Skip to content
Research Article Open access CC BY 4.0

Haemodynamic Responses to Tobacco Smoke Inhalation in Male Adolescents in Lusaka, Zambia

Chikopela Theresa, M. Goma Fastone

Cardiology and Angiology: An International Journal · pp. 160–169 · Published 10 Dec 2015

10.9734/CA/2015/22969

Abstract

Background: Tobacco smoke is said to cause changes in the levels of catecholamines in the blood, this leads to an increase in blood pressure and heart rate. This is due to nicotine which has also been noted to cause a decrease in vasodilatory activities leading to an increase in both the blood pressure and heart rate. Aim: To determine the acute effects of tobacco smoke on haemodynamics in black male adolescents in Lusaka, Zambia. Study Design: This was an observational study done at the University of Zambia School of Medicine Cardiovascular Research Laboratory in the month of December, 2014. Methodology: Twenty-two (22) black, male-adolescent (age range 19-25 years), active-smokers, consented to participate in the study. The Diasys Ambulatory Blood Pressure Monitoring system (Novacor, France) was used to obtain the Systolic and Diastolic blood pressures (SBP and DBP) and the heart rate. These were obtained 15 minutes before smoking at 5 minute intervals and averaged to obtain the baseline, during the 15 minutes of smoking and on immediate cessation of smoking and thereafter every 15 minutes up to an hour after smoking. Results: There was a significant rise in SBP (mmHg) during smoking (127.9±13.80 mmHg) from baseline values (113.5±13.15 mmHg) (P < .001). It took 30 minutes for the SBP to return to baseline after cessation of smoking. DBP (mmHg) also increased from baseline (79.5±8.79 mmHg) to 85.6±10.92 mmHg during smoking (P <.01). It returned to baseline values immediately after cessation of smoking. The heart rate (bpm) was also noted to significantly increase during smoking (95.2±16.72 bpm) from the values noted before smoking (74.3±13.75 bpm) (P < .05). The mean value for heart rate returned to baseline value by the 15th minute of recovery. Conclusion: The present study demonstrates that smoking may be the cause for the acute increases in SBP, DBP and heart rate in smokers. The smoking caused significant increases in all the haemodynamic indices considered in this study within 15 minutes. Both SBP and DBP increases are indices for stroke and coronary heart disease respectively. The effect of increased SBP was noted to last for 30 minutes while DBP returned to baseline immediately after smoking. A significant increase in heart rate was also noted in the study.  

Systolic Blood Pressure (SBP) Diastolic Blood Pressure (DBP) Heart Rate (HR) adolescents

References (33)

  1. 1 Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies [DOI]
  2. 2 Metabolism and Disposition Kinetics of Nicotine [DOI]
  3. 3 Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults. [DOI]
  4. 4 Norepinephrine and Epinephrine Release and Adrenergic Mediation of Smoking-Associated Hemodynamic and Metabolic Events [DOI]
  5. 5 Passive Smoking and Impaired Endothelium-Dependent Arterial Dilatation in Healthy Young Adults [DOI]
  6. 6 Racial and Ethnic Differences in Serum Cotinine Levels of Cigarette Smokers [DOI]
  7. 7 Interindividual variability in the metabolism and cardiovascular effects of nicotine in man. [DOI]
  8. 8 Role of human cytochrome P4502A6 in C-oxidation of nicotine. [DOI]
  9. 9 Mechanisms responsible for sympathetic activation by cigarette smoking in humans. [DOI]
  10. 10 Short- and long-term effects of cigarette smoking on heart rate variability [DOI]
  11. 11 Dysfunctional Endothelial Nitric Oxide Biosynthesis in Healthy Smokers With Impaired Endothelium-Dependent Vasodilatation [DOI]
  12. 12 Ethnic Differences in N-Glucuronidation of Nicotine and Cotinine [DOI]
  13. 13 Particulate and vapor phase constituents of cigarette mainstream smoke and risk of myocardial infarction [DOI]
  14. 14 Evaluation of methoxsalen, tranylcypromine, and tryptamine as specific and selective CYP2A6 inhibitors in vitro.
  15. 15 Deficiency in nitric oxide bioactivity in epicardial coronary arteries of cigarette smokers [DOI]
  16. 16 Acute and chronic effects of cigarette smoking on arterial stiffness [DOI]
  17. 17 Rise of blood pressure with age. New evidence of population differences. [DOI]
  18. 18 Site of nicotine absorption from a vapour inhaler - comparison with cigarette smoking [DOI]
  19. 19 Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase [DOI]
  20. 20 Emergence of Ethnic Differences in Blood Pressure in Adolescence [DOI]
  21. 21 Effect of cigarette smoke extract on arteriolar dilatation in vivo [DOI]
  22. 22 Ethnic differences in arterial stiffness and wave reflections after cigarette smoking [DOI]
  23. 23 Smoking and physical activity interrelations in health science students. Is smoking associated with physical inactivity in young adults?
  24. 24 An Acute Effect of Cigarette Smoking on Platelet Function [DOI]
  25. 25 Sources of variability in nicotine and cotinine levels with use of nicotine nasal spray, transdermal nicotine, and cigarette smoking [DOI]
  26. 26 Probucol preserves endothelial function by reduction of the endogenous nitric oxide synthase inhibitor level [DOI]
  27. 27 Myocardial infarction with normal coronary angiogram. Possible mechanism of smoking risk in coronary artery disease. [DOI]
  28. 28 Smoking and mechanisms of cardiovascular control [DOI]
  29. 29 Chronic nicotine administration does not affect peripheral vascular reactivity in the rat. [DOI]
  30. 30 Short-term effects of transdermal nicotine on acute tissue plasminogen activator release in vivo in man [DOI]
  31. 31 Effects of transdermal nicotine treatment on structure and function of coronary artery bypass grafts [DOI]
  32. 32 The Acute Impact of Smoking One Cigarette on Cardiac Hemodynamic Parameters [DOI]
  33. 33 Nicotine increases heart adenosine release, oxygen consumption, and contractility [DOI]

Cited by 0

No indexed citations yet.

Related research

Article metrics

Real usage data collected on this platform.

59

Page views

0

PDF downloads

15

Outbound clicks

0

Citations

Views over time

Views by country

Approximate, from request IP at view time — not citizenship or institution. Countries with fewer than 5 views are grouped as "Other".

Traffic sources

Referring site, by host.

Views and downloads exclude known bots/crawlers. Citations combines this platform's own DOI-resolved index with each external source's own reported total — see Cited by above for individually listed citing works. Last refreshed 0 seconds ago.