Comparison of Physostigmine and Neostigmine for Antagonism of Neuromuscular Block
Markku Salmenperä, E. Nilsson
Abstract
Markku Salmenperä, E. Nilsson
Abstract
The ability of physostigmine alone and in combination with neostigmine to reverse d-tubocurarine-induced neuromuscular block was evaluated in surgical patients. The relaxation was maintained at a level of 90% twitch suppression during balanced anesthesia, and antagonism was attempted with physostigmine 1.5 mg x 3; neostigmine 0.5 mg x 3; neostigmine 1.0 mg x 3; or with a combination of physostigmine 0.75 mg and neostigmine 0.5 mg x 3. The measured parameters included the twitch force or EMG amplitude of the adductor pollicis brevis muscle after supramaximal 0.1 Hz stimulation and fading of these responses after repetitive 2 and 50 Hz stimuli. Although the restitution rate of twitch height and EMG amplitude were essentially the same with both antagonists, there was a considerable time-lag in regeneration of the fades after repetitive stimuli with physostigmine as compared with the neostigmine group. The addition of physostigmine to a subeffective dose of neostigmine resulted in antagonism comparable to that seen in other groups. The clinical antagonism was satisfactory in all patients receiving physostigmine. The divergence of relaxation-indicating parameters (twitch responses and fades) after physostigmine suggests dissimilar modes of action of two antagonists at the neuromuscular junction.
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The ability of physostigmine alone and in combination with neostigmine to reverse d-tubocurarine-induced neuromuscular block was evaluated in surgical patients. The relaxation was maintained at a level of 90% twitch suppression during balanced anesthesia, and antagonism was attempted with physostigmine 1.5 mg x 3; neostigmine 0.5 mg x 3; neostigmine 1.0 mg x 3; or with a combination of physostigmine 0.75 mg and neostigmine 0.5 mg x 3. The measured parameters included the twitch force or EMG amplitude of the adductor pollicis brevis muscle after supramaximal 0.1 Hz stimulation and fading of these responses after repetitive 2 and 50 Hz stimuli. Although the restitution rate of twitch height and EMG amplitude were essentially the same with both antagonists, there was a considerable time-lag in regeneration of the fades after repetitive stimuli with physostigmine as compared with the neostigmine group. The addition of physostigmine to a subeffective dose of neostigmine resulted in antagonism comparable to that seen in other groups. The clinical antagonism was satisfactory in all patients receiving physostigmine. The divergence of relaxation-indicating parameters (twitch responses and fades) after physostigmine suggests dissimilar modes of action of two antagonists at the neuromuscular junction.
Key concepts: Neostigmine, Physostigmine, Medicine, Antagonism, Anesthesia, Neuromuscular transmission, Cholinesterase, Muscle relaxation