Carbon monoxide-induced arterial wall hypoxia and atherosclerosis.
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.
D000328:Adult; D001013:Aorta, Thoracic / Q000378:metabolism; D001158:Arteries / Q000378:metabolism; D001161:Arteriosclerosis / Q000097:blood*; D002248:Carbon Monoxide / Q000097:blood*; D002249:Carbon Monoxide Poisoning / Q000097:blood; D002263:Carboxyhemoglobin / Q000032:analysis; D003201:Computers; D006801:Humans; D000860:Hypoxia / Q000097:blood*; D010100:Oxygen / Q000097:blood; D012907:Smoking / Q000503:physiopathology; D014651:Vasa Vasorum / Q000378:metabolism
D002248:Carbon Monoxide; D002263:Carboxyhemoglobin; D010100:Oxygen