Mechanism of the toxic action of carbon monoxide.
Our studies indicate that a high concentration of carboxyhemoglobin (COHb) does not interfere with the O2--carrying capacity of the blood. In dogs, both the transfusion of erythrocytes containing 80 percent COHb and the i.p. injection of carbon monoxide (CO) gas do not produce CO toxicity even though the COHb is above 50 percent. Dogs inhaling CO (13 percent in air) for 15 minutes died within 15 minutes to 65 minutes with an average COHb level of 65 percent. The probable toxic action of CO is on the cellular respiration taking place in the mitochondria when CO competes with O2 for cytochrome a3. The presence of dissolved CO in plasma, which is necessary for CO to enter the tissue, probably occurs when the exchange takes place between alveolar air and the blood in the lungs. When air containing CO is inhaled, there will be a significant CO tension in the blood when it leaves the lungs and when it reaches the organs especially the heart and brain. While COHb level is useful as a clinical measure of CO exposure, the most important mechanism by which CO causes toxicity is its combination with cytochrome oxidase.
D000818:Animals; D002248:Carbon Monoxide / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D004285:Dogs; D004912:Erythrocytes / Q000378:metabolism; D006454:Hemoglobins / Q000378:metabolism; D007274:Injections, Intraperitoneal; D013997:Time Factors
D006454:Hemoglobins; D002248:Carbon Monoxide