Jeppsson_1988_Pharmacol.Toxicol_63_211

Bambuterol, the bis-dimethyl carbamate prodrug of terbutaline, and physostigmine were examined with respect to their ability to interfere with the neuromuscular transmission in an isolated vagus nerve-trachea preparation, a phrenic nerve-diaphragm preparation and the transmurally stimulated extensor digotorum longus (EDL) isolated from the guinea-pig. Physostigmine increased the contractile response of the trachea to stimulation of the vagus nerve. Bambuterol had an opposite effect in this respect and inhibited the effect of physostigmine. Both compounds, in high concentrations, increased the tension of the unstimulated tracheal smooth muscle. Physostigmine, but not bambuterol, caused a threefold increase in the twitch tension of the indirectly stimulated diaphragm. Bambuterol counteracted this increase almost completely. In the EDL, physostigmine caused a concentration-dependent and curare-sensitive increase in the force of both twitches and subtetanic contractions. This increase was completely inhibited by bambuterol which had no effect per se on the contractions. Both enantiomers of bambuterol appeared to be equally potent in counteracting the effect of physostigmine on the EDL. It is concluded that bambuterol, in concentrations which selectively and completely block the butyrylcholinesterase, has no effect on the neuromuscular transmission. In higher concentrations, at which bambuterol might interfere with acetylcholinesterase, it counteracts the effects of the unselective inhibitor of cholinesterases, physostigmine.