Acute Effects of Vaporized Nicotine Inhalation on Young Non‐Smokers

Abstract

Electronic cigarettes (e‐cig) are popular with smokers and former smokers, but are also becoming popular with non‐smokers who might never have considered smoking a cigarette. Obvious dangers of long‐term e‐cig use in non‐smokers include nicotine addiction, with associated cardiovascular implications. Nicotine is a sympathomimetic agent, which affects autonomic cardiovascular control. We therefore studied the acute autonomic and cardiovascular effects of e‐cig use in non‐smokers. The purpose of this study was to document autonomic and hemodynamic effects of vaporized nicotine inhalation via e‐cig on arterial pressure and autonomic cardiovascular regulation. Fourteen young, healthy non‐smokers (9 M, 5 F, 21±0.71 yr) participated. With subjects in a semi‐recumbent position, we recorded the electrocardiogram, beat‐by‐beat arterial pressure from which we also derived cardiac output via model‐flow (finger plethysmography), and muscle sympathetic nerve activity (peroneal nerve microneurography, MSNA). Subjects rested quietly for 10 minutes while breathing in time to a computer display prompting them to breathe at a frequency of 15 breaths/min. Subjects continued to breathe in time to the computer display, but inhaled once every thirty seconds on an e‐cig (n = 4, 18 mg/ml; n = 10, 59 mg/ml) for 10‐min followed by a 10‐min recovery. The 10‐min baseline variables were averaged and compared to the 10‐min of active vaping (VAPE) and 10‐min of recovery (REC). Variables were assessed with repeated measures ANOVA. Data are expressed as means±SE. Mean arterial pressure increased during VAPE and remained elevated into REC. (91.3±1 mmHg at BASE to 97.6±2.5 at VAPE and 96.1±2.2 at REC; all p<.008). MSNA bursts per min (n=10) tended to decrease from BASE to VAPE (p<0.1) and then decreased substantially during REC (25.4±3.7 bursts/min at BASE to 16.8±2.6 bursts/min at REC; p<.03) MSNA bursts per 100 heart beats (hb) decreased from BASE to VAPE and REC (36.7±4.9 burst/100hb at BASE to 26.1±2.1 bursts/100hb at VAPE & 23.80±3.3 bursts/100hb at REC; all p<.04). Cardiac Output increased during VAPE and returned to BASE values in REC (6.6±0.47 L/min at BASE to 7.54±0.62 L/min at VAPE; p<.001). Total peripheral resistance (TPR) increased during REC (14.62±0.91 mmHg*min*ml−1 at BASE to 15.3±0.95 mmHg*min*ml−1 at REC; p<.02). Use of e‐cigs has increased precipitously among young non‐smokers, largely due to the perception of lower risk relative to combustible tobacco. Our results suggest that acute vaporized nicotine inhalation delivers a stimulus that increases arterial pressure and decreases MSNA. Increases of arterial pressure and reductions of MSNA are likely due to sympathetic baroreflex inhibition. Cardiac output causes the increase in mean arterial pressure during VAPE, which is sustained during REC in association with elevated TPR. We conclude that non‐smokers who vape may be at risk for the development of nicotine‐induced hypertension.Support or Funding InformationBlue Cross Blue Shield of Michigan & The Portage Health FoundationThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.