Carbon monoxide vasodilation

Motterlini RA, Mann BE (2002) Preparation of metal complexes for therapeutic delivery of carbon monoxide as vasodilator. Patent WO 2002/092075... 

Furchgott, R.F., Jothianandin, S. (1991). Endothelium-dependent and -independent vasodilation involving cGMP relaxation induced by nitric oxide, carbon monoxide and light. Blood Vessels 28 52-61. 

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

McFaul, S.J., McGrath, J.J. (1987). Studies on the mechanism of carbon monoxide-induced vasodilation in the isolated perfused rat heart. Toxicol. Appl. Pharmacol. 87 464-73. 

Hypoxaemia (Pa02 < 70 mm Hg) is observed in 45-69% of patients suffering from cirrhosis or liver insufficiency. Only rarely has severe hypoxaemia been demonstrated (Pa02 < 50 mm Hg). (6, 32, 51, 52, 56) Intrapulmonary vasodilations could be ascertained in 13-47% of liver transplant candidates. (27) In about 50% of all cirrhotic patients, a decline in the diffusion capacity for carbon monoxide was detected. (24) About 30% of cirrhotic patients showed no (physiological) reduction in pulmonary vasoconstriction under conditions of hypoxia. The prevalence of HPS in cirrhotic patients varies between 4% and 19%. It occurs more... 

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. 

Flushed red skin may be caused by carbon monoxide poisoning, boric acid intoxication, chemical burns from corrosives or hydrocarbons, or anticholinergic agents. It may also result from vasodilation (eg, phenothiazines or disulfiram-ethanol interaction). 

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