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Mechanisms of Vascular Endothelial Dysfunction in Chronic E-Cigarette Users.
紀錄類型:
書目-語言資料,手稿 : Monograph/item
正題名/作者:
Mechanisms of Vascular Endothelial Dysfunction in Chronic E-Cigarette Users./
作者:
Halstead, Kristen.
面頁冊數:
1 online resource (53 pages)
附註:
Source: Masters Abstracts International, Volume: 85-01.
Contained By:
Masters Abstracts International85-01.
標題:
Clinical psychology. -
電子資源:
click for full text (PQDT)
ISBN:
9798379786090
Mechanisms of Vascular Endothelial Dysfunction in Chronic E-Cigarette Users.
Halstead, Kristen.
Mechanisms of Vascular Endothelial Dysfunction in Chronic E-Cigarette Users.
- 1 online resource (53 pages)
Source: Masters Abstracts International, Volume: 85-01.
Thesis (M.S.)--The University of Iowa, 2023.
Includes bibliographical references
Tobacco and nicotine use cause vascular endothelial dysfunction, thus increasing lifetime cardiovascular disease (CVD) risk. Whether this is also true for e-cigarette use remains unknown. Tobacco cigarette smoking leads to higher CVD burden in females compared to males, but no studies of e-cigarette use have examined sex-differences in vascular responses that inform lifetime CVD risk. Chronic e-cigarette use is reported to decrease endothelial function, a potent predictor of future CVD risk. However, the mechanism(s) mediating this reduction remain unclear.Using the cutaneous circulation as a model, we examined endothelium- and nitric oxide (NO)-dependent dilation, and the role of oxidative stress in attenuating these responses, in otherwise healthy, young chronic (≥6 months) e-cigarette users (EC) compared to healthy controls (HC). 20 HC (21±2 yrs; 10M/10F) and 20 EC (21±2 yrs; 10M/8F) underwent a standard local heating protocol (42°C; 0.1°C·s-1). Two intradermal microdialysis fibers were placed in the ventral forearm skin for local delivery of lactated Ringer's (control), or 10µM tempol (superoxide dismutase mimetic). After full expression of the local heating response, 15mM NG-nitro-L-arginine methyl ester (L-NAME; NO synthase-inhibition) was perfused. Red cell flux was measured continuously by laser-Doppler flowmetry, and cutaneous vascular conductance (CVC=flux/MAP) was standardized to maximum (%CVCmax; 28mM SNP + 43°C).Between groups, endothelium- (EC: 73.1 ± 14.3 vs HC: 86.5 ± 8.9 %CVCmax; p<0.001) and NO-dependent (EC: 49.5 ± 18.1% vs HC: 61.8 ± 14.7%) dilation were attenuated in EC compared to HC. Local tempol perfusion increased endothelium- (83.6 ± 11.6 %CVCmax; p=0.01) and NO-dependent (62.6 ± 13.5%; p=0.005) dilation in EC but had no effect in HC (all p>0.05). Within sex, female EC had lower endothelium- (EC: 71.0 ± 13.3 vs HC: 89.1 ± 7.3 %CVCmax; p=0.002) and NO-dependent (EC: 46.9±5.5 vs HC: 69.4±10.8%; p=0.005) dilation compared to female HC. There were no differences between these responses in HC and EC males (both p>0.05). Tempol perfusion augmented endothelium- (83.1 ± 12.8 %CVCmax; p=0.002) and NO-dependent (62.3 ± 13.1%; p=0.015) dilation in EC females but had no effect in EC males (both p>0.05). These data suggest that otherwise healthy young adult e-cigarette users have reduced microvascular endothelium- and NO-dependent dilation. Within e-cigarette users, these results are driven by greater reductions in females. Oxidative stress, and specifically superoxide anion, contributes to these impairments. Females who use e-cigarettes demonstrate greater reductions in endothelial function and may have increased risk for developing future CVD.
Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024
Mode of access: World Wide Web
ISBN: 9798379786090Subjects--Topical Terms:
649607
Clinical psychology.
Subjects--Index Terms:
Electronic cigarettesIndex Terms--Genre/Form:
554714
Electronic books.
Mechanisms of Vascular Endothelial Dysfunction in Chronic E-Cigarette Users.
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Tobacco and nicotine use cause vascular endothelial dysfunction, thus increasing lifetime cardiovascular disease (CVD) risk. Whether this is also true for e-cigarette use remains unknown. Tobacco cigarette smoking leads to higher CVD burden in females compared to males, but no studies of e-cigarette use have examined sex-differences in vascular responses that inform lifetime CVD risk. Chronic e-cigarette use is reported to decrease endothelial function, a potent predictor of future CVD risk. However, the mechanism(s) mediating this reduction remain unclear.Using the cutaneous circulation as a model, we examined endothelium- and nitric oxide (NO)-dependent dilation, and the role of oxidative stress in attenuating these responses, in otherwise healthy, young chronic (≥6 months) e-cigarette users (EC) compared to healthy controls (HC). 20 HC (21±2 yrs; 10M/10F) and 20 EC (21±2 yrs; 10M/8F) underwent a standard local heating protocol (42°C; 0.1°C·s-1). Two intradermal microdialysis fibers were placed in the ventral forearm skin for local delivery of lactated Ringer's (control), or 10µM tempol (superoxide dismutase mimetic). After full expression of the local heating response, 15mM NG-nitro-L-arginine methyl ester (L-NAME; NO synthase-inhibition) was perfused. Red cell flux was measured continuously by laser-Doppler flowmetry, and cutaneous vascular conductance (CVC=flux/MAP) was standardized to maximum (%CVCmax; 28mM SNP + 43°C).Between groups, endothelium- (EC: 73.1 ± 14.3 vs HC: 86.5 ± 8.9 %CVCmax; p<0.001) and NO-dependent (EC: 49.5 ± 18.1% vs HC: 61.8 ± 14.7%) dilation were attenuated in EC compared to HC. Local tempol perfusion increased endothelium- (83.6 ± 11.6 %CVCmax; p=0.01) and NO-dependent (62.6 ± 13.5%; p=0.005) dilation in EC but had no effect in HC (all p>0.05). Within sex, female EC had lower endothelium- (EC: 71.0 ± 13.3 vs HC: 89.1 ± 7.3 %CVCmax; p=0.002) and NO-dependent (EC: 46.9±5.5 vs HC: 69.4±10.8%; p=0.005) dilation compared to female HC. There were no differences between these responses in HC and EC males (both p>0.05). Tempol perfusion augmented endothelium- (83.1 ± 12.8 %CVCmax; p=0.002) and NO-dependent (62.3 ± 13.1%; p=0.015) dilation in EC females but had no effect in EC males (both p>0.05). These data suggest that otherwise healthy young adult e-cigarette users have reduced microvascular endothelium- and NO-dependent dilation. Within e-cigarette users, these results are driven by greater reductions in females. Oxidative stress, and specifically superoxide anion, contributes to these impairments. Females who use e-cigarettes demonstrate greater reductions in endothelial function and may have increased risk for developing future CVD.
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