Abstract

Pregnancy is a vulnerable time with significant cardiovascular changes that can lead to adverse outcomes, which can extend into the postpartum window. Exposure to emissions from electronic cigarettes (Ecig), commonly known as "vaping," has an adverse impact on cardiovascular function during pregnancy and post-natal life of offspring, but the postpartum effects on maternal health are poorly understood. We used a Sprague Dawley rat model, where pregnant dams are exposed to Ecigs between gestational day (GD)2-GD21 to examine postpartum consequences. Litter and dam health were monitored during the weaning period, and maternal vascular and endocrine function were assessed after weaning. Exposure to Ecig emissions during pregnancy led to fetal losses (i.e., reabsorption in utero) and reduced survival of pups during weaning compared to controls (air-exposed dams). We find that maternal vaping during pregnancy, with or without nicotine (or flavoring) results in maternal vascular and hormonal dysfunction (i.e., reduced prolactin, increased expression of sirtuin 1 deacetylase in the brain). Both 5 and 30W Ecig aerosol exposures resulted in significant impairment of middle cerebral artery reactivity to acetylcholine-mediated dilation (decreasing ~ 22 and ~ 50%, respectively). We also observed an increase in the number of extracellular vesicles (EVs) in plasma from 30-W group that persists up to 3-week postpartum and that these EVs impaired endothelial cell function when applied to in vitro and ex vivo assays. Our data suggest (1) Ecig vaping, even without nicotine or flavorings, during pregnancy alters maternal circulating factors that influence maternal and fetal health, (2) circulating EVs may contribute to the etiology of vascular dysfunction, and (3) that the window for recovery from vascular dysfunction in the dam is likely to be longer than the exposure window.

Department(s)

Biological Sciences

Publication Status

Open, Access

Keywords and Phrases

Brain; Middle cerebral artery; Myography; Pregnancy; Vaping

International Standard Serial Number (ISSN)

1559-0259; 1530-7905

Document Type

Article - Journal

Document Version

Citation

File Type

text

Language(s)

English

Rights

© 2025 Springer, All rights reserved.

Publication Date

01 Jan 2025

PubMed ID

39841346

Included in

Biology Commons

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