MECHANISMS OF CARBON-MONOXIDE TOXICITY

This review re-examines the possibility that some of the toxic effects of CO exposure in man could be due to CO binding within cells, as well as decreases in tissue pO2 resulting from the presence of carboxyhemoglobin (HbCO). Data are reviewed from experiments designed to measure adverse effects of CO on isolated smooth muscle. These data show that CO tensions greater than 1,000 times those seen in intact tissues when HbCO is 5 to 10% saturation have only a small effect on oxygen uptake. Thus, it is unlikely that in vivo CO toxicity occurs in this tissue as a result of binding to cytochrome oxidase. I reviewed existing data which indicate that CO binding to myoglobin, in heart and skeletal muscle, is significant, even at low CO exposure giving HbCO less than 5% saturation. Whether myoglobin-CO binding is a significant cause of CO toxicity during exercise, or of the sensitivity of the myocardium to CO, is unknown. © 1979.