ЖУРНАЛ КАРДИОРЕСПИРАТОРНЫХ ИССЛЕДОВАНИЙ | JOURNAL OF CARDIORESPIRATORY RESEARCH
№2 | 2021
26
Сачин Кумар Байта
Студент MBBS
Самаркандский Государственный Медицинский
Институт. Самарканд, Узбекистан
Ташкенбаева Элеонора Негматовна
д.м.н., проф., зав. кафедрой внутренних болезней №2
Самаркандский государственный медицинский институт
Самарканд, Узбекистан
Абдиева Гулнора Алиевна
ассистент кафедры внутренних болезней №2
Самаркандский государственный медицинский институт
Самарканд, Узбекистан
ВЛИЯНИЕ КУРЕНИЯ НА СЕРДЕЧНО-СОСУДИСТЫЕ ФУНКЦИИ: РОЛЬ НИКОТИНА И МОНООКСИДА УГЛЕРОДА
For citation:
Sachin Kumar B., Tashkenbaeva E.N., Abdieva G.A. Effects of smoking on cardiovascular function: the role of nicotine and carbon
monoxide. Journal of cardiorespiratory research. 2021, vol.2, issue 2, pp.26-33
http://dx.doi.org/10.26739/2181-0974-2021-2-4
АННОТАЦИЯ
Курение — это распространенное явление среди всех факторов сердечно-сосудистых заболеваний. Он влияет на миокард и его
кровоснабжение, усиливает атеросклероз и способствует развитию инфаркта миокарда, кардиомиопатии и заболеваний периферических
сосудов. Никотин, окись углерода и различные элементы табака оказывают непосредственное воздействие на эндотелий, вызывая
воспаление, атерому и тромбоз. В сигаретном дыме много свободных радикалов, которые провоцируют и усиливают воспалительный
каскад, увеличивая инфильтрацию лейкоцитов и производство цитокинов. Очень важно собирать правильные записи о привычке к
курению, однако накопление записей больше не должно зависеть от собственных записей, которые вводят в заблуждение, однако следует
использовать биохимические биомаркеры нескольких форм, в идеале котинин. Курильщики должны получить интенсивные
консультации, каждый с помощью квалифицированного персонала на месте и с помощью профессиональных служб по отказу от курения.
Курильщикам следует дать фундаментальное определение пагубным последствиям курения для ишемической болезни сердца и
атеросклероза. Пациентам следует рекомендовать применить все повторные рекомендации по консультированию и обратиться к
заместительной терапии или другим лекарственным средствам, чтобы бросить курить. Цель этой статьи - дать краткую оценку
результатов курения, и особенно результатов воздействия никотина и других веществ на сердечно-сосудистую систему. Никотин
деактивирует сердечную вегетативную функцию, усиливает эмпатию, увеличивает частоту сердечных сокращений (ЧСС) при
расслаблении, в то же время замедляя повышение частоты сердечных сокращений за счет инновационных упражнений и снижает
максимальное количество часов, которое может быть выполнено. В то же время образующийся курением ко связывается с гемоглобином
и миоглобином, снижает сатурацию артериальной крови 02, ставит под угрозу работу респираторных ферментов и вызывает нарушение
устройства производства, транспортировки и транспортировки 02, особенно при выполнении упражнений, в частности, снижая целевые
возможности и общая производительность циркуляционной машины.
Ключевые слова:
болезнь сердца, сердечно-сосудистая система, курение, табак.
Sachin Kumar Baitha
MBBS Student
Samarkand State Medical Institute
Samarkand, Uzbekistan
Tashkenbaeva Eleonora Negmatovna
Doctor of Medical Sciences, Professor, Head of the
Department of Internal Medicine №2
Samarkand State Medical Institute
Samarkand, Uzbekistan
Abdieva Gulnora Alievna
Assistant of the Department of Internal Medicine No. 2
Samarkand State Medical Institute
Samarkand, Uzbekistan
ЖУРНАЛ КАРДИОРЕСПИРАТОРНЫХ ИССЛЕДОВАНИЙ | JOURNAL OF CARDIORESPIRATORY RESEARCH
№2 | 2021
27
EFFECTS OF SMOKING ON CARDIOVASCULAR FUNCTION: THE ROLE OF NICOTINE AND CARBON MONOXIDE
ANNOTATION
Smoking is a widespread chance thing for all factors of cardiovascular disorder. It influences the myocardium and occludes the blood supply, will
increase atherosclerosis and contributes to myocardial infarction, cardiomyopathy and peripheral vascular disorder. Nicotine, carbon monoxide and
different tobacco elements have direct outcomes at the endothelium, inflicting inflammation, atheroma and thrombosis. Free radicals are ample in
cigarette smoke and those provoke and accentuate the inflammatory cascade, growing leukocyte infiltration and cytokine production. It is essential
to reap correct records approximately smoking habit, however records amassing ought to now no longer depend on self-record that is misleading,
however ought to use a few shapes of biochemical biomarker, ideally cotinine. Smokers ought to then be intensively counselled, each through in-
residence skilled personnel and thru the professional smoking cessation services. It ought to be defined to sufferers in fundamental phrases
approximately the deleterious outcomes of smoking on coronary heart disorder and atherosclerosis. Patients ought to be recommended to apply all
reasserts of counselling and to go to the substitute treatments or different pharmaceutical aids to quit. The purpose of this article is to provide a brief
evaluation of the outcomes of smoking, and especially the outcomes of nicotine and co on cardiovascular function. Nicotine deactivates cardiac
autonomic function, will increase empathy hobby, increases heart rate (HR) at relaxation, while blunting HR elevation all through innovative
exercise and lowering the maximum HR that may be executed. On the equal time, the smoking- generated co binds with haemoglobin and
myoglobin, reduces arterial 02 blood saturation, compromises the performance of respiratory enzymes, and reasons disorder of the 02 production,
transportation and transport device, specially all through exercise, notably decreasing the purposeful capability and the overall performance of the
circulatory machine.
Keywords:
heart disease, circulatory system, smoking, tobacco.
Sachin Kumar Baita
MBBS yo`nalishi bo`yicha talaba
Samarqand davlat tibbiyot instituti
Samarqand, O'zbekiston
Tashkenbayeva Eleonora Negmatovna
Tibbiyot fanlari doktori, prof., Ichki kasalliklar
kafedrasi mudiri №2
Samarqand davlat tibbiyot instituti
Samarqand, O'zbekiston
Abdiyeva Gulnora Aliyevna
2-son ichki kasalliklar kafedrasi assistenti
Samarqand davlat tibbiyot instituti
Samarqand, O'zbekiston
CHEKISHNING YURAK-QON TOMIR FUNKTSIYASIGA TA'SIRI: NIKOTIN VA UGLEROD MONOKSIDINING ROLI
ANNOTATSIYA
Chekish yurak-qon tomir kasalliklarining barcha omillari uchun keng tarqalgan imkoniyatdir. Bu miyokardga ta'sir qiladi va qon bilan
ta'minlanmaydi, aterosklerozni kuchaytiradi va miyokard infarkti, kardiyomiyopatiya va periferik qon tomir kasalliklariga yordam beradi. Nikotin,
uglerod oksidi va turli xil tamaki elementlari endoteliyda to'g'ridan-to'g'ri natijalarga ega bo'lib, yallig'lanish, ateroma va tromboz keltirib chiqaradi.
