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  • 1
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    Online Resource
    Abstract 11496: Increased Pulmonary Microvascular Endothelial Permeability by E-Cigarette Aerosol: The Pathway from Lung to Peripheral Blood Vessels
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 144, No. Suppl_1 ( 2021-11-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. Suppl_1 ( 2021-11-16)
    Abstract: Background: We reported that permeability of cultured microvascular endothelial cells is increased by incubation in e-cigarette (e-cig) users’ serum relative to that from smokers or non-users. It is unclear whether this is a direct effect of aerosol chemicals that reach the circulation, or an indirect response mediated by the e-cig users’ pulmonary epithelium. Hypothesis: Vaping increases microvascular endothelial permeability indirectly by signaling from alveolar epithelium. Methods: E-cig aerosol condensates were derived from e-liquids with and without nicotine (12 mg/mL free base), each containing menthol, vanillin, ethyl maltol, or cinnamaldehyde (2 mg/mL). Cell permeability was measured in human lung microvascular endothelial cells (HMVEC-Ls) using electric cell-substrate impedance sensing. Human Type II lung alveolar epithelial cells (ATII) were grown in serum-free air-liquid interface and exposed to e-cig aerosols with 0, 18, or 36 mg/mL nicotine (free base and salt), or air, 1 h/day for 3 days in an exposure chamber inside a CO 2 incubator. Results: Incubation of HMVEC-Ls with 0.3% v/v e-cig aerosol condensates from most e-liquids, with and without nicotine, decreased cell permeability (in contrast to the increased permeability that we reported from incubation with e-cig user serum). The exception was menthol + nicotine, which increased permeability (but reduced viability). When HMVEC-Ls were instead incubated with supernatant collected from ATII cells after exposure to e-cig aerosols, permeability was increased when supernatants were from exposure to aerosol with 36 mg/ml nicotine salt, but not 36 or 18 mg/mL freebase nicotine. Supernatants from similarly exposed ATII cells contained higher levels of the proinflammatory proteins MCP-1, IL-8, GROα, and MIP-1β when aerosol contained 36 mg/mL freebase nicotine (3/6 wells) or nicotine salt (5/6), but not 18 mg/ml nicotine (0/6). Conclusion: HVMEC-L permeability was not directly increased by e-cig aerosol condensate, but was increased by supernatant of alveolar epithelial cells exposed to high-nicotine aerosol, potentially mediated by elevated ATII cytokine production, indicating a potential indirect mechanism by which vaping increases pulmonary microvascular permeability.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.144.suppl_1.11496
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1466401-X
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  • 2
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    Abstract 10022: Marijuana Smoke or Vaporizer Aerosol Impairs Endothelial Function Regardless of Drying Regimen or Cannabinoid Profile
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Vol. 146, No. Suppl_1 ( 2022-11-08)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. Suppl_1 ( 2022-11-08)
    Abstract: Introduction: Marijuana smoke and vaporizer aerosol adversely affect the cardiovascular system. Most US marijuana research has used research marijuana from the University of Mississippi supplied through the National Institute on Drug Abuse (NIDA). NIDA marijuana is dried at high temperature with maximum of 10% THC, but real-world material is gently dried and is ~20% THC. Because NIDA marijuana differs from what is currently used by the public in terms of THC content and drying regimen, skepticism regarding relevance to the real world is limiting the impact of results obtained from this material. Here, we validated the use of NIDA research marijuana in the study of vascular effects of cannabis. Hypothesis: Exposure to marijuana smoke or vaporizer aerosol, regardless of the cannabinoid profile or drying regimen, impairs endothelial function. Methods: We exposed groups of rats (n=8) to smoke or Volcano vaporizer aerosol from materials obtained from U Miss (Placebo ( 〈 0.01% THC hot), 4.2% THC hot and gentle dried pair, 10% THC hot), from Biopharmaceutical Research Company (Castroville, CA) (20% THC gentle dried), commercial hemp with negligible THC content, and clean air. Exposure was pulsatile, 5s/min over 5 mins. Endothelial function was measured as flow-mediated dilation (FMD) and pre- vs. post-exposure FMD (10 and 30 mins after end of exposure) differences were analyzed. Results: We observed significant impairment of FMD after exposure to pulsatile smoke from marijuana with varied cannabinoid profiles and drying regimens (p≤.006), with no effect from clean air (p=.13). No significant recovery of FMD was observed in any group 30 mins after marijuana smoke exposure (p≥.32). Pulsatile exposure to aerosol generated from the same materials impaired FMD in all groups (p≤.001) except clean air (p=.23). Conclusions: Acute exposure to marijuana smoke/aerosol impairs endothelial function regardless of the drying regimens or the cannabinoid profile of the marijuana product.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.146.suppl_1.10022
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
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  • 3
