Penney D G, Howley J W
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201.
Environ Health Perspect. 1991 Nov;95:191-8. doi: 10.1289/ehp.9195191.
Exposure to carbon monoxide in our society is a frequent occurrence, from auto exhaust, industrial effluents, and cigarette smoke, and takes place over a wide range of concentrations. It has been suggested that chronic CO inhalation may alter blood pressure, even possibly provoking hypertension by acting alone or in combination with other environmental stressors. Some studies examining the response to CO exposure have reported decreases in blood pressure, whereas others have found increases or no change. Blood pressure in long-term cigarette smokers is generally decreased relative to nonsmokers, albeit a slight decrease. The strength of this finding is somewhat clouded by the effect of the lower body weight in smokers. The increases in blood pressure observed acutely with smoking are mainly due to nicotine. Chronically, the hypertensive action of nicotine is largely offset by the hypotensive action of CO. Several studies support the notion that environmental CO exposure or smoking accelerates or exacerbates hypertension in some people. It has been asserted that chronic CO exposure increases the development of atherosclerotic disease; however, convincing evidence from animal experiments is lacking. Nevertheless, CO may elevate plasma cholesterol and does appear to enhance atherosclerosis when serum cholesterol is greatly elevated by diet. Using the borderline hypertensive rat, an animal model reputed to have increased sensitivity to environmental stimuli, we found no evidence to suggest a provocatory role for CO in the development of hypertension; instead, CO exposure produced hypotension. On the whole, the human and animal literature, as well as our studies, fail to support the hypothesis that long-term CO exposure is capable of provoking an increase in blood pressure, even in borderline hypertensive or sensitive individuals.
在我们的社会中，接触一氧化碳的情况屡见不鲜，其来源包括汽车尾气、工业废水和香烟烟雾，且接触发生时的浓度范围很广。有人认为，长期吸入一氧化碳可能会改变血压，甚至可能单独或与其他环境应激源共同作用引发高血压。一些研究一氧化碳暴露反应的报告称血压下降，而另一些研究则发现血压升高或无变化。与不吸烟者相比，长期吸烟者的血压总体上有所下降，尽管降幅较小。吸烟者体重较低这一因素使这一发现的说服力有所减弱。吸烟时急性观察到的血压升高主要归因于尼古丁。从长期来看，尼古丁的升压作用在很大程度上被一氧化碳的降压作用所抵消。多项研究支持这样一种观点，即环境一氧化碳暴露或吸烟会使一些人的高血压病情加重或恶化。有人断言，长期接触一氧化碳会增加动脉粥样硬化疾病的发生；然而，缺乏来自动物实验的确凿证据。尽管如此，一氧化碳可能会升高血浆胆固醇，而且当饮食使血清胆固醇大幅升高时，一氧化碳似乎确实会加剧动脉粥样硬化。使用边缘性高血压大鼠这一据称对环境刺激敏感性增加的动物模型，我们没有发现证据表明一氧化碳在高血压发展过程中起激发作用；相反，接触一氧化碳会导致血压下降。总体而言，人类和动物研究文献以及我们的研究均未能支持长期接触一氧化碳会导致血压升高这一假说，即使是在边缘性高血压患者或敏感个体中也是如此。
