Abstract
SummaryDifferences have been shown between horse and human erythrocytes with regard to the regulation of methaemoglobinaemia. In general, horse erythrocytes are more prone than normal human erythrocytes to accumulation of methaemoglobin and to depletion of reduced glutathione. This greater susceptibility to methaemoglobinaemia seems related to decreased reductive capacity of the horse erythrocyte rather than to greater inherent susceptibility of horse haemoglobin to oxidation. The results suggest that horse erythrocytes utilise plasma lactate to keep haemoglobin reduced and in a functional state, in the face of relative inability to absorb and utilise glucose. Although adequate under normal conditions, this lactate‐dependent pathway of methaemoglobin reduction appears unable to respond substantially to the stress of erythrocytic exposure to catalytic oxidants.
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