Erkin radikallar sigaretaning tutunida juda ko'p bo'lib, ular yallig'lanish kaskadini qo'zg'atadi va ta'kidlaydi, leykotsitlar infiltratsiyasi va sitokin
ishlab chiqarishni ko'paytiradi. Taxminan chekishni odat qilish uchun to'g'ri yozuvlarni yig'ish kerak, ammo hozirda to'plangan yozuvlar
chalg'ituvchi o'z-o'zini yozib olishga bog'liq emas, ammo bir nechta biokimyoviy biomarker, ideal holda kotinindan foydalanish kerak. Keyinchalik
chekuvchilarga har birida yashash joyidagi malakali kadrlar va chekishni tashlash bo'yicha professional xizmatlar orqali intensiv ravishda maslahat
berish kerak. Chalinganlarga yurakning koronar buzilishi va ateroskleroz kasalligi bo'yicha chekishning zararli natijalarini asosiy iboralar bilan
aniqlash kerak. Bemorlarga maslahatning barcha qayta tiklanishlarini qo'llash va davolanishni to'xtatish uchun almashtirish muolajalariga yoki turli
xil farmatsevtik vositalarga murojaat qilish tavsiya etilishi kerak. Ushbu maqolaning maqsadi chekish natijalarini qisqacha baholash, xususan yurak-
qon tomir faoliyati bo'yicha nikotin va ko natijalarini baholashdir. Nikotin yurakning avtonom funktsiyasini o'chiradi, hamdardlik sevimli
mashg'ulotlarini kuchaytiradi, bo'shashganda yurak urishini (soat) oshiradi, shu bilan birga soat ko'tarilishini innovatsion mashqlar yordamida va
bajarilishi mumkin bo'lgan maksimal soatni pasaytiradi. Xuddi shu vaqtda, chekish natijasida hosil bo'lgan CO gemoglobin va miyoglobin bilan
bog'lanib, qonning qon bilan to'yinganligini pasaytiradi, nafas olish fermentlarining ish faoliyatini pasaytiradi va 02 ishlab chiqarish, tashish va
tashish moslamasining buzilishini, xususan, jismoniy mashqlar orqali, shu bilan birga maqsadga muvofiq qobiliyat va qon aylanish mashinasining
umumiy ishlashi.
Kalit so'zlar:
yurak kasalligi, qon aylanish tizimi, chekish, tamaki
Introduction
Smoking is a major hazard thing for cardiovascular morbidity and
mortality, and is considered to be the main preventable purpose of loss
of life within the global [61, 65]. Internationally, 25% of centre - aged
cardiovascular deaths because of smoking [7]. The European society of
cardiology said these days that smoking reasons 28% of cardiovascular
deaths in men aged 35 to 69 years and 13% in girls of the identical age
[40]. In the European region of the arena fitness organization (WHO),
smoking is the second one most vital chance issue inside the burden of
incapacity adjusted life years and is the primary danger aspect for
untimely mortality, related to about 1.6 million deaths every yr. [66]. In
the eu union (EU), 15 % of all -cause deaths are attributed smoking,
amounting to 655,000 smoking associated deaths each yr. [53]. At the
same time as in Greece, the share of deaths from any smoking related
cause, among individuals a while 35 and older, has been envisioned to
be 18.1%. Primarily based on estimates via the who, tobacco maintains
to kill nearly 6 million humans each year - together with more than
600,000 passive people who smoke – via coronary heart ailment, lung
cancer, and different ailments [65]; that is one and a 1/2 million extra
than the corresponding estimate for 1990 [7]. If contemporary
tendencies continue, the death toll is projected to attain extra than 8
million according to yr. by using 2030 [65].
Smoking ranks among the pinnacle causes of cardiovascular
ailment, together with coronary heart disease, ischemic stroke,
peripheral artery disorder and abdominal aortic aneurysm [40]. It's also
associated with an improved chance of sure styles of most cancers, and
is a primary purpose of chronic obstructive pulmonary disease [61, 65].
Smoking, both lively or passive, can cause cardiovascular ailment thru
a chain of interdependent approaches, consisting of superior oxidative
pressure,
hemodynamic
and
autonomic
changes,
disorder,
ЖУРНАЛ КАРДИОРЕСПИРАТОРНЫХ ИССЛЕДОВАНИЙ | JOURNAL OF CARDIORESPIRATORY RESEARCH
№2 | 2021
28
inflammation, hyperlipidemia, or different outcomes [11]. Endothelial
thrombosis, even exposure to small portions-e.g., Occasional smoking,
passive smoking, some cigarettes in keeping with day-is enough to have
deleterious results [60]. Cigarette smoke carries extra than 4000
chemical substances which have dangerous effects on cardiovascular
function [17]. These include nicotine, carbon monoxide (CO), oxidative
gases, polycyclic fragrant hydrocarbons, carbonyls, butadiene,
minerals, carbon disulphide, and benzene. Even though the various toxic
materials contained in tobacco smoke are ordinary merchandise of the
combustion of natural substances, exposure to smoking entails contact
with materials which can be unique to tobacco smoke and are regarded
to be unfavorable to the fitness: nicotine and co [62].
No matter all the exposure regarding the documented unfavorable
consequences of smoking on public health, smoking prevalence
nevertheless remains excessive in the ecu, where about 30% of citizens
are people who smoke. Greece suffers from a widespread smoking-
associated public health hassle, having the very best share of people who
smoke within the EU (42%). In keeping with who estimates, in Greece
63.1% of grownup males and 39% of ladies ≥15 years are people who
smoke [67], while in young adults, aged 19-30 years, the smoking
incidence is 37,6% [51], the motive of this article is to provide a quick
description of the results of smoking, and especially the outcomes of
nicotine and co, on cardiovascular characteristic, supplying essential
statistics that would make a contribution to decreasing the smoking
epidemic and its effects for cardiovascular health.
Nicotine
Nicotine causes your blood vessels to constrict or narrow, that
limits the number of blood that flows to your organs. Over time, the
constant constriction leads to blood vessels that are stiff and fewer
elastic. Constricted blood vessels decrease the amount of atomic number
8 associated nutrients your cells receive. to satisfy the requirement for a
lot of oxygen, your pulse could increase. phytotoxin is classed as an
alkaloid (like opiate and cocaine) and meets the factors of an extremely
addictive drug. One coffin nail delivers 1.2-2.9 mg of nicotine, and also
the typical one pack-per-day smoker absorbs 20-40 mg of nicotine on a
daily basis [43]. As associate addictive drug, phytotoxin has a pair of
terribly potent effects: it's a stimulant and it is additionally a depressant
[28]. phytotoxin deregulates viscus function, sixteen sympathetic
activations, raises heart rate, causes coronary and involuntary boosts
peripheral vasoconstriction, will increase cardiac muscle workload, and
stimulates adrenal and neuronic hormone release [3]. In addition,
nicotine is related to hypoglycemic agent resistance, increased humor
super molecule levels, and intravascular inflammation that contributes
to the event of atherosclerosis [3].
