Abstract
The influence of carbon dioxide changes on the neuromuscular blocking effect of tubocurarine in the anaesthetized human subject has been investigated. To assess neuromuscular transmission a simple spring myograph attached to a finger was used and the motor nerve stimulated with supramaximal tetanic stimuli. The plasma levels of tubocurarine were estimated using extraction into ethyl dichloride and a spectrophotometric method of assay. Respiratory acidaemia in one group of patients was associated with high plasma levels of the drug and prolonged neuromuscular block; respiratory alkalaemia in a further group resulted in low plasma levels of the drug after the same initial dose and rapid recovery from the block. It is suggested that a likely explanation of these findings is related to the fact that the tubocurarine molecule contains, besides its quaternary ammonium groups, two phenolic hydroxyl groups which have pK2 values of 8.1 and 9.1 and so vary their degree of ionization within the range of pH changes associated with variations in pulmonary ventilation.