PARIS, Oct. 27 (Benin News) –
Two related studies, one in humans and the other in rats, found that the cardiovascular effects of tobacco and e-cigarettes are strikingly similar and that these adverse effects on blood vessel function are likely due to a respiratory tract irritation from inhaling a foreign substance, rather than a specific component of cigarette smoke or e-cigarette vapor (aerosol), according to new research published in the journal Arteriosclerosis, Thrombosis and Vascular Biology (ATVB) from the American Heart Association.
According to the study, smoking and e-cigarette use are known to cause endothelial dysfunction – the inability of large blood vessels to open wide enough to supply enough blood to the heart and other tissues.
It can be an early indicator of cardiovascular disease because endothelial cells line the inside of all blood vessels and regulate the opening of vessels, the exchange of substances between the bloodstream and surrounding tissues, as well as as immune and inflammatory responses.
“The objective of this project was to determine why an increasing number of inhaled tobacco products, including combustible cigarettes, heated tobacco products and e-cigarettes, all impair endothelial function despite fundamental differences between these products” , explains the principal investigator of the two studies, Matthew L. Springer, MD, professor of medicine in the division of cardiology at the University of California in San Francisco (United States).
Thousands of chemicals have been identified in tobacco smoke, some of which are also present in e-cigarette aerosols, either as the original ingredient or as a chemical reaction product of the heating process,” he adds. -he. We are trying to find out which specific component of e-cigarette smoke or vapor may be responsible for interfering with the ability of blood vessels to function effectively.
Springer and his colleagues conducted two studies to assess the effects of smoking and vaping on cardiovascular function in rats and humans.
The impairment of endothelial function by cigarette smoke is not due to a specific component of the smoke, but to the aspiration of air through the respiratory tract
In the rat study, flow-mediated arterial dilation (FAD), which is the ability of blood vessels to widen, was measured before and after exposure to smoke from four types of traditional combustible cigarettes : classic nicotine, reduced nicotine, classic nicotine with added menthol and reduced nicotine with added menthol.
They point out that menthol is added to tobacco products (not in the European Union, where it has been banned since last May), and that it can reduce the irritation caused by smoking, especially in new smokers, and play an important role in facilitating nicotine addiction.
Study results revealed that blood vessel dilation was reduced after using all four types of cigarettes, and the magnitude of the reduction ranged from 20 to 46 percent, depending on the type of cigarette. Nicotine was not necessary for the alteration of vascular function; however, higher levels of nicotine were associated with a greater reduction in FMD than lower levels of nicotine, and menthol was associated with a smaller reduction in FMD than products without menthol.
Springer emphasized that the finding that the addition of menthol reduced the severity of flow-mediated dilation impairment should not be over-interpreted to suggest that menthol is a beneficial additive in smoking products. and to vape, because the alteration was still significant and the menthol has other deleterious effects.
The rats were also exposed to two of the main gases found in e-cigarette smoke and aerosol, as well as pure carbon nanoparticles, to assess the effects of these types of compounds on vessel dilation. blood. Carbon gases and particles had effects similar to whole tobacco smoke, although they represent completely different chemical and physical components of smoke.
“Since flow-mediated expansion was affected by whole smoke, gas-phase smoke components, and individual carbon particles, with no single component being solely responsible, we investigated whether the mechanism involved a common airway irritation response affecting the vagus nerve,” says Springer.
The vagus nerve is a major component of the parasympathetic nervous system, which controls the involuntary functions of internal organs. It is responsible for regulating digestion, heart rate, respiratory rate, vascular dilation, inflammatory responses, and lung functions such as the cough reflex and mucus production.
To test this hypothesis, the researchers exposed anesthetized rats to smoke after severing the vagus nerves. They found that preventing nerve signals from the rats’ lungs from reaching the rest of the body completely prevented any vascular functional impairment due to smoke. These results suggest that endothelial dysfunction may be caused by a vagus nerve-dependent mechanism resulting from irritation of respiratory and pulmonary sensory nerves.
“We were surprised to find that it is not the inhalation of a specific foreign material that causes adverse cardiovascular effects, but the fact that some kind of irritant is inhaled in the first place, whatever its nature. says Mr. Springer. It is likely that all inhalants have similar adverse effects on vascular function.
Springer points out that the lack of a specific toxin to explain vascular disorders means that regulators cannot rely on banning specific ingredients to prevent adverse effects from inhalants.