赞比亚卢萨卡男性青少年对烟草烟雾吸入的血流动力学反应。

Cardiology and angiology Pub Date : 2015-01-01 Epub Date: 2015-12-10 DOI:10.9734/ca/2015/22969
Theresa Chikopela, Fastone M Goma
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引用次数: 0

摘要

背景:吸烟引起血液中儿茶酚胺水平的变化。这会导致血压和心率升高。这是由于尼古丁引起的,尼古丁也会导致血管舒张活动的减少,从而导致血压和心率的增加。目的:确定烟草烟雾对赞比亚卢萨卡黑人男性青少年血液动力学的急性影响。研究设计:这是一项观察性研究,于2014年12月在赞比亚大学医学院心血管研究实验室完成。方法:二十二(22)名黑人男性青少年(年龄范围19-25岁),积极吸烟,同意参加本研究。使用Diasys动态血压监测系统(Novacor, France)获取收缩压和舒张压(SBP和DBP)和心率。这些数据在吸烟前15分钟每隔5分钟获得一次,在吸烟15分钟期间和立即戒烟期间以及之后每15分钟直至吸烟后一小时平均获得基线。结果:吸烟期间收缩压(mmHg)较基线值(113.5±13.15 mmHg)显著升高(127.9±13.80 mmHg) (P = .00)。戒烟后,收缩压恢复到基线需要30分钟。吸烟时DBP (mmHg)也从基线(79.5±8.79 mmHg)增加到85.6±10.92 mmHg (P = 0.01)。戒烟后立即恢复到基线值。吸烟时的心率(bpm)(95.2±16.72 bpm)也比吸烟前(74.3±13.75 bpm)显著增加(P = 0.05)。恢复后15分钟,心率平均值恢复到基线值。结论:吸烟可能是引起吸烟者收缩压、舒张压和心率急性升高的原因。吸烟在15分钟内引起本研究考虑的所有血流动力学指标的显著增加。收缩压和舒张压升高分别是脑卒中和冠心病的指标。收缩压升高的效果持续30分钟,而舒张压在吸烟后立即恢复到基线。研究还指出,心率显著增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Haemodynamic responses to tobacco smoke inhalation in male adolescents in Lusaka, Zambia.

Haemodynamic responses to tobacco smoke inhalation in male adolescents in Lusaka, Zambia.

Haemodynamic responses to tobacco smoke inhalation in male adolescents in Lusaka, Zambia.

Haemodynamic responses to tobacco smoke inhalation in male adolescents in Lusaka, Zambia.

Background: Tobacco smoke causes 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 = .00). 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 increase 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.

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