scholarly journals Vascular endothelial function is impaired by aerosol from a single IQOS HeatStick to the same extent as by cigarette smoke

2018 ◽  
Vol 27 (Suppl 1) ◽  
pp. s13-s19 ◽  
Author(s):  
Pooneh Nabavizadeh ◽  
Jiangtao Liu ◽  
Christopher M Havel ◽  
Sharina Ibrahim ◽  
Ronak Derakhshandeh ◽  
...  

BackgroundHeated 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.MethodsWe 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.ResultsFMD 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.ConclusionsAcute exposures to IQOS aerosol impairs FMD in rats. IQOS use does not necessarily avoid the adverse cardiovascular effects of smoking cigarettes.

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Kazuki Hotta ◽  
Wayne B Batchelor ◽  
James Graven ◽  
Vishal Dahya ◽  
Thomas E Noel ◽  
...  

Patients with peripheral artery disease (PAD) frequently have walking impairment due to lower extremity claudication. Our preliminary results in a rat model of aging indicate that a program of daily calf muscle stretching improves endothelium-dependent dilation of soleus muscle arterioles and increases soleus muscle blood flow during exercise. However, the effects of muscle stretching on the function of arteries supplying the legs of PAD patients is unknown. We hypothesized that daily calf muscle stretching improves vascular endothelial function and walking distance in PAD patients. To test our hypothesis, a randomized, non-blinded, crossover study was performed. Four weeks of muscle stretching (30 min/d, 5 days/wk) and 4 weeks of sedentary lifestyle (no stretching) were performed in random order. Thirteen patients with PAD participated in this study (71 ± 2 years old; 7 males and 6 females). During the stretching intervention both ankle joints were maintained at 15o of dorsiflexion using ankle dorsiflexion splints to stretch their calf muscles at home. Flow-mediated dilation (FMD; dilation to post-occlusion reactive hyperemia) and nitroglycerin-induced dilation (dilation to sublingual 0.4 mg nitroglycerin) of the popliteal artery were measured after 4 weeks of muscle stretching and after the no stretching period using ultrasound. A six-minute walk test was also performed to obtain walking distance. After 4 weeks of muscle stretching, FMD and 6-minute walking distance significantly improved as compared to the values measured after 4 weeks of no stretching (FMD: 5.2 ± 0.6 % vs. 3.7 ± 0.4 %, P=0.003 stretching vs. no stretching, 6-minute walking distance: 355 ± 32 m vs. 311 ± 31 m, P=0.007, stretching vs. no stretching; mean ± SE). No difference in nitroglycerin-induced dilation was found between groups (10.9 ± 1.4 vs. 9.9 ± 1.1 %, P=0.54, stretching vs. no stretching). Percentage change of walking distance (%change = [(stretching - no stretching) / no stretching] x 100) significantly correlated with the %change of FMD (R 2 =0.65, P=0.03). These results indicate that static calf muscle stretching enhances vascular endothelial function of the popliteal artery, contributing to improvement of walking tolerance in PAD patients.


2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Poonam Rao ◽  
Pooneh Nabavizadeh Rafsanjani ◽  
Daniel Han ◽  
Suzaynn Schick ◽  
Matthew Springer

Introduction: Exposure to tobacco and marijuana smoke impairs vascular endothelial function. While the particulate phase of smoke is heavily implicated, the role of volatile constituents is unclear. Smoke contains aldehydes, which are known to cause endothelial dysfunction. We explored whether two aldehydes found in smoke, acrolein and acetaldehyde, can induce endothelial dysfunction. Hypothesis: Aldehydes in smoke impair endothelial function. Methods: We exposed 4 groups of anesthetized rats to 3 ppm acrolein and 10-11.5 ppm acetaldehyde gases (concentrations relevant to levels in secondhand smoke), Marlboro Red cigarette sidestream smoke at modest levels (600 μg/m 3 PM2.5) as a positive control, and clean air through the gas generation system as a negative control. Exposure was continuous for 10 minutes. Endothelial function (flow-mediated dilation; FMD) was quantified pre- and post-exposure by measuring femoral artery diameter with ultrasound before and after 5 min of transient ischemia and expressed as % vasodilation. Results: Impairment of FMD was observed for acrolein (10.8±1.7(SD)% vs. 5.8±2.9%, p=.001), acetaldehyde (8.8±2.0% vs. 6.0±2.5%, p=.001), and cigarette smoke (9.4±2.9% vs. 5.8±2.0%, p=.002), but not for air (7.9±2.0% vs. 9±3.2%, p=.44) (figure; each colored line denotes a rat pre- and post-exposure; bars denote means). Conclusions: Acrolein and acetaldehyde at levels found in secondhand smoke impair endothelial function. Our results suggest that despite a potential role of particles, volatile aldehydes may mediate part of the endothelial dysfunction caused by exposure to smoke.


