Background: Despite a lack of empirical data, an unprecedented rise in electronic cigarettes (ECs) has been widely perceived as safe. Multiple studies support a causal link between tobacco cigarette (TC) use and cardiovascular (CV) diseases; however, there is a lack of data with EC use. We have previously shown that chronic and acute EC use decreases heart rate variability (HRV) in humans, likely via increased sympathetic nervous system activation. Objective: We aimed to evaluate HRV effects induced by brief EC exposures utilizing an in-vivo model for freely moving C57BL/6 mice. Methods and Results: Telemetry devices were implanted in the abdomen of six 10-week-old C57BL/6 male mice to monitor electrocardiographic activity continuously. Mice underwent an exposure protocol designed to reflect human vaping topography with two EC exposures, each lasting 15-minutes (4-sec puff/ 26-sec Air) followed by 45-min post-exposure periods. Air (primary control) and PBS (secondary control) were also included, each with their own post-exposure events. During EC exposures, we observed bradycardic effects in heart rate (HR) with the standard deviation of NN intervals (SDNN), root mean square of successive differences (RMSSD), and the proportion of adjacent normalized RR intervals that differed by more than 6 ms (pNN 6 ) significantly (p< 0.05) altered as compared to Air exposures. After EC exposures, SDNN, RMSSD and pNN 6 parameters significantly decreased compared to Air. No significant differences between Air and PBS were observed in these parameters. Frequency domain parameters also indicated significant changes in HRV; the low frequency (LF) and high frequency (HF) bands showed marked increases during and after the EC exposures, while the log (LF/HF) ratio remained relatively unchanged, suggesting a possible coactivation of both parasympathetic and sympathetic branches of the autonomic nervous system. Conclusion: Short-term EC exposures lower heart rate and altered HRV in mice in an acute manner, suggesting that ECs may not be safe as previously assumed. This work was funded by the Tobacco-Related Disease Research Program (TRDRP) which included the High Impact Pilot Research Award [28IP-0036], the Cornelius Hopper Diversity Award Supplement and the Student Research Award Supplement, the UCLA Center for Occupational and Environmental Health (COEH) Student Project Award, and in part by the National Institute of Environmental Health Sciences (NIEHS) via the Student-to-Scientist Bridge program at California State University, Northridge [5R25ES025507]. 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.
Read full abstract