Penn A, Currie J, Snyder C
Norton Nelson Institute of Environmental Medicine, New York University Medical Center, NY 10016.
Eur J Pharmacol. 1992 Sep 1;228(2-3):155-64. doi: 10.1016/0926-6917(92)90025-8.
The effects of chronic exposure to moderate levels of carbon monoxide (CO) upon the augmentation of arteriosclerotic plaque development were investigated in a series of in vivo studies. Cockerels were exposed to carefully regulated CO levels in dynamic exposure chambers. The plaque volume percentage in the aortic walls of experimental and control animals was determined by point-counting. Chronic CO inhalation, at levels up to 200 ppm, did not stimulate arteriosclerotic plaque development (at 200 ppm CO, carboxyhemoglobin (COHb) levels 10 min after exposures ended were 11-12%). When administered concomitantly with cholesterol feeding, CO did not augment plaque development. When administered after either carcinogen-associated or diet-promoted plaque size increases had occurred, CO elicited no further plaque size increases. Thus, in this animal model, daily exposures to moderately high CO levels were without discernable effect upon arteriosclerotic plaque development, although high COHb levels were attained.
在一系列体内研究中，研究了长期暴露于中等水平一氧化碳（CO）对动脉粥样硬化斑块发展加剧的影响。将公鸡置于动态暴露舱中，使其暴露于经过精确调节的CO水平。通过点计数法测定实验动物和对照动物主动脉壁中的斑块体积百分比。吸入高达200 ppm的慢性CO，并未刺激动脉粥样硬化斑块的发展（在200 ppm CO时，暴露结束后10分钟的碳氧血红蛋白（COHb）水平为11 - 12%）。当与胆固醇喂养同时进行时，CO并未加剧斑块发展。当在致癌物相关或饮食促进的斑块大小增加之后给予CO时，CO并未引起斑块大小的进一步增加。因此，在这个动物模型中，尽管达到了高COHb水平，但每日暴露于中等偏高的CO水平对动脉粥样硬化斑块发展没有明显影响。
