Abstract
Introduction: Obstructive sleep apnea (OSA) is a major public health issue because of its prevalence and morbidity. Pregnancy is associated with a high prevalence of OSA. However, the consequences of gestational OSA are poorly known. We hypothesized that intermittent hypoxia (IH), an hallmark of OSA, induces prenatal and neurodevelopmental abnormalities of cardiorespiratory and cognitive functions. Theses anomalies could be related to a systemic and tissue inflammation.
Methods: A classic model of IH was applied to pregnant mice using 5% FiO2, 30 cycles /h 10 hours a day, during the last 10 days of gestation. The IH model was characterized by monitoring transcutaneous oxygen saturation and the mothers' weight. The pups' evaluation consisted of daily weighing, measuring cardio respiratory parameters at basal state and during hypoxic and hypercapnic challenges at 5 and 12 days of age. Cognitive functions were evaluated by the object recognition test (ORT) at 60 days of age. Cytokine assay was performed in serum and tissue samples (Merck Millipore, Magpmag-24k -Billerica, Massachusetts).
Results: The IH induced oxygen desaturations and delayed weight gain in pregnant mice without showing serum and tissue inflammation. The study of IH exposed pups revealed: 1 / transient respiratory anomalies such as an increase in basal normoxic ventilation (Ve, Ttot), 2 / a persistent growth retardation at all postnatal ages till 30 days and 3 / no differences in cognitive function evaluated by the ORT.
Discussion: These results are consistent with the current literature and suggest an impact of IH. The prospects inspired by our work are the study of the consequences of a less severe IH model, closer to human pathology.
- © 2014 ERS