygen transfer in the placenta, that oxygen partial pressure (PO 2 ) swings resulting from obstructive apneas mimicking OSA are mitigated in the fetal circulation. METHODS: To this end, 4 anesthetized ewes close to term pregnancy were subjected to obstructive apneas consisting of 25-s airway obstructions. Real time PO 2 was measured in the maternal carotid artery and in the umbilical vein using fast-response fiberoptic oxygen sensors. RESULTS: The amplitude of PO 2 swings in the umbilical vein were considerably smaller (3.1±1.0 vs. 21.0±6.1 mmHg (m±SE); p<0.05). Corresponding estimated swings in fetal and maternal oxyhemoglobin saturation tracked PO 2 swings. CONCLUSION: This study provides novel insights into fetal oxygenation in a model of gestational OSA, and highlights the importance of further understanding the impact of sleep-disordered-breathing on fetal and offspring development.

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