2018 ◽  
Vol 119 (3) ◽  
pp. 259-270 ◽  
Author(s):  
Joshua D. McDonald ◽  
Chureeporn Chitchumroonchokchai ◽  
Jinhui Li ◽  
Eunice Mah ◽  
Allison N. Labyk ◽  
...  

AbstractEggs attenuate postprandial hyperglycaemia (PPH), which transiently impairs vascular endothelial function (VEF). We hypothesised that co-ingestion of a glucose challenge with egg-based meals would protect against glucose-induced impairments in VEF by attenuating PPH and oxidative stress. A randomised, cross-over study was conducted in prediabetic men (n20) who ingested isoenegertic meals (1674 kJ (400 kcal)) containing 100 g glucose (GLU), or 75 g glucose with 1·5 whole eggs (EGG), seven egg whites (WHITE) or two egg yolks (YOLK). At 30 min intervals for 3 h, brachial artery flow-mediated dilation (FMD), plasma glucose, insulin, cholecystokinin (CCK), lipids (total, LDL- and HDL-cholesterol; TAG), F2-isoprostanes normalised to arachidonic acid (F2-IsoPs/AA), and methylglyoxal were assessed. In GLU, FMD decreased at 30–60 min and returned to baseline levels by 90 min. GLU-mediated decreases in FMD were attenuated at 30–60 min in EGG and WHITE. Compared with GLU, FMDAUCwas higher in EGG and WHITE only. Relative to baseline, glucose increased at 30–120 min in GLU and YOLK but only at 30–90 min in EGG and WHITE. GlucoseAUCand insulinAUCwere also lower in EGG and WHITE only. However, CCKAUCwas higher in EGG and WHITE compared with GLU. Compared with GLU, F2-IsoPs/AAAUCwas lower in EGG and WHITE but unaffected by YOLK. Postprandial lipids and methylglyoxal did not differ between treatments. Thus, replacing a portion of a glucose challenge with whole eggs or egg whites, but not yolks, limits postprandial impairments in VEF by attenuating increases in glycaemia and lipid peroxidation.


2008 ◽  
Vol 52 (3) ◽  
pp. 262-267 ◽  
Author(s):  
J.F Argacha ◽  
D Fontaine ◽  
D Adamopoulos ◽  
A Ajose ◽  
P van de Borne ◽  
...  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Mobin Malik ◽  
Michael E Widlansky ◽  
Tisha Suboc ◽  
Allison Coulliard ◽  
Jidong Su ◽  
...  

Introduction: There is a significant unmet clinical need to identify novel therapies to prevent and treat the progression of cardiovascular disease. This requires identification of additional contributory processes to the pathogenesis of heart disease so that mechanism-based interventions may be developed. Hypothesis: Our objective was to translate the recently discovered mechanistic link in rats between changes in the intestinal microbiota and the pathogenesis of cardiovascular disease to humans. Methods: Twenty male adult patients with stable coronary heart disease on stable doses of vasoactive medications and HMG-CoA reductase inhibitors consumed a probiotic drink containing Lactobacillus plantarum 299v (3 oz. serving containing 20 billion colony forming units) once a day for 42 days. Vascular endothelial function was measured at the beginning and end of the study period by brachial flow-mediated dilation. Results: The probiotic improved brachial artery flow mediated dilation, a surrogate marker of cardiovascular risk, by 33% from 3.55 + 1.96% to 4.73 + 2.33% with a trend towards decreased LDL-cholesterol by 8% from 96 + 11 mg/dl to 88 + 10 mg/dl. Probiotic therapy decreased circulating levels of the inflammatory cytokines IL-8 by 24% (17±2 to 13±1 pg/ml) and IL-12 by 20% (56±7 to 45±6 pg/ml). Whole microbiome analysis based on abundance of 2,206 taxa using hierarchical clustering revealed no separation of the overall intestinal microbial population between pre- and post-probiotic treatment samples. Bacterial genus richness ranged from 334 to 530 and archaeal ranged from 8 to 25, with no significant differences between pre- and post-probiotic samples. Lactobacillus and Bacillus species were enriched in post-probiotic samples. Lactobacillus plantarum 299v levels were elevated in post-probiotic samples, confirming patient compliance. Conclusions: Our discovery of a relationship between Lactobacillus plantarum 299v, improved vascular endothelial function and decreased inflammation indicates intestinal microbiota may be developed as therapies to prevent and treat the progression of cardiovascular disease.


