Effects of carbon monoxide on isolated heart muscle cells. Research report, March 1989-February 1992

By sequestering intracellular myoglobin of cardiac muscle cells in the nonfunctioning carboxymyoglobin form, carbon monoxide blocks myoglobin-facilitated diffusion of oxygen, as well as myoglobin-mediated oxidative phosphorylation. The authors explored the hypothesis that the carbon monoxide blockade of myoglobin function may be responsible at the cellular level for a component of the cardiotoxicity of carbon monoxide observed during exercise. At physiological oxygen pressures no greater than 5 torr, after sequestration of approximately 50% of the myoglobin, steady-state oxygen uptake decreased significantly less than the respiration of cell groups for which the fraction of carboxymyoglobin was 0% to 40%. When respiration is diminished, the rate of oxidative phosphorylation also decreases. Thus, they concluded that sequestering intracellular myoglobin as carboxymyoglobin significantly decreased the rate of oxidative phosphorylation of isolated cardiac myocytes. They estimate that intracellular myoglobin-dependent oxidative phosphorylation will be inhibited when approximately 20% to 40% of the arterial hemoglobin in the whole animal is carboxyhemoglobin.