Schneiderman G, Goldstick T K
Atherosclerosis. 1978 May;30(1):1-15. doi: 10.1016/0021-9150(78)90148-x.
The elevated carbon monoxide level found in tobacco smokers has been suggested as one etiologic factor linking it with atherosclerosis. Unquestionably carbon monoxide does induce some arterial wall hypoxia, which has been established as an atherogenic factor, but without knowing the extent and location of this hypoxia the importance of this mechanism could not previously be assessed. Carbon monoxide acts both by inducing hypoxemia and shifting the oxyhemoglobin equilibrium curve, with these effects acting on the oxygen transport system from both the luminal blood and the vasa vasorum. We have studied this system using a computer simulation of the human arterial wall and found significant, mid-medial hypoxia with blood carbon monoxide levels routinely found in smokers. Because these levels fluctuate, the hypoxia they induce would be expected to be uncompensated by increased vascularization and therefore potentially represent a much more significant factor in atherogenesis than chronic hypoxia alone.
吸烟者体内一氧化碳水平升高被认为是将吸烟与动脉粥样硬化联系起来的一个病因。毫无疑问，一氧化碳确实会导致一定程度的动脉壁缺氧，而缺氧已被确认为一种致动脉粥样硬化的因素，但在不清楚这种缺氧的程度和位置之前，此前无法评估该机制的重要性。一氧化碳通过诱导低氧血症和改变氧合血红蛋白平衡曲线发挥作用，这些作用从管腔内血液和血管滋养管两方面作用于氧运输系统。我们使用人体动脉壁的计算机模拟研究了这个系统，发现吸烟者血液中常见的一氧化碳水平会导致中膜显著缺氧。由于这些水平会波动，预计它们所诱导的缺氧无法通过增加血管生成来补偿，因此在动脉粥样硬化形成中，这可能是一个比单纯慢性缺氧更为重要的因素。
