Postpartum Maternal Vascular Function in a Rat Model of Gestational Obstructive Sleep Apnea

Introduction: De novo obstructive sleep apnea (OSA) in pregnancy is associated with adverse gestational outcomes. In pregnant mice, exposure to chronic intermittent hypoxia (CIH), a model of OSA, induces endothelial dysfunction in maternal uterine arteries. It is currently unknown whether gestational OSA has a long-term effect on maternal vascular function. We hypothesized that exposure to gestational CIH during pregnancy will result in postpartum maternal vascular dysfunction. Methods: Pregnant rats were assigned to Normoxia and CIH groups. The CIH group was exposed to five days of intermittent hypoxia [6 min cycles of 3 min hypoxia (10% O2) and 3 min normoxia (21% O2)]. Endothelial function was assessed in isolated maternal uterine arteries at weaning (postnatal day 28). Vascular reactivity to acetylcholine (ACh) was examined in the presence and absence of uterine perivascular adipose tissue (PVAT) using wire myography. Results: In the absence of PVAT, uterine arteries from dams exposed to gestational CIH had exaggerated responses to ACh compared to dams exposed to normoxia [(-)PVAT/pEC50, Normoxia: 6.77±0.08 vs. CIH: 7.13±0.09, p< 0.01], while PVAT normalized this difference [(+)PVAT/pEC50, Normoxia: 6.67±0.08 vs. CIH: 6.70±0.07, p=0.99]. The effects of PVAT were due to its anti-dilatory influences on uterine arteries from CIH-treated rats ([CIH (-PVAT) vs. CIH (+PVAT), p = 0.003), whereas it had no effect on arteries from normoxic rats (p = 0.77). Conclusion: Exposure to gestational CIH exaggerated postpartum uterine vascular smooth muscle relaxation responses. Gestational OSA may impair maternal vascular recovery after birth.