Effect On Tissue

Decrease in peripheral oxygen delivery is not the sole mechanism of CO toxicity. Extravascular uptake of CO has been estimated at 10-50% of the total body CO8. Goldbaum et al.9 showed that with the same blood level of carboxyhemoglobin, dogs inhaling CO died, whereas dogs transfused only with CO incubated erythrocytes did not. He concluded that the decrease in oxygen delivery induced by the interaction of CO with hemoglobin was not the most important fact in CO toxicity, and that extravascular CO had a toxic action probably by interfering with oxygen utilization. In a experimental CO poisoning in rabbits, Ludbrook et al confirmed that abnormalities in organ function (i.e., brain function) occurred without any decrease in organ oxygen delivery10.

Carbon monoxide reacts with a number of other heme moieties besides hemoglobin. These include myoglobin, hydroperoxidase, cytochrome oxidase (also called cytochrome a-a3), and cytochrome p-45011-13. Although its affinity for these heme-like compounds is lower than its affinity for hemoglobin, as the blood oxygen pressure falls, a tissue PO2 level can be reached at which CO avidly binds to myoglobin and cytochrome oxidase.

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