Toxicology Graduate Program, University of Saskatchewan, Saskatoon, SK, Canada.
Environ Toxicol Pharmacol. 2011 May;31(3):453-9. doi: 10.1016/j.etap.2011.02.008. Epub 2011 Feb 26.
The aim of this study was to determine if carbon monoxide (CO) is responsible for acute adverse cardiovascular effects of different sources of smoke: second-hand tobacco smoke (SHS), incense and candle smoke. Endothelial function was tested using flow-mediated dilation (FMD) in pigs and was shown to be sensitive to nitric oxide synthase blockade. Subsequent experiments showed that FMD was significantly impaired compared to sham-exposed pigs at 30 min after a 30-min exposure to all three sources of smoke. In contrast, SHS significantly increased systolic, diastolic and pulse pressures compared to sham-exposure, while both incense and candle smoke exposure had no effect. The FMD impairment correlated well with CO levels in the exposure chamber, but not total particulates or venous CO-hemoglobin. Therefore, this study suggests a gas phase component of smoke that accompanies CO, but not CO itself, is responsible for acute endothelial dysfunction after SHS, incense or candle smoke exposure.
本研究旨在确定一氧化碳（CO）是否是导致不同来源烟雾（二手烟草烟雾（SHS）、香薰和蜡烛烟雾）急性不良心血管效应的原因。我们使用血流介导的扩张（FMD）来测试内皮功能，结果表明它对一氧化氮合酶阻断敏感。随后的实验表明，与假暴露组相比，所有三种烟雾暴露 30 分钟后 30 分钟，FMD 显著受损。相比之下，与假暴露组相比，SHS 显著增加了收缩压、舒张压和脉搏压，而香薰和蜡烛烟雾暴露没有影响。FMD 损伤与暴露室内的 CO 水平密切相关，但与总颗粒物或静脉 CO-血红蛋白无关。因此，本研究表明，伴随 CO 的烟雾气相成分，但不是 CO 本身，是导致 SHS、香薰或蜡烛烟雾暴露后急性内皮功能障碍的原因。
