OBJECTIVES: To investigate the impact of cigarette smoking and oral contraceptive (OC) use on hemodynamic stress responses of women. Also, to examine gender differences in stress reactivity as a function of smoking status and acute nicotine administration. METHODS:Thirty men and 46 women, differing in smoking status and OC use, were tested for cardiovascular stress responses to a variety of behavioral and physical stressors. Each was tested twice, once under a transdermal nicotine patch condition and once under a placebo patch condition. Impedance cardiography was used to estimate hemodynamic reactivity noninvasively. RESULTS: In response to behavioral stressors, women smokers, irrespective of OC use or nicotine vs placebo, demonstrated significantly blunted cardiac output and heart rate reactivity to stressors, and showed significantly greater estimated total peripheral resistance (TPR) under stress relative to women nonsmokers. There were no differences in hemodynamic stress reactivity between men smokers and nonsmokers. The only significant effect involving nicotine administration on stress reactivity was seen in men where, regardless of smoking status, nicotine increased heart rate reactivity to all stressors relative to placebo responses. CONCLUSIONS: Results suggest that cigarette smoking may act differently in men and women to increase risk for cardiovascular disease (CVD). For men, nicotine may exert pathogenic influences via increasing the magnitude of heart rate reactivity to stressors. For women, however, smoking seems to have deleterious effects on hemodynamic stress reactivity patterns, reducing myocardial but increasing TPR contributions to blood pressure responses.
RCT Entities:
OBJECTIVES: To investigate the impact of cigarette smoking and oral contraceptive (OC) use on hemodynamic stress responses of women. Also, to examine gender differences in stress reactivity as a function of smoking status and acute nicotine administration. METHODS: Thirty men and 46 women, differing in smoking status and OC use, were tested for cardiovascular stress responses to a variety of behavioral and physical stressors. Each was tested twice, once under a transdermal nicotine patch condition and once under a placebo patch condition. Impedance cardiography was used to estimate hemodynamic reactivity noninvasively. RESULTS: In response to behavioral stressors, women smokers, irrespective of OC use or nicotine vs placebo, demonstrated significantly blunted cardiac output and heart rate reactivity to stressors, and showed significantly greater estimated total peripheral resistance (TPR) under stress relative to women nonsmokers. There were no differences in hemodynamic stress reactivity between men smokers and nonsmokers. The only significant effect involving nicotine administration on stress reactivity was seen in men where, regardless of smoking status, nicotine increased heart rate reactivity to all stressors relative to placebo responses. CONCLUSIONS: Results suggest that cigarette smoking may act differently in men and women to increase risk for cardiovascular disease (CVD). For men, nicotine may exert pathogenic influences via increasing the magnitude of heart rate reactivity to stressors. For women, however, smoking seems to have deleterious effects on hemodynamic stress reactivity patterns, reducing myocardial but increasing TPR contributions to blood pressure responses.
Authors: Brittany E Evans; Kirstin Greaves-Lord; Anja S Euser; Joke H M Tulen; Ingmar H A Franken; Anja C Huizink Journal: PLoS One Date: 2013-04-19 Impact factor: 3.240