The effects of vaping with electronic cigarettes (e‐cigs) on cardiovascular health are still under investigation. An important question that still remains unknown is the role of individual constituents within the e‐liquid used for vaping. In this study, we examine the sole effect of either vegetable glycerin (VG) or propylene glycol (PG), without the presence of any flavors or nicotine, on aortic reactivity. Healthy C57BL/6J mice were exposed to e‐cig vapor for 4 weeks (5d/wk, 1‐hour/day, 60 puffs/day) to e‐cig aerosol from either 100% VG or 100% PG e‐liquid using a whole‐body chamber exposure system (SCIREQ InExpose). Control mice were exposed to ambient air. E‐cig aerosol was produced by a Joyetech eGRIP OLED device at 17.5 watts, with 5‐second puff duration. Mice were sacrificed >24 hours after their final exposure, and thoracic aortas were excised, cleaned of perivascular adipose tissue, and were cut into 2mm ring segments. Aortic rings were mounted on wire myograph system (DMT, AD Instruments) containing warm aerated Krebs‐Henseleit buffer solution. The vessels were pre‐constricted with 50 µL of U46619 [7.5e‐9 M], and then exposed to a serial dilution of methacholine [MCh 10‐9 to 10‐5 M] to assess endothelial‐dependent (EDD) vasodilation, and separately to serial dilutions of sodium nitroprusside [SNP 10‐9 to 10‐5 M] to assess endothelium‐independent (EID) vasodilation. In PG‐exposed mice, max aortic EDD was reduced by 18±2% (P<0.05) compared to controls, and reduced by 14±2% (P<0.05) compared to VG‐exposed mice. VG‐exposed mice were not significantly different compared to controls. Maximal aortic EID was slightly impaired in PG‐ mice compared to control (8±2% P<0.05) and VG (5±1% P<0.05) groups. In summary, chronic exposure to e‐cig aerosol from PG in the base solution resulted in aortic EDD and EID dysfunction, however VG‐exposed mice were not affected. These data suggest that both endothelial‐dependent and ‐independent mechanisms are adversely affected by PG, and therefore vaping with PG in the base solution alone poses a significant risk for adverse cardiovascular health effects.
Electronic cigarettes (E‐cigs) have been marketed as safer alternative to traditional tobacco cigarettes; however, little has been done to assess the impact of various settings (such as wattage) towards vascular health, specifically cerebrovascular function. Using a whole‐body chamber (SCIREQ InExpose), mice (n=5‐6/group) were exposed to aerosol produced from a Joyetech eGrip OLED E‐cig device with no nicotine using 5‐sec puffs at either 5 (W)atts or 30 W for 100 puffs/day, 5 days/week, for 4 weeks. Control mice were exposed to ambient air. Twenty‐four hours after the final exposure mice were euthanized and the middle cerebral arteries (MCA) were removed and positioned in a pressurized myobath. To test for vessel health, the MCA was exposed to increasing concentrations of acetylcholine (Ach; 10‐9M to 10‐4M), phenylephrine (PE; 10‐9M to 10‐4M), and sodium nitroprusside (SNP; 10‐9M to 10‐4M). Maximal MCA dilation was impaired in both the 5W and 30W groups (7.5±1.3um vs 2.7±2.9um respectively, p<0.0001) compared to controls (16.7±0.7um), with the 30W groups displaying greater (84%) impairment compared to the 5W group (55%)(p<0.05). Both the 5W and 30W groups exhibited an impaired response to SNP compared to controls (7.3±2.5um, 5.8±3.5um respectively vs 15±1.8um, p<0.05) while only the 30W groups exhibited an impaired response to PE compared to controls (‐9.8±3.7um vs ‐17.1±3.3um). These data show that vaping E‐cigs at low wattage induces >50% reduction in cerebrovascular reactivity, and that increasing the wattage (i.e. temperature) produced greater impairment. For both wattage conditions, dysfunction was observed in endothelial‐dependent and ‐independent mechanisms, demonstrating that vaping results in significant cerebrovascular health risks.