Vascular Function
There are sample published data suggesting that prolonged exposure
to tobacco smoke causes pathological alteration of endothelial function.
Endothelial dysfunction can be caused by metabolic (dyslipidemia),
environmental (smoking), and physiological (arterial hypertension)
factors, or by inflammation that provokes pathological conditions [41].
It is characterized by an imbalance between vasodilatory and
vasoconstrictive
substances
derived
from
the
endothelium,
anticoagulant and procoagulant mechanisms, growth factors and growth
inhibitors [41]. Under normal circumstances, free radicals circulating in
the human div are neutralized by defensive mechanisms. However, if
their concentrations within the blood must rise greatly due to excessive
exposure to harmful factors such as smoking, they cannot be controlled
and dangerous mutations that destroy cells can occur. Oxidative stress
is seen to arise under these conditions [17].
The term “oxidative stress” refers to the whole of the intracellular
and extracellular situations that result in chemical or metabolic
manufacturing of reactive oxygen species (ROS) [62]. Smoke exists
specifically in states: the gaseous (which incorporates CO) and the solid
(tar). In each those states, it consists of a big number of unfastened
radicals [11]. Pryor and Stone decided that 1 g of tar from cigarette
smoke consists of greater than 10 long-lived unfastened radicals (hours
to months), while1 g risky fraction of smoke consists of 10 [3] short-
lived unfastened radicals (seconds). Chronic publicity to tobacco
additionally weakens the antioxidant shielding mechanisms that alter
those big numbers of smoking-caused unfastened radicals, main to a
sizeable growth in oxidative stress [41]. Oxidative stress, the oxidation
of lipids, proteins, and DNA, is without delay related to atherogenesis
[17]. An indicative locating is that once stages of isoprostanes (indexes
of lipid peroxidation and oxidative damage) have been measured in
smokers, their stages have been determined to be better than in non-
smokers [62]. The response of nitric oxide (NO) with the unfastened
radicals contained in smoke reduces NO’s bioavailability, interfering
with its vasodilatory, antithrombotic, anti-inflammatory, and
antioxidant effects, in addition to its have an impact on endothelium
permeability and myocardial function (lowering the diastolic
distensibility of the left ventricle) [35]. The alteration in biosynthesis of
NO and its reduced activity [8], in mixture with the smoking-caused
discount in prostacyclin manufacturing [22] and the direct poisonous
impact of nicotine on endothelial cells that reasons direct structural
damage [3], are crucial elements which can result in endothelial
dysfunction Using an extract of cigarette tobacco or its remoted
ingredients, along with nicotine, many in vitro research have determined
that smoking is related to decreased NO availability. It has been proven
that nicotine attention in smokers’ blood serum reduces the supply of
NO in human umbilical vein endothelial cells (HUVECs), in addition to
in human coronary artery endothelial cells, main to a discount
withinside the brachial artery’s endothelium-established vasodilation
[11]. Using this model, Barua et al. confirmed that publicity to smokers’
sera reduced NO availability in each HUVECs and human coronary
artery endothelial cells, with the aid of using changing the expression
and pastime of the endothelial NO synthase enzyme [8]. In addition,
they cited a large correlation among glide-mediated brachial artery
endothelium-established vasodilation and NO bioavailability from
cultured HUVECs uncovered to serum from the identical individuals.
On the alternative hand, CO, that is extensively expanded in smokers,
inhibits the advent of NO and takes its vicinity in hemoglobin bonds
[27]. These findings result in the realization that the big portions of
unfastened radicals contained in smoke decorate oxidative pressure and,
in aggregate with decreased NO bioavailability, nicotine-triggered
vasoconstriction and impaired vasodilation, can also additionally result
in endothelial dysfunction.
The consequent endothelial harm contributes to the formation and
development of atheromatous plaque, and decreases blood glide thru
thrombosis and vasospasm, therefore inflicting cardiovascular disease
[5, 41].
Lipid Metabolism
Tobacco smoke, and especially nicotine, has a significant effect
on lipid metabolism and the regulation of lipid levels in the blood [46].
Therefore, cigarette smoke may promote atherosclerosis partly through
its effects on the lipid profile [11]. It has been shown that, in the
presence of already increased serum lipid levels, smoking Event [33].
Smoking is related to extensively increased serum concentrations of
general LDL cholesterol and triglycerides [46]. In addition, numerous
researches have proven a bent for low-density lipoprotein (LDL) and
really low-density lipoprotein (VLDL) LDL cholesterol to be barely
better in smokers [47]. These institutions appear to be dose dependent
[46]. On the alternative hand, smoking lowers serum concentrations of
high-density lipoprotein (HDL) LDL cholesterol, an effective shielding
issue in opposition to the improvement of atherosclerosis [64]. The
distinction is generally small, five mg/dl or less, however this distinction
represents a 10crease and could be predicted to have an effect on
atherogenesis to a great degree [47]. Giving up smoking improves HDL
levels, irrespective of frame weight, contributing to a development in
cardiovascular fitness after smoking cessation [45].
It is feasible that oxidative harm to protein and lipid components
may also give an explanation for the manner wherein cigarette smoke
impacts plasma LDL and HDL. Cigarette smoking will increase the
oxidative change of LDL. Exposure to cigarette smoke extract
ЖУРНАЛ КАРДИОРЕСПИРАТОРНЫХ ИССЛЕДОВАНИЙ | JOURNAL OF CARDIORESPIRATORY RESEARCH
№2 | 2021
29
additionally decreases the plasma hobby of paraoxonase, an enzyme that
protects in opposition to LDL oxidation [11]. There are capability
mechanisms through which reactive smoke additives can produce their
deleterious results on critical plasma components: 1) indirectly,
fueloline-section cigarette smoke may also spark off macrophages and
neutrophils withinside the lung, which may also launch enzymes and
oxidants able to adverse lipids and proteins; 2) directly, for the reason
that lung possesses a really big floor place for fueloline exchange, it's
miles feasible that fueloline-section cigarette smoke additives have
interaction with plasma components withinside the interstitial fluid [64].
Arteriosclerosis
Arteriosclerosis is a general term that includes almost all
arterial disorders that cause thickening and hardening of all types of
arteries. Atherosclerosis is a specific form of arteriosclerosis, the most
characteristic feature of which is the concentration of lipids in the intima
of large elastic arteries (aorta) and medium-sized muscular arteries
(coronary, femoral, carotid, etc.) [45]. Smoking is considered a
significant risk factor for the development of atherosclerosis. The
atherosclerotic effects of cigarette smoke are largely due to events
related to thrombosis. The accumulation of platelets coating the artery
wall in sites where there is turbulent blood flow or endothelial injury
may be the prodromal stage for the formation of atheromatous plaque
[54].