2020 ◽  
Vol 37 (5) ◽  
pp. 2169-2183
Author(s):  
Tamio Teramoto ◽  
Hirotaka Shibata ◽  
Yuki Suzaki ◽  
Shingo Matsui ◽  
Naoto Uemura ◽  
...  

Abstract Introduction Omega-3 fatty acid ethyl esters (omega-3), an eicosapentaenoic acid and docosahexaenoic acid preparation (Lotriga®, Takeda Pharmaceutical Company Limited), are approved in Japan to treat triglyceridemia. We investigated the effects of omega-3 on vascular endothelial function, measured by flow-mediated dilation (FMD). Methods Patients with dyslipidemia receiving 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors were randomized 1:1 to receive omega-3 at 2 g (QD) or 4 g (2 g BID) for 8 weeks. The primary end point was the change from baseline of fasting  %FMD in each treatment group. Secondary end points included the 4-h postprandial  %FMD and 4-h postprandial triglyceride (TG) level. Results Thirty-seven patients were randomized to receive omega-3 at 2 g (n = 18) or 4 g (n = 19). Mean fasting %FMD did not increase from baseline to week 8 in the 2-g group (− 1.2%) or 4-g group (− 1.3%). Mean 4-h postprandial %FMD did not change from baseline to week 8 in the 2-g group (0.0%), but increased in the 4-g group (1.0%). Mean 4-h postprandial TG level decreased by 34.7 mg/dl from baseline over week 8 in the 2-g group, with a significantly larger decrease in the 4-g group of 75.9 mg/dl (p < 0.001). No new safety concerns were identified. Conclusions Fasting %FMD did not improve after 8 weeks of omega-3 treatment at 2 g or 4 g. After 8 weeks, 4-h postprandial TG levels showed improvement at both doses, with a greater reduction in the 4-g group. Trial Registration ClinicalTrials.gov, ID: NCT02824432.


Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1872 ◽  
Author(s):  
Maho Sasaki ◽  
Yuri Nonoshita ◽  
Takashi Kajiya ◽  
Nobuhiko Atsuchi ◽  
Megumi Kido ◽  
...  

Vascular disease poses a major public health problem worldwide. Trigonelline isolated from Raphanus sativus cv. Sakurajima Daikon (Sakurajima radish) induces nitric oxide production from vascular endothelial cells and enhances vascular function. Here, we investigated the characteristics of trigonelline and its effects on endothelial function after consumption of Sakurajima radish by humans. Our results show that Sakurajima radish contains approximately 60 times more trigonelline than other radishes and squashes. Additionally, no significant differences were observed between varieties of Sakurajima radish, suggesting that any type of Sakurajima radish can be ingested for trigonelline supplementation. The effects of cooking and processing Sakurajima radish were also evaluated, as were the effects of freezing, and changes in osmotic pressure and pH. A first-in-human trial using Sakurajima radish showed that ingestion of 170 g/day of Sakurajima radish for ten days increased blood trigonelline concentrations and significantly improved flow-mediated dilation, which is a measure of vascular endothelial function. Overall, our findings suggest that the trigonelline contained in Sakurajima radish may contribute to improved human vascular endothelial function. Hence, Sakurajima radish may enhance vascular endothelial function as a functional food.


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