Effects of electronic cigarette E-liquid and device wattage on vascular function

Abstract

Electronic cigarettes (e-cigs) are customizable tobacco products that allow users to select e-liquid composition, flavors, and (in some devices) adjust wattage or heat used to generate e-cig aerosol. This study compared vascular outcomes in a conducting vessel (thoracic aorta) and a resistance artery (middle cerebral artery, MCA) in C57Bl/6 mice exposed to e-cig aerosol generated from either pure vegetable glycerin (VG) or pure propylene glycol (PG) over 60-min (Study 1), and separately the effect of using 5- vs. 30-watt settings with an exposure of 100-min (Study 2). In Study 1, aortic endothelial-dependent-dilation (EDD) was only impaired with PG- exposure (p < 0.05) compared with air. In the MCA, EDD response was impaired by ∼50% in both VG and PG groups compared with air (p < 0.05). In Study 2, the aortic EDD responses were not different for either 5- or 30-watt exposed groups compared with air controls; however, in the MCA, both 5- and 30-watt groups were impaired by 32% and 55%, respectively, compared with air controls (p < 0.05). These pre-clinical data provide evidence that chronic exposure to aerosol produced by either VG or PG, and regardless of the wattage used, leads to vascular dysfunction at multiple levels within the arterial system. For all exposures, we observed greater impairment of arterial reactivity in a resistance artery (i.e. MCA) compared with the aorta. These data could suggest the smaller arteries may be more sensitive or first to be affected, or that different mechanism(s) for impairment may be involved depending on arterial hierarchy.

Keywords: Aorta; Brain; Middle cerebral artery; Myography; Vaping.

Figure 1.

Aorta vasodilation responses to increasing concentration of methacholine (MCh, panels A & B) and sodium nitroprusside (SNP, panels C & D) in mice exposed to air (control), 100% vegetable glycerin (VG) or 100% propylene glycol (PG) e-liquid base solution (no nicotine, no flavor). Maximal responses ([10⁻⁵]M) for MCh and SNP are shown in panels B and D, respectively. Mean±SE. ^ signifies PG different than Air.

Figure 2.

Middle cerebral artery (MCA) vasodilation responses to increasing concentration of acetylcholine (ACh, panels A & B) and sodium nitroprusside (SNP, panels C & D) in mice exposed to air (control), 100% vegetable glycerin (VG) or 100% propylene glycol (PG) e-liquid base solution (no nicotine, no flavor). Maximal responses ([10⁻⁴]M) for MCh and SNP are shown in panels B and D, respectively. Mean±SE. * signifies VG different than Air, p<0.05; ^ signifies PG different than Air, p<0.05.

Figure 3.

Aorta vasodilation responses to increasing concentration of methacholine (MCh, panels A & B) and sodium nitroprusside (SNP, panels C & D) in mice exposed to air (control), e-cig device at 5- or 30-(W)atts. Maximal responses ([10⁻⁵]M) for MCh and SNP are shown in panels B and D, respectively. E-liquid was 50:50 VG:PG with no nicotine and no flavor. Mean±SE. * signifies 5w different than Air, p<0.05; ^ signifies 30w different than Air, p<0.05.

Figure 4.

Middle cerebral artery (MCA) vasodilation responses to increasing concentration of acetylcholine (ACh, panels A & B) and sodium nitroprusside (SNP, panels C & D) in mice exposed to air (control), or e-cig device operating at either 5- or 30-(W)atts. Maximal responses ([10⁻⁴]M) for MCh and SNP are shown in panels B and D, respectively. E-liquid was 50:50 VG:PG with no nicotine and no flavor. Mean±SE. * signifies 5w different than Air, p<0.05.

Figure 5.

Maximal dilation response of middle cerebral artery (MCA) to acetylcholine (ACh[10⁻⁴]) (A & C) and aorta to methacholine (MCh [10⁻⁵](B & D) showing the effect of NOS inhibition using L-NAME from Study 1 (E-liquid composition, top panels A & B) and Study 2 (Watts, bottom panels C & D). Mean±SE. *signifies p<0.05 for ACh+LNAME compared to ACh within the same condition. § signifies p<0.05 for the difference in ACh minus ACh+LNAME compared Air.