Nicotine is idea to be chargeable for the boom in blood
viscosity and platelet aggregation, because it inhibits the manufacturing
of prostacyclin which might restrict platelet aggregation [33]. Increases
manufacturing of platelet adhesion thrombi, divides coronary artery
intima, quickens the procedure of atheromatous plaque formation, and
is related to an extended threat of cardiac ischemia [5]. In addition,
nicotine influences prostaglandin metabolism, weakening the vessel’s
defense towards platelet deposition [56]. The boom in platelet
aggregation, the impact of nicotine on blood coagulation time, and the
boom in blood viscosity, in aggregate with the boom in stages of LDL
and VLDL, the discount in HDL, and inflammatory processes, sell the
advent of atheromatous plaque and the improvement of atherosclerosis
[3, 28, 47]. It is hence probable that continual smoking, via way of
means of growing peripheral vascular resistances on this way, can also
additionally result in a boom in cardiac afterload and a consequent
discount in stroke volume [50].
The circulating degree of fibrinogen in people who smoke is one of
the maximum effective predictive markers of coronary events.
The boom in fibrinogen tiers acts in mixture with the boom in purple
mobileular mass from long-time period publicity to CO, growing blood
viscosity and boosting the activation of platelets, for this reason growing
the chance of atherogenesis. Increased fibrinogen tiers withinside the
blood flow also can result in the improvement of atherosclerosis, with
an instantaneous impact at the boom in platelet aggregation [39].
Tissue factor (TF)—in any other case referred to as tissue platelet
issue, or issue III, or thrombokinase, or CD142—is a protein discovered
in endothelial tissue, platelets, and leucocytes, and is important for the
initiation of thrombus formation with the aid of using zymogen
prothrombin [21]. TF is expressed with the aid of using cells which can
be commonly now no longer uncovered to blood flow, together with
sub-endothelial cells (e.g. smooth-muscle cells) and the cells that
surround blood vessels (e.g. fibroblasts). This can extrade whilst blood
vessels are damaged—for instance with the aid of using bodily injury,
or rupture, or atherosclerotic plaque. TF is found in atherosclerotic
plaque and might sell thrombogenesis and likely propagation of the
thrombus to the already present atherosclerosis. Sambola et al.
discovered that smoking multiplied plasma TF ranges in people who
smoke who smoked 10 or greater cigarettes consistent with day, with a
smoking record of 10 or more years [57].
Atherogenesis and coronary artery disorder are the end result of
inflammatory processes. The reality that smoking is related to infection
means that infection can be one of the mechanisms thru which cigarette
smoking ends in cardiovascular dysfunction. C-reactive protein (CRP)
and degrees of white blood cells are markers of infection, and are hence
related to atherosclerosis and an extended chance of cardiovascular
disorder [2]. Levels of CRP and white blood cells appear like better in
people who smoke than in non-people who smoke [24]. Furthermore,
there seems to be a relation among the volume of smoking and the white
blood mobiliary count. Dietrich et al. claimed that the boom in CRP
found in people who smoke is proportional to each the amount and the
years of smoking [24].
Overall, Nicotine increases sympathetic activity, stimulates the
release of neurotransmitters, causes coronary and peripheral
vasoconstriction, and elevates blood pressure.
In addition, nicotine enhances lipolysis, increases free fatty acid
levels, increases oxidative stress, endothelial damage and dysfunction,
and promotes vessel inflammation, contributing significantly to the
development of atherosclerosis and heart disease.
Autonomic Nervous System
There is a long-time hyperlink among atypical coronary heart rate
(HR) responses at relaxation and throughout exercise, autonomic
disorder and cardiovascular health [57]. On the opposite hand, persistent
smoking is related to disorder of the autonomic anxious device [10, 63],
and the atypical HR responses to tobacco can be implicated withinside
the hyperlink among smoking and cardiovascular disease [4, 20].
Although the ideal mechanism of movement of smoke components
remains beneath Neath investigation, all proposed hypotheses nation
that the principal outcomes of smoking on cardiovascular characteristic
are related to the direct or oblique movement of nicotine at the
nutriregulation of the circulatory device, in which sympathetic hobby is
accelerated and parasympathetic hobby is reduced.
The nicotine-caused sympathetic overdrive reasons the adrenal
medulla to boom the secretion of each epinephrine and norepinephrine
into the circulating blood [4]. In addition, nicotine stimulates the
vasomotor center of the medulla, inflicting secretion of norepinephrine
from neighborhood deposits. Subsequently, secretion of catecholamines
from the loose nerve endings of the sympathetic nerves and the
neighborhood launch of epinephrine and norepinephrine are
accelerated. In addition, vasoconstriction of coronary vessels occurs, the
biosynthetic ability of prostacyclin is reduced, and endothelial
characteristic is impaired [58]. The stimulation of catecholamine
secretion, in mixture with the depressed manufacturing of prostacyclin
(strong vasodilators), outcomes in an acute upward thrust in blood
pressure, a substantial upward thrust in HR, an boom in cardiac
contractility, and a substantial boom in myocardial work. Nicotine
impacts cardiovascular characteristic each directly, as defined
previously, and indirectly, via a sequence of neurohormonal changes
[9]. In particular, nicotine molecules engage with and prompt the brain's
acetylcholine receptors (nAChRs), whose extended activation might
also additionally desensitize a percentage of them .The activation of
nAChRs via way of means of nicotine boosts the discharge of
neurotransmitters, whilst changing the characteristic of a number of
them—which includes norepinephrine, dopamine, serotonin (5-HT),
and endogenous opioid peptides—accordingly enhancing the movement
of the peripheral anxious device and inflicting cigarette addiction [15].
Heart Rate at Rest
Smoking has been related to expanded resting HR values in
wholesome adults, irrespective of age or sex. Minami et al. located that
the HR is on common 7 bpm quicker in people who smoke than in non-
people who smoke [13]; this locating is consistent with records
mentioned via way of means of Papathanassiou et al., indicating that
people who smoke had a drastically better resting HR as compared with
non-people who smoke in each female (76.4 bpm vs. 70.0 bpm,
p=0.001) and male (72.8 vs. 66.3, p=0.004) subjects [50]. In particular,
smoking is related to selective changes in cardiac autonomic
control[51]. More specifically, smoking, performing at peripheral
sympathetic sites, will increase circulating tiers of catecholamines,
augments sympathetic outflow, and reasons a long-time period discount
in vagal drive. This sympathetic predominance, visible even in younger
heavy people who smoke, is likewise related to impaired baroreflex
function, main to a marked boom in HR at rest.
