Combinatorial effect of nicotine and black tea on heart rate variability: Useful or harmful?

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It has been reported that among more than 9000 chemical agents in cigarette smoke, oxidizing chemicals, carbon monoxide, volatile organic compounds, particulates, heavy metals and nicotine are the main responsible of cardiovascular diseases (CVD).1 The cardiovascular pathogenesis of smoking can be mediated through various pathways such as the induction of oxidative injury, endothelial dysfunction, thrombogenesis, inflammation, hemodynamic stress, dyslipidemia and atherogenesis, insulin resistance and arrhythmogenesis.2 Myocardial ischaemia and sudden cardiac death are important side effects of smoking and nicotine,2 these effects may be partly mediated by autonomic imbalance9 and changes in heart rate variability (HRV).10 It is believed that the activation of sympathetic nerves in the heart leads to an increase in the heart rate and a decrease in HRV, indicators of susceptibility to arrhythmias. However, activation of parasympathetic nerves innervating the heart induces a reduction in heart rate and HRV increment: signs of normal heart function.11 Previous studies regarding the effect of nicotine on HRV mostly has been conducted in smokers, smokers using nicotine patches to quit smoking, smoking quitters or has been evaluated in healthy volunteers in single doses or after short‐term administration. It has been reported that smoking causes an acute and transient decrease in HRV, and heavy smoking but not moderate smoking causes long‐term reduction in vagal cardiac control in young people and blunted postural responses in autonomic cardiac regulation.12 Another study indicated a graded pattern of increasing HRV following stopping smoking and transitioning to using nicotine patch and finally fully abstinent from tobacco.11 In addition, single dose (4 mg) of nicotine induces a significant decrease in HRV in healthy young non‐smokers.13 However, Druyan et al14 indicated that a single dose (2 mg) of nicotine had no significant effect on HRV of non‐smokers. We previously showed that despite the increase of plasma atherogenic index in rats which treated with nicotine for 4 weeks,15 the susceptibility to lethal cardiac arrhythmia16 and cardiac injury17 did not increase in these animals. It seems the findings of previous studies especially human studies have been confounded by abundant factors such as degree of physical activity, diet regimen, environmental conditions, race, sex, dose and duration of nicotine consumption, period of study, desensitization of receptors, tolerance phenomena and withdrawal effects. Because of these uncertainties, a part of the aim of this study was the assessment of the long‐term effect of nicotine on cardiac autonomic function assessed by measuring HRV in the absence of most of above confounding factors. Some studies have reported differences between the sexes with respect to nicotine consumption‐related phenomena in rats, such as less compensatory smoking response to nicotine reduction in females,18 the more important conditioning effect of nicotine in males,19 and also opposite effect of nicotine self‐administration on tissue levels of substance P in the males and females.20 Thus, male rats were exclusively used in this study.
It has been reported that cigarette smokers drink more tea and coffee than non‐smokers.21 Bertoia et al23 did not find an association between risk of sudden cardiac death in women and caffeinated tea. However, the effect of tea and nicotine in combine on HRV has not been reported. Thus, another part of the objective of this study was the evaluation of the effect of nicotine along with black tea on HRV.
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