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    Vascular endothelial function is impaired by aerosol from a single IQOS HeatStick to the same extent as by cigarette smoke
    BMJ ; 2018
    In:  Tobacco Control Vol. 27, No. Suppl 1 ( 2018-11), p. s13-s19
    Details
    In: Tobacco Control, BMJ, Vol. 27, No. Suppl 1 ( 2018-11), p. s13-s19
    Abstract: Heated tobacco products (also called ‘heat-not-burn’ products) heat tobacco at temperatures below that of combustion, causing nicotine and other compounds to aerosolise. One such product, IQOS from Philip Morris International, is being marketed internationally with claims of harm reduction. We sought to determine whether exposure to IQOS aerosol impairs arterial flow-mediated dilation (FMD), a measure of vascular endothelial function that is impaired by tobacco smoke. Methods We exposed anaesthetised rats (n=8/group) via nose cone to IQOS aerosol from single HeatSticks, mainstream smoke from single Marlboro Red cigarettes or clean air for a series of consecutive 30 s cycles over 1.5–5 min. Each cycle consisted of 15 or 5 s of exposure followed by removal from the nose cone. We measured pre-exposure and postexposure FMD, and postexposure serum nicotine and cotinine. Results FMD was impaired comparably by ten 15 s exposures and ten 5 s exposures to IQOS aerosol and to cigarette smoke, but not by clean air. Serum nicotine levels were similar to plasma levels after humans have smoked one cigarette, confirming that exposure conditions had real-world relevance. Postexposure nicotine levels were ~4.5-fold higher in rats exposed to IQOS than to cigarettes, despite nicotine being measured in the IQOS aerosol at ~63% the amount measured in smoke. When IQOS exposure was briefer, leading to comparable serum nicotine levels to the cigarette group, FMD was still comparably impaired. Conclusions Acute exposures to IQOS aerosol impairs FMD in rats. IQOS use does not necessarily avoid the adverse cardiovascular effects of smoking cigarettes.
    Type of Medium: Online Resource
    ISSN: 0964-4563 , 1468-3318
    URL: Article
    DOI: 10.1136/tobaccocontrol-2018-054325
    Language: English
    Publisher: BMJ
    Publication Date: 2018
    detail.hit.zdb_id: 2010882-5
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  • 4
    Online Resource
    Online Resource
    Chronic E-Cigarette Use Impairs Endothelial Function on the Physiological and Cellular Levels
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 42, No. 11 ( 2022-11), p. 1333-1350
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 42, No. 11 ( 2022-11), p. 1333-1350
    Abstract: The harmful vascular effects of smoking are well established, but the effects of chronic use of electronic cigarettes (e-cigarettes) on endothelial function are less understood. We hypothesized that e-cigarette use causes changes in blood milieu that impair endothelial function. Methods: Endothelial function was measured in chronic e-cigarette users, chronic cigarette smokers, and nonusers. We measured effects of participants’ sera, or e-cigarette aerosol condensate, on NO and H 2 O 2 release and cell permeability in cultured endothelial cells (ECs). Results: E-cigarette users and smokers had lower flow-mediated dilation (FMD) than nonusers. Sera from e-cigarette users and smokers reduced VEGF (vascular endothelial growth factor)-induced NO secretion by ECs relative to nonuser sera, without significant reduction in endothelial NO synthase mRNA or protein levels. E-cigarette user sera caused increased endothelial release of H 2 O 2 , and more permeability than nonuser sera. E-cigarette users and smokers exhibited changes in circulating biomarkers of inflammation, thrombosis, and cell adhesion relative to nonusers, but with distinct profiles. E-cigarette user sera had higher concentrations of the receptor for advanced glycation end products (RAGE) ligands S100A8 and HMGB1 (high mobility group box 1) than smoker and nonuser sera, and receptor for advanced glycation end product inhibition reduced permeability induced by e-cigarette user sera but did not affect NO production. Conclusions: Chronic vaping and smoking both impair FMD and cause changes in the blood that inhibit endothelial NO release. Vaping, but not smoking, causes changes in the blood that increase microvascular endothelial permeability and may have a vaping-specific effect on intracellular oxidative state. Our results suggest a role for RAGE in e-cigarette-induced changes in endothelial function.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.121.317749
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1494427-3
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  • 5
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    Circulating angiogenic cell function is inhibited by cortisol in vitro and associated with psychological stress and cortisol in vivo
    Elsevier BV ; 2016
    In:  Psychoneuroendocrinology Vol. 67 ( 2016-05), p. 216-223
    Details
    In: Psychoneuroendocrinology, Elsevier BV, Vol. 67 ( 2016-05), p. 216-223
    Type of Medium: Online Resource
    ISSN: 0306-4530
    URL: Article
    DOI: 10.1016/j.psyneuen.2016.02.019
    RVK:
    YH 2600
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2016
    detail.hit.zdb_id: 1500706-6
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  • 6
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    Overexpression of Nitric Oxide Synthase Restores Circulating Angiogenic Cell Function in Patients With Coronary Artery Disease: Implications for Autologous Cell Therapy for Myocardial Infarction
