Carbon monoxide vasodilator effects

Lin, H., McGrath, J.J. (1988). Vasodilating effect of carbon monoxide. Drug Chem. Toxicol. 11 371-85. 

Carbon monoxide is eliminated via the lungs. Dissociation and excretion of carbon monoxide occur rapidly after cessation of exposure but slow as carboxyhemoglobin levels decrease. Cardiovascular injury can result from carboxymyoglobin formation and vasodilation from cellular effects of carbon monoxide. Clinical neurological effects and any delayed neurological sequelae can be attributed to asphyxia as well as lipid peroxidation, and hypotension, which induce ischemic-reperfusion injury. 

The second type of asphyxiants is that which works at the cellular level. Here, they interfere with the mitochondrial cytochrome oxidase s function in the electron transport chain. Because this is the fuel cell for the body, energy production ceases within the cell, with cell death following close behind. The key substance implicated here is cyanide, which is usually found only in a chemical laboratory setting, but can also be a side effect of smoke inhalation. As previously mentioned, hydrogen sulfide and carbon monoxide also have some effect at this site. In addition, azides are cellular asphyxiants. The azides, along with the nitro-ate-ites, are also vasodilators and can cause headaches and hypotension. 

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