Cardiovascular effects of ozone exposure in human volunteers
Cardiovascular effects of ozone exposure in human volunteers
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DOI：
10.1164/ajrccm.158.2.9709034
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发表时间：
1998-08-01
影响因子：
24.7
通讯作者：
Prasad, SB
中科院分区：
文献类型：
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作者：
Gong, H;Wong, R;Prasad, SB
我们假设臭氧(O-3)暴露会严重影响人类的心血管血流动力学，特别是在高血压患者中。我们研究了10名非药物高血压患者和6名健康男性成年人。每个受试者在右心和桡动脉插管后，每天暴露在环境控制室中的过滤空气(FA)中，第二天暴露在0.3ppmO-3中，进行间歇性运动3h。与FA暴露相比，O-3暴露对心脏指数、心功能、肺动脉压、肺血管阻力、体循环阻力、心电、血清心肌酶、血浆儿茶酚胺和心钠素以及Sa(O2)均无显著影响。总体结果显示，无论是高血压患者还是对照组，都没有发现O-3对心血管的重大急性影响。然而，对于心率-压力乘积(1,353次/分钟/毫米汞柱)和心率(8次/分钟)，使用O-3的暴露前的平均变化显著大于使用FA的(p<；0.02)；这些反应在高血压组和对照组之间没有显著差异。在平均FEV1(-6%)和Aapo(2)(>；10 mm Hg增加)方面也观察到了显著的O-3效应，这在两组之间没有显著差异。这些结果表明，接触O-3可以增加心肌作功和损害肺气体交换，其程度可能对既有严重心血管损害、有或不伴有肺部疾病的人具有临床意义。
We hypothesized that ozone (O-3) exposure acutely affects cardiovascular hemodynamics in humans and, in particular, in subjects with essential hypertension. We studied 10 nonmedicated hypertensive and six healthy male adults. Each subject, after catheterization of the right heart and a radial artery, was exposed in an environmentally controlled chamber to filtered air (FA) on one day and to 0.3 ppm O-3 On the following day for 3 h with intermittent exercise. Relative to FA exposure, O-3 exposure induced no statistically significant changes in cardiac index, ventricular performance, pulmonary artery pressure, pulmonary and systemic vascular resistances, EGG, serum cardiac enzymes, plasma catecholamines and atrial natriuretic factor, and Sa(O2). The overall results did not indicate major acute cardiovascular effects of O-3 in either the hypertensive or the control subjects. However, mean preexposure to postexposure changes were significantly (p < 0.02) larger with O-3 than with FA for rate-pressure product (1,353 beats/min/mm Hg) and for heart rate (8 beats/min); these responses were not significantly different between the hypertensive and the control subjects. Significant O-3 effects were also observed for mean FEV1 (-6%), and AaPO(2) (> 10 mm Hg increase), which were not significantly different between the two groups. These results suggest that O-3 exposure can increase myocardial work and impair pulmonary gas exchange to a degree that might be clinically important in persons with significant preexisting cardiovascular impairment, with or without concomitant lung disease.