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Journal of the American Heart Association Vol. 5, No. 1 ( 2016-01-13)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 5, No. 1 ( 2016-01-13)
    Abstract: Circulating angiogenic cells ( CAC s) are peripheral blood cells whose functional capacity inversely correlates with cardiovascular risk and that have therapeutic benefits in animal models of cardiovascular disease. However, donor age and disease state influence the efficacy of autologous cell therapy. We sought to determine whether age or coronary artery disease ( CAD ) impairs the therapeutic potential of CAC s for myocardial infarction ( MI ) and whether the use of ex vivo gene therapy to overexpress endothelial nitric oxide ( NO ) synthase ( eNOS ) overcomes these defects. Methods and Results We recruited 40 volunteers varying by sex, age ( 〈 or ≥45 years), and CAD and subjected their CAC s to well‐established functional tests. Age and CAD were associated with reduced CAC intrinsic migration (but not specific response to vascular endothelial growth factor, adherence of CAC s to endothelial tubes, eNOS mRNA and protein levels, and  NO production. To determine how CAC function influences therapeutic potential, we injected the 2 most functional and the 2 least functional CAC isolates into mouse hearts post MI . The high‐function isolates substantially improved cardiac function, whereas the low‐function isolates led to cardiac function only slightly better than vehicle control. Transduction of the worst isolate with eNOS cDNA adenovirus increased NO production, migration, and cardiac function of post‐ MI mice implanted with the CAC s. Transduction of the best isolate with eNOS small interfering RNA adenovirus reduced all of these capabilities. Conclusions Age and CAD impair multiple functions of CAC s and limit therapeutic potential for the treatment of MI . eNOS gene therapy in CAC s from older donors or those with CAD has the potential to improve autologous cell therapy outcomes.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.115.002257
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2653953-6
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  • 7
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    Brief Exposure to Secondhand Smoke Reversibly Impairs Endothelial Vasodilatory Function
    Oxford University Press (OUP) ; 2014
    In:  Nicotine & Tobacco Research Vol. 16, No. 5 ( 2014-5), p. 584-590
    Details
    In: Nicotine & Tobacco Research, Oxford University Press (OUP), Vol. 16, No. 5 ( 2014-5), p. 584-590
    Type of Medium: Online Resource
    ISSN: 1469-994X , 1462-2203
    URL: Article
    DOI: 10.1093/ntr/ntt189
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2014
    detail.hit.zdb_id: 2020202-7
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  • 8
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    Abstract P355: Comparable Impairment Of Vascular Endothelial Function By A Wide Range Of Electronic Nicotine Delivery Devices
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Research Vol. 129, No. Suppl_1 ( 2021-09-03)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 129, No. Suppl_1 ( 2021-09-03)
    Abstract: Introduction: Electronic nicotine delivery systems (ENDS; i.e., vaping devices) such as e-cigarettes, heated tobacco products, and newer coil-less ultrasonic vaping devices are promoted as less harmful alternatives to combustible cigarettes. However, the cardiovascular health effects of these devices are understudied. We investigated whether exposure to aerosol from a wide range of ENDS devices with and without nicotine, including a new ultrasonic vaping device, impairs endothelial function. Hypothesis: ENDS aerosols irrespective of nicotine, flavors, and heating coil impair endothelial function comparably to smoke from cigarettes. Methods: We exposed 11 groups (n=8), of anaesthetized rats to aerosol from propylene glycol (PG), vegetable glycerin (VG), PG+VG without nicotine, a USONICIG Zip ultrasonic vaping device, previous generation e-cigarettes (tank style with freebase nicotine), 5% nicotine JUUL pods of three flavors (Virginia tobacco, Mango, and Menthol), and an IQOS heated tobacco product; with Marlboro Red cigarette smoke and clean air as controls, to a single session of 10 cycles of pulsatile 5s exposure over 5 minutes. Endothelial function was quantified as arterial flow-mediated dilation (FMD) using micro-ultrasound. Results: Aerosol/smoke from all conditions except air significantly impaired FMD (Figure: each colored line denotes one rat, black horizontal bars denote means). The extent of impairment ranged from 40%-67% although there were no significant differences between groups. Nicotine absorption into the blood varied widely from these undiluted aerosols (those containing nicotine), with IQOS being the highest, and USONICIG and previous generation e-cig being the lowest. Conclusions: A single session of exposure to aerosol from a wide range of ENDS, including multiple types of e-cigarettes, a heated tobacco product, and an ultrasonic vaping device, all impair endothelial vascular function comparably to combusted cigarettes. Key words: JUUL, IQOS, ultrasonic vaping device, e-liquids, flow-mediated dilation
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.129.suppl_1.P355
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
