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Studies show that the cardiovascular effects of cigarettes and e-cigarettes are surprisingly similar

Studies show that the cardiovascular effects of cigarettes and e-cigarettes are surprisingly similar


Two relevant studies in humans and rats found that the cardiovascular effects of tobacco and e-cigarettes were strikingly similar, and that these detrimental effects on vascular function were caused by airway irritation from inhalation of foreign substances. It turns out that there is a high possibility that Not specific components of cigarette smoke or e-cigarette vapor (aerosols), according to new research published today in the American Heart Association’s peer-reviewed journal. Atherosclerosis, Thrombosis and Vascular Biology (ATVB).

Both cigarette smoking and e-cigarettes are known to cause endothelial dysfunction, in which the large blood vessels do not open enough to supply enough blood to the heart and other tissues. , may be an early predictor of cardiovascular disease. Endothelial cells line all blood vessels and regulate vascular openings, material exchange between the bloodstream and surrounding tissues, and immune and inflammatory responses.

The goal of this project is the growing number of inhaled tobacco products such as combustible tobacco, heat-not-burn tobacco products, and e-cigarettes, all of which impair endothelial function despite their fundamental differences. It was to find out why. Thousands of chemicals have been identified in tobacco smoke, some of which are also present in e-cigarette aerosols, either as original ingredients or as chemical reaction products of the heating process. , we sought to find out which specific constituents of smoke and e-cigarette vapor are responsible for preventing the efficient functioning of blood vessels.”

Matthew L. Springer, Ph.D., Principal Investigator of both studies, Professor of Medicine, Department of Cardiology, University of California, San Francisco

Springer and colleagues conducted two studies to assess the effects of smoking and e-cigarettes on cardiovascular function in both rats and humans.

Tobacco smoke-induced impairment of endothelial function is not caused by specific smoke constituents, but by vagal input from the respiratory tract.

In a rat study, arterial flow-mediated dilatation (FMD), the ability of blood vessels to dilate, was measured before and after smoking four conventional combustible cigarettes: conventional, low-nicotine, and conventional nicotine. Nicotine with menthol and reduced nicotine with menthol. Menthol is added to many tobacco products and may reduce the irritation caused by smoking and may play a major role in promoting nicotine addiction, especially among new smokers.

The study found that vasodilation decreased after the use of all four types of tobacco, with the degree of reduction ranging from 20 to 46% depending on the type of tobacco. Although not required, higher nicotine levels reduced FMD more significantly than lower nicotine levels, and menthol reduced FMD less than non-menthol products.

Springer overinterpreted the finding that the addition of menthol reduced the severity of bloodstream-mediated diastolic impairment, citing that the impairment was still substantial and that menthol had other hazards, suggesting that menthol should not be used. Emphasized that it should not imply beneficial additives in smoking and e-cigarette products.

Rats were also exposed to the two major gases found in both smoke and e-cigarette aerosols, as well as clean carbon nanoparticles, to assess the effects of these types of components on vasodilation. Gases and carbon particles had similar impairment effects to total tobacco smoke, even though they represent completely different chemical and physical constituents of the smoke.

“Flow-mediated dilation is compromised by smoke as a whole, gas phase components of smoke, and simple carbon particles, and no single component is uniquely responsible, suggesting that the mechanism is to diverge from the respiratory tract, including the vagus nerve.” We investigated whether it was involved in the general stimulus response,” Springer said.

The vagus nerve is a major component of the parasympathetic nervous system that controls involuntary visceral functions. It is involved in the regulation of lung functions such as digestion, heart rate, respiratory rate, vasodilation, inflammatory response, cough reflex and mucus production.

To test this hypothesis, researchers exposed anesthetized rats to smoke after cutting the vagus nerve. They found that by preventing nerve signals in the lungs of rats from reaching the rest of the body, smoke-induced vascular dysfunction could be completely prevented. These findings suggest that endothelial dysfunction may be caused by vagus-dependent mechanisms arising from respiratory stimulation and pulmonary sensory nerves.

“I was surprised to discover that it was not the specific inhaled foreign substance that caused the adverse cardiovascular effects. A few “All inhaled products are likely to have similar detrimental effects on vascular function,” Springer said.

Springer pointed out that the lack of specific toxins that cause vascular damage means that regulators cannot rely on banning specific ingredients to avoid adverse effects in inhaled products.

Co-authored by Pooneh Nabavizadeh, MD. Jiangtao Liu, MD; Poonam Rao, MD; Sharina Ibrahim, MSc. Daniel D. Han, Bachelor. Ronak Derakhshandeh, Master of Science. Huiliang Qiu, MD. Xiaoyin Wang, MD; Stanton A. Grantz, Ph.D. and Suzaynn F. Schick, Ph.D. Author disclosures are provided in the manuscript.

