SUMMARYThe increase in permeability of human erythrocytes to glucose produced by carbon dioxide was confirmed. The effect of certain membrane inhibitors was studied. It was found that while mercuric chloride inhibited the effect of carbon dioxide, ouabain and butanol did not. Inhalation anesthetics in therapeutic concentrations were found to inhibit the stimulatory effect of carbon dioxide. It was concluded that while the means by which carbon dioxide stimulates glucose entry into red cells remains undefined, the inhibitory effect of anesthetics is not related to their ability to “stabilize” membranes, to their effects on energy‐linked metabolic processes, or to their interactions with sulfhydryl or amino groups in cell membranes. The inhibitory effect of anesthetics on carbon dioxide‐stimulated glucose entry is compatible with the hypothesis that they act as competitive penetrating inhibitors of glucose transport mechanisms in human red cell membranes. The depressant effect of anesthetics on carbon dioxide‐induced increases in respiration resemble their depressant effects on carbon dioxide‐induced increases in glucose transport. This raises the possibility that anesthetics have as a common property inhibition of normal responses to carbon dioxide, including responses other than those involving pulmonary