Electronic cigarettes (E‐cigs) have been marketed as a safer alternative to traditional cigarettes and as a smoking cessation aid. The main components comprising the E‐cig liquid are vegetable glycerin (VG) and propylene glycol (PG), but few studies have examined the chronic effects of either VG or PG e‐cig aerosol on cerebrovascular health. Wild type C57BL/6J mice (n=6/group) were placed in whole‐body chambers (SCIREQ InExpose) and exposed to aerosol produced from e‐cigs (Joyetech eGrip OLED using 5‐sec puffs at 17.5 W) with either 100% VG or 100% PG liquid using 60 puffs/day, 5 days/week, for 4 weeks. Control group of mice were exposed to ambient air. One‐day after the last exposure, the mice were sacrificed and the middle cerebral artery (MCA) responsiveness to acetylcholine (ACh; 10‐9M to 10‐4M), phenylephrine (PE; 10‐9M to 10‐4M), and sodium nitroprusside (SNP; 10‐9M to 10‐4M) were examined using a pressure myography. Maximal MCA dilation to ACh (10‐4M) was impaired by ~50% in both VG and PG exposed groups (max response = 8.2±1.1 and 8.2±1.8 μm, respectively, p<0.05) compared to control mice (17.2±0.8 μm). Maximal endothelial‐independent dilator response to SNP (10‐4 M) showed 25‐42% impairment with VG (14.8±2.7 μm) and PG (13.0±2.9 μm) compared to control mice (17.4±0.9 μm, p<0.05). Maximal vasoconstriction response to PE (10‐4 M) was 15% lower (‐12.8±1.9 μm) with VG and 40% lower (‐9.0±2.6 μm, p<0.05) with PG compared to control mice (‐15.0±2.4 μm). Mice exposed to e‐cig aerosol produced solely from base compounds used in e‐liquid (VG or PG) show significant cerebrovascular dysfunction (up to 50%), with a greater deficit observed in endothelial‐dependent mechanisms. However, endothelial‐independent mechanisms are also involved.
Electronic cigarettes (e‐cigs) are being marketed as a healthier alternative to traditional cigarettes, yet the health consequences of e‐cig usage (also called vaping) are still being investigated. E‐cigs are easily customized for user preferences. For example, choice of flavors, nicotine concentration, and/or temperature (i.e. wattage) used to combust the e‐liquid can be selected in many devices. Emerging evidence suggest vaping during pregnancy impairs cerebral vascular function in rodent offspring. In this study, we sought to investigate the potential effects of changes in e‐cig device wattage (i.e. 5 watts vs 30 watts) with maternal vaping during pregnancy of vascular function in postnatal life of offspring. METHODS: Adult female Sprague Dawley rats were time‐mated to allow for maternal e‐cig exposure beginning on gestation day 2 until birth. Maternal vaping occurred for 1 h/day, 5 days/wk using a whole‐body chamber system. E‐cig aerosol was generation using D19 Joyetech atomizer with nicotine‐free (0 mg/mL) 50:50 VG:PG e‐liquid without flavoring. Puff topology was 83 ml with 5‐sec puff duration. Pregnant dams were randomly assigned to control (air‐exposed), 5 watt or 30‐watt exposure groups. Rat offspring (n=2/dam) were studied at 30‐, 90‐, and 180‐days after birth, where in vivo pulse wave velocity (an index of arterial stiffness) was assessed using VisualSonics Vevo 2100 ultrasound, thereafter animals were euthanized and thoracic aortas were excised, cleaned, and cut into 2mm rings for wire myography (DMT, AD instruments). Aortic rings were mounted and warmed in aerated Krebs‐Henseleit buffer solution. Vessel reactivity was measured using serial dilutions of methacholine [MCh 10‐9to 10‐5M] and sodium nitroprusside [SNP 10‐9 to 10‐5 M] to assess endothelial‐dependent vasodilation (EDD) and endothelium‐independent vasodilation (EID), respectively. RESULTS: At the 30‐days, max aortic EDD was not different between either 5W (79±17%, mean±SD) or 30W (86±4%) groups compared to controls (88±4%)(p>0.36). At 90‐days, max aortic EDD was lower with 30W (58±18%, p<0.001), but not 5W (78±4%, p=0.11) compared to controls (95±6%). Carotid PWV was elevated in 5W (3.49 m/s) and 30W (3.83 m/s) groups compared to controls (2.98 m/s, p<0.05) suggesting 17‐29% increase in arterial stiffness. At 180 days, max aortic EDD was also lower with 30W (75±12%, p<0.01), but not 5W (81±9x%, p=0.11) compared to controls (100±10%). Carotid PWV was elevated further in 5W (3.96 m/s) and 30W (4.29 m/s) groups compared to controls (3.13 m/s, p<0.05) revealing 27‐37 % increase in arterial stiffness. Maximal aortic EID response (to SNP) was not different by wattage group or age. CONCLUSIONS: These findings show that e‐cig device power used during maternal vaping plays a role in increasing arterial stiffness and blunting EDD vascular function in the postnatal life of offspring with effects worsening with age. These data suggest vaping during pregnancy is not safe and has long‐lasting consequences to vascular health of progeny.
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