Abstract

Developmental harm to offspring from maternal exposure to electronic cigarettes (E‐cig) during pregnancy is still poorly understood. Similar to cigarettes, we hypothesized the even low‐level E‐cig exposure would produce similar evidence of cerebral vascular dysfunction compared to a higher exposure dose. We examined the effects of maternal E‐cig exposure (Joyetech eGrip OLED using 5‐sec puffs @17.5 W) on cerebrovascular function in offspring (n=2–4 from each dam) from Sprague‐Dawley rat dams exposed to air (Control), E‐cig with 18 mg/ml nicotine (E‐cig18) and without nicotine (E‐cig0). Dams were exposed to low (20 puffs) or high (60 puffs) dose for 1‐hour each day, 5 days/week, starting on gestational day 2 and continued until pups were weaned. Pups themselves we never directly exposed to E‐cig aerosol. Middle cerebral arteries (MCA) were obtained from pups at 3‐months of age, isolated and positioned in a pressurized myobath, and exposed to increasing concentrations of acetylcholine (ACh; 10 ‐9 M to 10 ‐4 M), serotonin (5‐ HT;10 ‐9 M to 10 ‐4 M), and sodium nitroprusside (SNP; 10 ‐9 M to 10 ‐4 M), and in the presence or absence of Tempol (a superoxide dismutase mimetic). At the lower dose, MCA dilation to ACh was impaired by 60±1% and 50±0.1% in E‐cig0 and E‐cig18 groups, respectively, compared to controls (p<0.05). At the higher dose, MCA dilation to ACh was similarly impaired by 63±1% and 60±0.2% in E‐cig0 and E‐cig18 groups, respectively (p<0.05). Incubation with tempol reversed the cerebrovascular dysfunction seen in both E‐cig groups at both doses, suggesting the superoxide pathway is involved in the impairment observed in offspring. At both low and high doses, the vasocontrictory response to 5‐HT, and dilation response to SNP (non‐endothelial‐dependent mechanism), were similar across all groups. These data show that maternal E‐cig usage results in similar cerebrovasculature impairment with either 20 or 60 puffs/day during pregnancy and lactation in adolescent offspring with prior in utero exposure from maternal vaping at suggesting that even low‐levels of maternal E‐cig use confers significant post‐natal vascular health risks for the offspring.Support or Funding InformationWVU Cancer Institute Philip R Dino Innovative Research Grant (IMO); APS STRIDE Fellowship (JO); NIHGMS 5U54GM104942‐03 (PDC)

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