This work was supported by grants from the National Heart, Lung, and Blood Institute, a division of the National Institutes of Health (NIH), and the US Food and Drug Administration Center for Tobacco Products. It is supported by NIH’s National Cancer Institute and the Elfenworks Foundation (in memory of Deb O’Keefe) and the Roy E Thomas Medical Foundation.

Chronic e-cigarette use impairs endothelial function at the physiological and cellular level

A second study was conducted in multiple centers and included individuals who reported smoking combustible tobacco regularly, those who reported using e-cigarette products regularly, and those who used nicotine products. Cardiovascular health status of all participants was assessed by researchers measuring endothelial function and performing cell culture experiments to assess the effects of chronic e-cigarette use and vascular disorders. was assessed at one point in time by assessing its association with the level of Measures include the production of nitric oxide, a key molecule for the proper functioning of blood vessels, and endothelial cell permeability, which reflects how easily substances escape from blood vessels. Increased vascular permeability leads to the leakage of larger molecules and may contribute to edema, or swelling caused by excess fluid in tissues, inflammation, heart disease, and other diseases such as cancer.

“Since flammable cigarette smoke and e-cigarette aerosols inhaled by humans do not directly contact blood vessels, but also blood, serum (the clear liquid in the blood that remains after blood clots) was collected from all participants. We took a sample and brought it into contact with endothelial cells in a culture dish to assess how different serum samples affected the functional behavior of those cells,” Springer said. “This allows us to examine the effect of substances in smoke/aerosols absorbed from the lungs and entering the bloodstream on endothelial cells and on other circulating molecules that the body may produce in response to smoke or aerosol inhalation. We were able to investigate the effects, including proteins involved in the inflammatory response.”

The study included 120 adults aged 21 to 50 years without cardiovascular disease. Participants included those who smoked 5 or more combustible cigarettes a day for at least 1 year. People who used e-cigarettes more than 5 times a week for more than 3 months. And those who do not currently smoke or smoke e-cigarettes.

The analysis found that prolonged e-cigarettes and smoking both cause blood changes that affect endothelial function, albeit in different ways.

  • Serum-soaked endothelial cells from both those who smoked regularly and those who smoked e-cigarettes on a regular basis showed that nitric oxide release was impaired, implying that endothelial cell function was compromised. It was less.
  • Condensed e-cigarette aerosols did not directly reduce nitric oxide production. This indicates that the substances in the blood that impair nitric oxide production did not come directly from aerosols, but were produced by the body in response to inhalation.
  • Serum from regular e-cigarette smokers, but not from regular e-cigarette smokers, increases the permeability of endothelial cells, allowing more substances to pass through the cells, causing tissue edema. It behaves like a possible leaky blood vessel.
  • Serum from participants who smoked e-cigarettes regularly caused endothelial cells to produce molecules that trigger oxidative stress, an imbalance between free radicals and antioxidants in the body, which can lead to cell and tissue damage. .
  • People who regularly use e-cigarettes or smoke combustible cigarettes have altered circulating biomarkers of inflammation, blood clotting factors, and cell adhesion compared to those who do not smoke or smoke e-cigarettes regularly. was seen.
  • Certain inflammatory biomarkers in the serum of people who regularly smoked combustible cigarettes were elevated, but not among those who used e-cigarettes. Sexual biomarkers were elevated in the serum of people who smoked e-cigarettes regularly, but not those who smoked combustible cigarettes regularly.

“Distinct patterns of these heart disease risk biomarkers in the sera of frequent users of combustible tobacco and e-cigarette products show that e-cigarette use and smoking are fundamentally different, despite similar physiological effects.” have been shown to provoke molecular reactions: no smoking of combustible cigarettes but causes blood changes that increase the likelihood of leakage in blood vessels, both smoking and e-cigarettes cause blood changes that lead to endothelial function It causes disability and increases the risk of future cardiovascular events in otherwise healthy people,” Springer said.

In this study, flow-mediated We also found significantly (more than 5%) lower swelling. A previous study showed that a 2% reduction in vasodilation was associated with a 15% increase in heart disease risk, suggesting that the effects of smoking and e-cigarettes are clinically important.

“It’s important that regulators, clinicians, and the general public recognize that e-cigarettes are not harmless,” Springer said. “While smoking and e-cigarettes can have similar detrimental cardiovascular effects, each condition causes adverse effects that may not occur otherwise. Cigarette smoking and e-cigarette product use can actually be bad for your blood vessels. healthier than


Journal reference:

Nabavizadeh, P. and others. (2022) Tobacco smoke-induced impairment of endothelial function is caused by vagal input from the respiratory tract rather than by specific smoke constituents. Atherosclerosis Thrombosis and Vascular Biology.

Mohammadi, L. and others. (2022) Chronic e-cigarette use impairs endothelial function at the physiological and cellular level. Atherosclerosis Thrombosis and Vascular Biology.




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