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  • 9
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    Abstract 224: Sub-cytotoxic Levels of Heavy Metals Induce Pro-inflammatory Signaling in the Aortic Endothelium without Impairing Flow-Mediated Dilation in Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Circulation Research Vol. 125, No. Suppl_1 ( 2019-08-02)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. Suppl_1 ( 2019-08-02)
    Abstract: Introduction: Acute exposure to tobacco or marijuana secondhand smoke (SHS) causes endothelial dysfunction. The identity of specific SHS constituents that cause vascular toxicity is unclear. Heavy metals are present in SHS and at elevated levels in the blood of smokers, and may mediate acute endothelial dysfunction through reactive oxygen species formation and decreasing NO bioavailability. We assessed the effects of exposure to cadmium, lead, mercury, and arsenic at levels present in the blood of human smokers on flow-mediated dilation (FMD) as a measure of endothelial function in rats. We also evaluated the effects of heavy metal exposure on intimal structure, protein localization pattern, and inflammatory gene expression in the aortic endothelium. Hypothesis: Sub-cytotoxic levels of heavy metals impair FMD, alter intimal structure, and induce pro-inflammatory signaling in endothelium. Methods: We injected rats (n=8/group) with heavy metal cocktail or vehicle intravenously and quantitated pre- and post-exposure FMDs measures defined as percent vasodilation of femoral artery after transient ischemia. We performed en face aorta immunostaining and assessed endothelial cell axis alignment, cell length ratio, and localization pattern of PECAM-1, VE-cadherin, and vimentin. We also quantified gene expression of key endothelial proteins in aorta homogenates. Results: FMD was not impaired in the heavy metal group (8.8±3.6(SD)% vs. 12.9±8.0%, p=.31 or controls (7.5±2.7% vs. 8.8±5.8%, p=.63). No significant difference in cell length ratio and endothelial x and y axes of alignment were detected between groups (p 〉 .8) and localization of PECAM-1, VE-cadherin, and vimentin in the aorta endothelium remained unaltered following heavy metal injection. However, expression of PECAM-1 and VE-cadherin was significantly lower in the heavy metal-treated rats, while VCAM-1 gene expression was significantly higher (p 〈 .05). Conclusion: Acute exposure to sub-cytotoxic levels of heavy metals can induce pro-inflammatory signaling in endothelium, which could potentially lead to vascular injury. However, FMD and endothelial structure remain unchanged by heavy metal exposure.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.125.suppl_1.224
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
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  • 10
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    Abstract 54: The Effect of Nicotine and Menthol in Secondhand Smoke on Endothelial Function
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Circulation Research Vol. 121, No. suppl_1 ( 2017-07-21)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 121, No. suppl_1 ( 2017-07-21)
    Abstract: Introduction: We have previously shown that even one minute of exposure to secondhand smoke (SHS) of tobacco and marijuana can impair arterial flow-mediated dilation (FMD) in rats. The identity of specific constituents of SHS that cause vascular toxicity remains unclear. Nicotine is a vasoconstrictor that potentially can affect vascular function. Menthol is a cigarette additive popular with African Americans, women, youth, and other ethnicities. Menthol interacts with smoke constituents and irritants such as acrolein through receptor ion channels and also affects the metabolism rate of nicotine. Hypothesis: We tested three hypotheses pertaining to acute effects of brief exposures to SHS: (1) nicotine increases the extent of endothelial functional impairment; (2) menthol decreases the extent of endothelial functional impairment; and (3) there is an interaction between the effects of nicotine and menthol. Methods: We exposed 8 groups of rats (n=8-10/group) for 10 minutes to two different levels of SHS from the following four different types of research reference tobacco: conventional nicotine (~15 mg/g tobacco), reduced nicotine (~0.4 mg/g tobacco), and both conventional and reduced nicotine with added menthol (~1.15 mg/g tobacco) in a 2x2 factorial (ANOVA) design. We also examined a clean air negative control group (n=9). FMD was measured before and after exposures in each rat. To calculate FMD, the femoral artery diameter was measured with micro-ultrasound before and after a 5-min transient ischemia induced by an external vascular occluder. FMD was quantified as the % vasodilation. Results: FMD was not affected in the clean air controls (p=0.13). Higher nicotine levels were associated with increased % reduction of FMD impairment (19.22±9.53% vs. 41.07±4.54% (SD); p=0.047). Adding menthol was associated with decreased % reduction of FMD impairment (40.52±4.85% vs. 18.50±9.81%; p=0.048). These two effects were independent (p for nicotine x menthol interaction = 0.6). Conclusion: Reduction of nicotine level and addition of menthol each lessen the acute impairment of FMD in rats exposed briefly to tobacco SHS.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.121.suppl_1.54
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1467838-X
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