Heart Rate during Exercise
During exercising, the accelerated metabolic needs are met via way
of means of an accelerated cardiac output, carried out via an
augmentation in HR and stroke volume. The elevation of HR, that is
related to age, HR relaxation and exercising capacity, is regulated via
way of means of exercising-caused autonomic control, in which
ЖУРНАЛ КАРДИОРЕСПИРАТОРНЫХ ИССЛЕДОВАНИЙ | JOURNAL OF CARDIORESPIRATORY RESEARCH
№2 | 2021
30
sympathetic hobby will increase and vagal tone is reduced. The HR
elevation peaks at maximal exercising, whilst healthful topics acquire a
real HR max close (±10 bpm) to their age-anticipated HR max [32]. An
impaired HR reaction to exercising and failure to reach >80% of the
age-anticipated HR max, referred to as chronotropic incompetence, are
related to autonomic imbalance and are vital prognostic markers of
cardiovascular health. In many HR-associated researches in healthful
adults, smoking become located to blunt HR elevation throughout
innovative exercising and to decrease the most HR carried out, posing
an accelerated hazard to smokers’ health. diversifications to continual
smoking, inclusive of down law of β-adrenergic receptors, were used to
provide an explanation for smokers’ blunted HR reaction to exercising.
long-time period smoking has been located to lower the density of
lymphocyte or adipose tissue β-receptors, down-regulating the β-
receptors of the cardiovascular system [29].
Heart rate recovery
On the final touch of full of life exercising, sympathetic pastime
withdraws and vagal reactivation mediates the price at which HR
decreases, making the post-exercising HR decline a crucial reference
marker for cardiac autonomic control. attenuated HR decline for the
duration of healing is a crucial surrogate for underlying autonomic
disorder this is related to extended cardiovascular morbidity and
mortality [30]. in lots of epidemiological HR-associated research in
wholesome middle-elderly populations, smoking became inversely
related to HR decline for the duration of healing.
Smoking and insulin resistance
Insulin has an impact on almost all of the tissues of the div, both
immediately or indirectly, and is characterized as a garage hormone due
to its anabolic motion on all 3 important nutritional groups: namely,
carbohydrates, fats, and proteins [25].
Insulin is related to precise receptors withinside the cell membrane.
the primary capabilities of the insulin receptor are to recognize and to
bind the hormone with the goal cell, and to transmit its metabolic action.
if any such capabilities are disturbed, insulin resistance is manifested.
insulin resistance, metabolic syndrome, and glucose intolerance are
seemed as disturbances with a not unusual place history and sturdy
interrelations [55].
Nicotine is known to growth sympathetic activity, to elevate
circulating
degrees
of
catecholamines,
increase
hormone,
adrenocorticotropic hormone, cortisol, prolactin, and beta-endorphin,
and to lower estrogen degrees these kinds of consequences are strongly
adversarial to insulin’s action. Thus, smoking reduces insulin
production, slowing glucose catabolism and main to its accumulation
withinside the div [36]. Nicotine might also growth insulin resistance
directly. It has been proven that the growth in insulin resistance become
halted after nicotine substitute become stopped, or even progressed
throughout non-stop weight benefit, implying that nicotine as opposed
to weight benefit can be answerable for the preliminary growth in
insulin resistance found in a few smoking-associated studies. The
smoking-brought on insulin resistance is likewise related to an growth
in triglyceride count, due to the fact in fatty tissue glucose is transformed
to triglycerides [1]. In turn, because of multiplied serum concentrations
of FFA and triglycerides, insulin-inspired glucose delivery in skeletal
muscle of routine cigarette people who smoke is exceptionally impaired
in contrast with non-people who smoke. Insulin resistance and the
growth in triglycerides found in people who smoke are sizable threat
elements for the destiny improvement of arteriosclerosis and as a result
cardiovascular disease [12].
Carbon Monoxide
Carbon monoxide (CO) is made from the unfinished combustion of
carbon-containing substances, inclusive of fuel and tobacco. The history
stage of CO withinside the surroundings may be very low and has little
impact on humans, even as maximum of the CO produced with the aid
of using herbal or technological tactics is oxidized to CO2 withinside
the top surroundings. Comparatively, then, the 3-6% CO in cigarette
smoke (and the 2-3 instances better concentrations in pipe and cigar
smoke) constitute notably better tiers than are generally encountered
[20].
Carbon monoxide publicity has been implicated withinside the
procedure of atherosclerosis, contributing to the buildup of LDL
cholesterol withinside the aorta and coronary arteries. In addition, CO
publicity complements endothelial damage, main to destructive
outcomes withinside the presence of ischemic coronary heart or
peripheral vascular disorder. The deleterious outcomes of CO are extra
profound withinside the myocardium than in peripheral tissues, due to
the very excessive oxygen extraction with the aid of using the
myocardium at rest [26]. There is epidemiological proof that employees
uncovered to excessive CO concentrations have better cardiovascular
morbidity and mortality as compared to the predicted charge withinside
the preferred population. The foremost mechanism with the aid of using
which CO reasons coronary heart disorder is thru hypoxia. Inhalation of
cigarette smoke, with the aid of using both lively or passive smokers,
will increase the tiers of carboxyhemoglobin (COHb) withinside the
blood, lowering the delivery of O2 to the tissues. In addition, myoglobin
binds with CO in order that the coronary heart muscle does now no
longer take in the essential O2 and does now no longer carry out
optimally. The decreased O2 uptake due to smoking, collectively with
a growth in serum lactic acid tiers (lactic acidosis), ends in a discount in
top cardio capability and to a great lower in most O2 uptake (VO2max)
[49].
CO and Haemoglobin
The robust chemical affinity among haemoglobin (Hb) and CO is
well-known. It has been predicted that the affinity among Hb and CO is
two hundred instances extra than the affinity among Hb and oxygen
(O2). A direct outcome of this distinction is the considerable binding of
Hb via way of means of CO withinside the blood, the advent of COHb
[34], and a awesome growth in its serum levels, ensuing in a extensive
lower in oxygen uptake via way of means of peripheral tissues. More
specifically, the CO in smoke binds Hb, developing COHb thru the
subsequent reaction:
HbO2 + CO COHb + O2
CO and Myoglobin
Myoglobin can also additionally integrate with CO and, like Hb, has
a more affinity (30-50 times) with CO than with O2, intensifying the
hypoxaemia of peripheral tissues and mainly the lively muscles.
However, myoglobin binds to 1 molecule of O2, while Hb binds to four.
Thus, the bad consequences of improved COHb tiers are a lot greater
hanging than the ones of COMb, efficiently lowering each the O2
deliver to the tissues and the O2 uptake of running muscles.
CO and lactic acidosis
The term “lactic acidosis” refers to excessive stages of lactic acid
withinside the blood. The decreased performance of the Ο2
transportation and deliver device in people who smoke inhibits
mitochondrial function. The publicity of mitochondria to smoking-
brought on oxidative materials consequences in harm to the
mitochondrial DNA, lowering adenosine triphosphate manufacturing in
coronary heart and muscle cells [66]. Essentially, smoking disturbs the
enzyme activity (adenine nucleotide translocator and mitochondrial
superoxide dismutase) in mitochondria this is crucial for his or her
proliferation, for this reason lowering their numbers. Because of this
harm, the muscular tissues can't get the electricity they want to function
(on account that they not have enough mitochondria); they consequently
are seeking for electricity thru some other route: anaerobic metabolism
[52]. The latter process, however, has lactic acid as its very last product,
so that the amount of circulating lactic acid will increase significantly
(lactic acidosis), growing the blood’s acidity, compromising cardio
tolerance, and impairing workout capacity [6].
