Effects of Chronically Inhaled Nicotine on Cardiac Function

Abstract

Nicotine is the addictive chemical in tobacco‐related products, such as cigarettes, water pipes, e‐cigs, and chewing tobacco. While the effects of smoke from cigarettes and cigars are well known, the rise in popularity of smokeless electronic cigarettes (e‐cigs) brings new questions about the effects of nicotine itself on the development of cardiovascular disease. These “smoke‐less” products have grown in popularity due to reduced costs, increased social acceptance, and a belief that e‐cigs are a less dangerous alternative to smoking, but very little is known about the cardiac effects of chronically inhaled nicotine.Thus the goal of our study is to investigate the effects of chronic nicotine exposure on cardiac function.C57BL/6 female mice aged 20 weeks were used in this study. Mice were exposed to nicotine vapors using a nicotine exposure chamber, in which home cages are placed in sealed chamber that provide control of air flow, chronicity, and nicotine vapor dose. Mice are exposed for 12 hours/day corresponding with the dark cycle during which they are active. Female mice exposed to nicotine vapor for five weeks showed a significant increased mean arterial blood pressure from baseline, (94.3 ± 1.1 mm Hg at baseline vs. 102.4 ± .1.8 mm Hg at five weeks; p<0.001). In addition, after five weeks nicotine exposure females were found to have decreased cardiac output (18.41 ± 2.23 ml/min for air exposed mice vs. 16.17 ± 2.08 ml/min for nicotine exposed mice; p<0.05) as well as thinner posterior walls at diastole (0.71 ± 0.1 mm for air exposed mice vs. 0.64 ± 0.1 mm for nicotine exposed mice; p<0.05).These findings suggest that nicotine inhalation alters cardiovascular function, leading to increased mean arterial blood pressure, reduced cardiac output, and thinned cardiac walls. This data indicates that nicotine may play a role in cardiac functional and structural decline. Potential future directions include investigating modulators of blood pressure, such as the renin‐angiotensin system, and measuring expression levels of pathways known to adversely regulate cardiomyocyte size, such as Atrogin‐1 and MuRF‐1, following nicotine exposure.Support or Funding InformationNIH NHLBI R01 HL135635This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.