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Vaping to Vascular Damage: The Role of E‐Cigarettes on Vascular Function
Author(s) -
Clayton Stuart,
DeVallance Evan,
Branyan Kayla,
Pitzer Christopher,
Breit Matthew,
Hoskinson Hannah,
Klinkhachorn Powsiri,
Erdreich Brett,
Chantler Paul,
Olfert Mark
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb651
Subject(s) - myograph , medicine , electronic cigarette , cardiology , thoracic aorta , nicotine , context (archaeology) , pulse wave velocity , aorta , vasodilation , blood pressure , pathology , biology , paleontology
Background Electronic cigarettes (E‐cigs) have exponentially increased in popularity and usage due to the perception that e‐cigs are safe, their usefulness as a cigarette‐smoking cessation tool, and the appeal of heavily marketed flavors. There is little known about the long‐term effects of E‐cig vapor exposure, particularly in the context of vascular dysfunction. We hypothesize that the long‐term use of E‐cig vapor decreased aortic function, and increase aortic stiffness. Methods Data were obtained from C57BL/6 female mice exposed to 3R4F reference cigarette (N=5–7), cappuccino flavored E‐vapor (18 mg/ml nicotine, N=7), or filtered air (N=7–8) for 4 h/day, 5 d/wk for 8 months. Food and water were administered ad libitum. Before and after the exposure, in‐vivo aortic stiffness (pulse wave velocity) was measured using B‐mode and Doppler ultrasound by obtain blood flow signals at the aortic arch and before the carotid bifurcation from a single image, which were gated to the EKG. At the end of the exposure the thoracic aorta was dissected, sectioned into rings and mounted onto an ex‐vivo wire tension myograph system. Force transduction was used to measure the changes in aortic tension in response to methacholine, or sodium nitroprusside. Results Aortic stiffness increased (0.45±0.20 m/s) in the air‐exposed group, reflecting the normal aging process. However, an accelerated age‐associated aortic stiffness was noted in the cigarette (1.28±0.27 m/s) and E‐cig (1.14±0.24 m/s) groups (ANOVA, p<0.05). In animals exposed to filtered air, the maximal aortic relaxation achieved to methacholine was 90%, compared to 60% and 70% in the cigarette and E‐cig groups, respectively (p<0.05). No differences were noted in sodium nitroprusside dilation between groups. Conclusion Our data suggests that 8 months of E‐cig significantly accelerated the age‐associated increase in aortic stiffness, and significantly impaired aortic endothelial‐dependent but not endothelial‐independent dilation. These data show the E‐cigs induce similar vascular dysfunction to cigarette smoke exposure suggesting that E‐cig have similar risk to develop accelerated cardiovascular aging and disease. Support or Funding Information National Institutes of Health Grant: 1P20 GM‐109098 West Virginia University – Marshall University Collaborative Health Research Grants