CO and Exercise Capacity
Smoking even one cigarette can right now have an effect on bodily
workout ability. The results of CO, including the considerable binding
of Hb and the decreased arterial O2 blood saturation, the insufficiency
of respiration enzymes, in aggregate with the binding of myoglobin and
the results of CO on cardio metabolism, bring about disorder of the O2
manufacturing, transportation, and transport system, especially for the
duration of workout [19]. Briefly, the decreased portions of transported
O2 and the reduced O2 deliver to and uptake from the energetic tissues,
mixed with the binding of myoglobin via way of means of CO,
appreciably lower maximal oxygen uptake (VO2max) lowering the
ЖУРНАЛ КАРДИОРЕСПИРАТОРНЫХ ИССЛЕДОВАНИЙ | JOURNAL OF CARDIORESPIRATORY RESEARCH
№2 | 2021
31
purposeful ability and the overall performance of the circulatory system
[37].
There is an observable lower, of round 10%, withinside the period
of workout till exhaustion in smokers, that is on account of a discount
in O2 manufacturing withinside the metabolically energetic tissues, due
to arterial O2 desaturation, and to the insufficiency of the O2
transportation, deliver and uptake system [14]. This impaired workout
tolerance and the reduced maximal workout ability were recorded even
in younger wholesome smokers.
Similar outcomes of smoke at the O2 transportation and deliver
system are visible in people who aren't lively people who smoke. Since
non-people who smoke are extra liable to CO than people who smoke,
absolutely being uncovered to cigarette smoke may also lessen their
VO2max. The quantity to which VO2max is decreased relies upon on
the quantity of CO that people who smoke inhale. Horvath et al. claimed
that no massive discount in VO2max became discovered till stages of
COHb reached or surpassed 4.3%, a degree exhibited with the aid of
using maximum people who smoke.100 From the instant COHb stages
attain 4.3%, VO2max decreases [23] according with the subsequent
equation
VO2max = 0.91(%COHb) + 2.2
Conclusions
Smoking, through its primary components nicotine and CO, will
increase oxidative stress, endothelial harm and disorder, is related to
appreciably better serum concentrations of overall ldl cholesterol and
triglycerides, reduces the aerobic defensive HDL, and via way of means
of selling intravascular irritation represents a big hazard issue for the
improvement of atherosclerosis and cardiovascular disease [48]. In
addition, nicotine deregulates cardiac autonomic function, boosts
sympathetic activity, and will increase HR at rest, whilst it blunts HR
elevation all through modern workout and lowers the most HR that may
be achieved. In parallel, the smoking-caused CO binds with
haemoglobin and myoglobin, reduces arterial O2 blood saturation, and
compromises the performance of respiration enzymes, ensuing in
disorder of the O2 production, transportation and shipping system,
specifically all through workout; this will extensively lessen the
purposeful potential and the overall performance of the circulatory
system [38]. Altogether, smoking is the maximum essential modifiable
hazard issue for cardiovascular disease, a first-rate hazard issue for
cardiovascular morbidity and mortality, and is taken into consideration
to be the main preventable reason of demise withinside the world [18].
Список литературы/ Iqtiboslar/References
1.
Alves-Bezerra M, Cohen DE. Triglyceride Metabolism in the Liver. Compr Physiol. 2017;8(1):1-8. Published 2017 Dec 12.
doi:10.1002/cphy.c170012
2.
Asthana A, Johnson HM, Piper ME, Fiore MC, Baker TB, Stein JH. Effects of smoking intensity and cessation on inflammatory markers in a
large cohort of active smokers. Am Heart J. 2010; 160(3):458-463
3.
Atherosclerosis. Author manuscript; available in PMC 2013 Aug 28.Published in final edited form as: Atherosclerosis. 2011 Apr; 215(2): 281–
283. Published online 2011 Feb 1. doi: 10.1016/j.atherosclerosis.2011.01.003
4.
Audrey A. Wickiser , Plasma catecholamine and ascorbic acid levels in smokers and nonsmokers as a function of stress , University of Nebraska
at Omaha DigitalCommons@UNO, 5-1984
5.
Badimon L, Padró T, Vilahur G. Atherosclerosis, platelets and thrombosis in acute ischaemic heart disease. Eur Heart J Acute Cardiovasc Care.
2012;1(1):60-74. doi:10.1177/2048872612441582 42:1149– 1160.
6.
Baker JS, McCormick MC, Robergs RA. Interaction among Skeletal Muscle Metabolic Energy Systems during Intense Exercise. J Nutr Metab.
2010;2010:905612. doi:10.1155/2010/905612.
7.
Banks, E., Joshy, G., Korda, R.J. et al. Tobacco smoking and risk of 36 cardiovascular disease subtypes: fatal and non-fatal outcomes in a large
prospective Australian study. BMC Med
17,
128 (2019). https://doi.org/10.1186/s12916-019-1351-4 (last day accessed 3 July 2019)
8.
Barua RS, Ambrose JA, Eales-Reynolds LJ, DeVoe MC, Zervas JG, Saha DC. Dysfunctional endothelial ntric oxide biosynthesis in healthy
smokers with impaired endothelium-dependent vasodilatation. Circulation. 2001; 104:1905-1910.
9.
Benowitz NL, Burbank AD. Cardiovascular toxicity of nicotine: Implications for electronic cigarette use. Trends Cardiovasc Med.
2016;26(6):515-523. doi:10.1016/j.tcm.2016.03.001
10.
Benowitz NL. Cigarette smoking and cardiovascular disease pathophysiology and implications for treatment. Prog Cardiovasc Dis. 2003;
46:91-111.
11.
Bhujade R, Ibrahim T, Wanjpe AK, Chouhan DS. A comparative study to assess general health status and oral health score of tobacco users
and nonusers in geriatric population in central India. J Family Med Prim Care. 2020;9(7):3387-3391. Published 2020 Jul 30.
doi:10.4103/jfmpc.jfmpc_157_20.
12.
Bitzur R, Cohen H, Kamari Y, Shaish A, Harats D. Triglycerides and HDL cholesterol: stars or second leads in diabetes?. Diabetes Care.
2009;32 Suppl 2(Suppl 2):S373-S377. doi:10.2337/dc09-S343
13.
Bourassa KJ, Ruiz JM, Sbarra DA. Smoking and Physical Activity Explain the Increased Mortality Risk Following Marital Separation and
Divorce: Evidence From the English Longitudinal Study of Ageing. Ann Behav Med. 2019;53(3):255-266. doi:10.1093/abm/kay038.
14.
