LAUSR

Maternal obesity increases the risk of preterm delivery which may result in rapid transition of their offspring from a relatively hypoxemic environment to normal or elevated oxygen environment, especially if the baby receives oxygen therapy. This exposure of premature infants to increased oxygen levels could induce oxidative stress and detrimental effects on organ development and maturation. Previous studies have shown that early-life exposure to high oxygen levels (hyperoxia) induces cardiovascular disease later in life. In the present study, we tested the hypothesis that neonatal exposure to hyperoxia (HO) leads to elevated blood pressure (BP) at adulthood in offspring from lean mothers and exacerbates the adverse impact of maternal obesity on offspring BP regulation. Male (n=5-7) and female (n=5-7) offspring from lean and high fat diet-fed obese mothers were exposed to room air (21% O2) or hyperoxia (80% O2) between postnatal (P) days P3-P10, and then returned to room air. The rats were provided food and water ad libitum and followed until 12-13 weeks of age when telemetry probes were implanted to measure BP and heart rate (HR) 24-hrs/day. After 10 days of recovery from surgery, BP and HR were measured for 5 consecutive days. Contrary to our hypothesis, neonatal HO was associated with lower BP compared to control offspring from lean mothers (males: 111±1 vs. 105±1 mmHg and females: 108±0.4 vs. 102±0.4 mmHg). Neonatal HO exposure was also associated with similar reductions in BP in hypertensive obese offspring from obese mothers (males: 123±1 vs. 117±1 mmHg and females: 116±1 vs. 113±1 mmHg). Offspring exposed to neonatal HO showed a tendency for reduced HR compared to lean and obese offspring not submitted to HO with significant reduction observed in obese female offspring from obese mothers (393±3 vs. 379±2 bpm). These results suggest that exposure to hyperoxia in early postnatal life is not associated with elevated BP in adulthood and it does not exacerbate the hypertensive effects of maternal obesity on offspring BP regulation. NIDDK 1R01121411, NIGMS P20GM104357 and NIGMS U54GM115428 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.