Abstract
The discovery that N-allylnormorphine was a specific antagonist to morphine gave hope that an anti-barbiturate agent might be discovered. Shaw et al. (11) noted that in dogs, BB-methyl-ethylglutarimide (bemegride) dispelled the EEG changes induced by barbituric acid, and suggested that it may act as a barbiturate antagonist. Subsequent studies by Louw and Sonne (5) and Pederson (9) did not lend support to this theory, and Peacock (8) could find no specific pattern of EEG changes which could be attributed to the administration of bemegride. Ackner and Pampiglione (1) concluded that the demonstration of persistence of barbiturate-fast activity in the EEG after arousal did not support the hypothesis of a direct pharmacological antagonism, and suggested that bemegride was not a direct stimulant but caused an increased responsiveness in the patient.
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