Breenfeldt Andersen A, Bejder J, Bonne T, Olsen NV, Nordsborg N. Repeated Wingate sprints is a feasible high-quality training strategy in
moderate hypoxia. PLoS One. 2020;15(11):e0242439. Published 2020 Nov 13. doi:10.1371/journal.pone.0242439.
15.
Brunzell DH, Stafford AM, Dixon CI. Nicotinic receptor contributions to smoking: insights from human studies and animal models. Curr Addict
Rep. 2015;2(1):33-46. doi:10.1007/s40429-015-0042-2.
16.
Buckler, Keith J; Turner, Philip J, Oxygen sensitivity of mitochondrial function in rat arterial chemoreceptor cells PubMed Central , 2013-01-
01
17.
Bullen CH. Impact of tobacco smoking and smoking cessation on cardiovascular risk and disease. Expert Rev Cardiovasc Ther. 2008; 6(6):883-
895.
18.
Buttar HS, Li T, Ravi N. Prevention of cardiovascular diseases: Role of exercise, dietary interventions, obesity and smoking cessation. Exp
Clin Cardiol. 2005;10(4):229-249.
19.
Carbon Monoxide Specifically Inhibits Cytochrome C Oxidase of Human Mitochondrial Respiratory Chain September 2003Pharmacology &
Toxicology 93(3):142-6 DOI:10.1034/j.1600-0773.2003.930306.x SourcePubMed Authors: Jose Ramon Alonso Hospital Clínic de Barcelona.
20.
Centers for Disease Control and Prevention (US); National Center for Chronic Disease Prevention and Health Promotion (US); Office on
Smoking and Health (US). Atlanta (GA): Centers for Disease Control and Prevention (US); 2010.
21.
Chu AJ. Tissue Factor, Blood Coagulation, and Beyond: An Overview. Int J Inflam. 2011; 2011:367284. doi: 10.4061/2011/367284. Epub 2011
Sep 20.
ЖУРНАЛ КАРДИОРЕСПИРАТОРНЫХ ИССЛЕДОВАНИЙ | JOURNAL OF CARDIORESPIRATORY RESEARCH
№2 | 2021
32
22.
Csordas, A., Bernhard, D. The biology behind the atherothrombotic effects of cigarette smoke. Nat Rev Cardiol
10,
219–230 (2013).
https://doi.org/10.1038/nrcardio.2013.8
23.
De Borba, A.T., Jost, R.T., Gass, R. et al. The influence of active and passive smoking on the cardiorespiratory fitness of adults. Multidiscip
Respir Med
9,
34 (2014). https://doi.org/10.1186/2049-6958-9-34
24.
Dietrich T, Garcia RI, de Pablo P, Schulze PC, Hoffmann K. The effects of cigarette smoking on C- reactive protein concentrations in men and
women
and
its
modification
by
exogenous
oral
hormones
in
women.
Eur
J
Cardiovasc Prev Rehabil. 2007; 14(5):694-700.
25.
Dimitriadis G, Mitrou P, Lambadiari V, Maratou E, Raptis SA. Insulin effects in muscle and adipose tissue. Diabetes Res Clin Pract. 2011
Aug;93 Suppl 1:S52-9. doi: 10.1016/S0168-8227(11)70014-6. PMID: 21864752.
26.
Duncker DJ, Bache RJ. Regulation of coronary blood flow during exercise. Physiol Rev. 2008 Jul;88(3):1009-86. doi:
10.1152/physrev.00045.2006. PMID: 18626066
27.
Flammer AJ, Anderson T, Celermajer DS, et al. The assessment of endothelial function: from research into clinical practice. Circulation.
2012;126(6):753-767. doi:10.1161/CIRCULATIONAHA.112.093245.
28.
G. Silveri , L. Pascazio , A. Miladinović , M. Ajčević and A. Accardo, Smoking effect on the circadian rhythm of blood pressure in
hypertensive subjects, Department of Engineering and Architecture, University of Trieste, Trieste 34127, Italy 2 Department of Medical, Surgical
and Health Care, CS of Geriatrics, University of Trieste, Trieste 34127, Italy GNB2020, June 10th-12th 2020
29.
Gök, I; Celebi, I; Hüseyinoğlu, N; Ozic, C, Roles of beta2-adrenergic receptor gene polymorphisms in a Turkish population with
obstructive sleep apnea syndrome or obesity. Science.gov (United States) 2014-10-20
30.
Garcia M, Mulvagh SL, Merz CN, Buring JE, Manson JE. Cardiovascular Disease in Women: Clinical Perspectives. Circ Res.
2016;118(8):1273-1293.doi:10.1161/CIRCRESAHA.116.307547
31.
George Papathanasiou, Anastasia Mamali, Spyridon Papafloratos
and Efthimia Zerv
,
Effects of smoking on cardiovascular function: the role of
nicotine and carbon monoxide George Papathanasiou Proussis 22, Athens 17123 Greece
32.
George , Effects of Smoking on Heart Rate at Rest and During Exercise, and on Heart Rate Recovery, in Young Adults may 2013Hellenic
journal of cardiology: HJC = Hellēnikē kardiologikē epitheōrēsē 54(3):168-177.
33.
Gepner AD, Piper ME, Johnson HM, Fiore MC, Baker TB, Stein JH. Effects of smoking and smoking cessation on lipids and lipoproteins:
outcomes from a randomized clinical trial. Am Heart J. 2011;161(1):145-151.
34.
Gille T, Sesé L, Aubourg E, et al. The Affinity of Hemoglobin for Oxygen Is Not Altered During COVID-19. Front Physiol. 2021;12:578708.
Published 2021 Apr 12. doi:10.3389/fphys.2021.578708
35.
Gusarov I, Shatalin K, Starodubtseva M, Nudler E. Endogenous nitric oxide protects bacteria against a wide spectrum of antibiotics. Science.
2009; 325:1380-1384. Harvard School of Public Health. The Greek Tobacco Epidemic. Centre for Global Tobacco Control. Boston, December
2011; available at: www.smokefreegreece.org (last day accessed 27 March 2013).
36.
Harris KK, Zopey M, Friedman TC. Metabolic effects of smoking cessation [published correction appears in Nat Rev Endocrinol. 2016 Nov;12
(11):684]. Nat Rev Endocrinol. 2016;12(5):299-308. doi:10.1038/nrendo.2016.32
37.
Hogan MC, Bebout DE, Wagner PD. Effect of increased Hb-O2 affinity on VO2max at constant O2 delivery in dog muscle in situ. J Appl
Physiol (1985). 1991 Jun;70(6):2656-62. doi: 10.1152/jappl.1991.70.6.2656. PMID: 1885462.163(1):81-87.e1.
38.
https://aklectures.com/lecture/respiratory-system/carbon-monoxide-and-hemoglobin
39.
Hunter KA, Garlick PJ, Broom I, Anderson SE, McNurlan MA. Effects of smoking and abstention from smoking on fibrinogen synthesis in
humans. Clin Sci (Lond). 2001; 100(4):459-465.
40.
Komatsu, H., Yagasaki, K. & Yoshimura, K. Current nursing practice for patients on oral chemotherapy: a multicenter survey in Japan. BMC
Res Notes
7,
259 (2014). https://doi.org/10.1186/1756-0500-7-259 (last day accessed 23 April 2014).
41.
Kurt Brassington , Stanley Chan , Huei Seow , Aleksandar Dobric , Steven Bozinovski , Stavros Selemidis , and Ross Vlahos, Ebselen reduces
cigarette smoke-induced vascular endothelial dysfunction in mice , 1RMIT University , September 11, 2020.
42.
Leaderer, B.P., Stolwijk, J.A.J. & Zagraniski, R.T. Health benefits due to reductions of CO levels. Environmental Management
1,
131–137
(1977). https://doi.org/10.1007/BF01866103
43.
Lande RG. Nicotine Addiction. Pathophysiology. Walter Reed Army Medical Center. Department of Psychiatry. Medscape Updated, December
13, 2012; available at: http://emedicine.medscape.com/article/2875 55-overview#a0104 (last day accessed 27 October 2013).
44.
Levine PH. An acute effect of cigarette smoking on platelet function. A possible link between smoking and arterial thrombosis. Circulation.
1973; 48(3):619-623.
45.
Lusis AJ. Atherosclerosis. Nature. 2000;407(6801):233-241. doi:10.1038/3502520331. Mjos OD. Effect of free fatty acids on myocardial
function and oxygen consumption in intact dogs. J Clin Invest. 1971; 50:1386- 1389.
46.
Ma, B., Chen, Y., Wang, X. et al. Cigarette smoke exposure impairs lipid metabolism by decreasing low-density lipoprotein receptor expression
in hepatocytes. Lipids Health Dis
19,
88 (2020).
47.
McGill HC. The cardiovascular pathology of smoking. Am Heart J. 1988; 115:250-257
48.
Michael Pittilo R. Cigarette smoking, endothelial injury and cardiovascular disease. Int J Exp Pathol. 2000;81(4):219-230. doi:10.1046/j.1365-
2613.2000.00162.x.
49.
Miura H, Araki H, Matoba H, Kitagawa K. Relationship among oxygenation, myoelectric activity, and lactic acid accumulation in vastus
lateralis muscle during exercise with constant work rate. Int J Sports Med. 2000 Apr;21(3):180-4. doi: 10.1055/s-2000-301. PMID: 10834349.
50.
Myrna B. Schnur, MSN, RN , Systemic Vascular Resistance and Pulmonary Vascular Resistance: What’s the Difference, May 25 2017
51.
Papathanasiou G, Papandreou M, Galanos A, Kortianou E, Tsepis H, Kalfakakou V, et al. Smoking and physical activity interrelations in health
science students. Is smoking associated with physical inactivity in young adults? Hellenic J Cardiol. 2012; 53:17-25.
52.
Park SY, Gifford JR, Andtbacka RH, et al. Cardiac, skeletal, and smooth muscle mitochondrial respiration: are all mitochondria created
equal?. Am J Physiol Heart Circ Physiol. 2014;307(3):H346-H352. doi:10.1152/ajpheart.00227.2014.
53.
Peto R, Lopez AD, Boreham J, Thun M. Mortality from smoking in developed countries 1950 -2000, 2nd edition: revised June 2006; available
at: http://www.ctsu.ox.ac.uk/~tobacco/C0002.pd f (last day accessed 27 March 2013).
54.
Rafieian-Kopaei M, Setorki M, Doudi M, Baradaran A, Nasri H. Atherosclerosis: process, indicators, risk factors and new hopes. Int J Prev
Med. 2014;5(8):927-946.
ЖУРНАЛ КАРДИОРЕСПИРАТОРНЫХ ИССЛЕДОВАНИЙ | JOURNAL OF CARDIORESPIRATORY RESEARCH
№2 | 2021
33
55.
Roberts CK, Hevener AL, Barnard RJ. Metabolic syndrome and insulin resistance: underlying causes and modification by exercise
training. Compr Physiol. 2013;3(1):1-58. doi:10.1002/cphy.c110062
56.
Ross R, Glomset J, Harker L. Response to injury and atherogenesis. Am J Pathol. 1977; 86(3):675-84.
57.
Sambola A, Osende J, Hathcock J, Degen M, Nemerson Y, Fuster V, et al. Role of Risk Factors in the Modulation of Tissue Factor Activity
and Blood Thrombogenicity. Circulation. 2003; 107:973-977.
58.
Sandoo A, van Zanten JJ, Metsios GS, Carroll D, Kitas GD. The endothelium and its role in regulating vascular tone. Open Cardiovasc Med J.
2010;4:302-312. Published 2010 Dec 23. doi:10.2174/1874192401004010302.
59.
Tayade MC, Kulkarni NB. The effect of smoking on the cardiovascular autonomic functions: a cross sectional study. J Clin Diagn Res.
2013;7(7):1307-1310. doi:10.7860/JCDR/2013/5526.3133
60.
U.S. Department of Health and Human Services. Public Health Service. How Tobacco Smoke Causes Disease: The Biology and Behavioural
Basis for Smoking-Attributable Disease. A Report of the Surgeon General. USA, July 2013.
61.
U.S. Department of Health and Human Services. National Centre for Chronic Disease Prevention and Health Promotion. Office on Smoking
and Health. The Health Consequences of Smoking: A Report of the Surgeon General. Atlanta, 2004; available at:
http://www.cdc.gov/tobacco/data_statistics/s gr/2004/complete report/index.htm (last day accessed 22 September 2013)
62.
USA Institute of Medicine of the National Academies. Secondhand Smoke Exposure and Cardiovascular Effects: Making Sense of the Evidence.
Washington DC: The National Academies Press, National Academy of Sciences, July 2013.
63.
Yun AJ, Bazar KA, Lee PY, Gerber A, Daniel SM. The smoking gun: many conditions associated with tobacco exposure may be attributable
to paradoxical compensatory autonomic responses to nicotine. Med Hypotheses. 2005;64(6):1073-9. doi: 10.1016/j.mehy.2004.11.040. PMID:
15823687.
64.
Wan Ahmad WN, Sakri F, Mokhsin A, Rahman T, Mohd Nasir N, Abdul-Razak S, Md Yasin M, Mohd Ismail A, Ismail Z, Nawawi H. Low
serum high density lipoprotein cholesterol concentration is an independent predictor for enhanced inflammation and endothelial activation. PLoS
One. 2015 Jan 23;10(1):e0116867.
65.
World Health Organization. Report on the Global Tobacco Epidemic. Geneva, 2008; available at: http://www.who.int/tobacco/mpower/mpow
(October 2013).
66.
World Health Organization. Regional Office for Europe. The European Tobacco Control Report 2007. Geneva, October 2013.
67.
World Health Organization. World Health Statistics. Geneva, 2011; available at: http://www.who.int/gho/publications/world_ health
statistics/2011/en/ (last day accessed 24 September 2013).
