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A Study of the Anti-barbiturate Effects of Bemegride

Published online by Cambridge University Press:  29 January 2018

A. Orwin ,
M. Sim  and
J. A. H. Waterhouse
A. Orwin
Affiliation:
Department of Psychological Medicine, United Birmingham Hospitals
M. Sim
Affiliation:
Department of Psychological Medicine, United Birmingham Hospitals
J. A. H. Waterhouse
Affiliation:
Department of Social Medicine, University of Birmingham
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Extract

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.

Type
Research Article
Information
The British Journal of Psychiatry , Volume 111 , Issue 475 , June 1965 , pp. 531 - 533
Copyright
Copyright © Royal College of Psychiatrists, 1965 

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References

1 Ackner, B., and Pampiglione, G. (1959). “Observations on arousal following Megimide (bemegride) during light barbiturate narcosis.” J. Ment. Sex., 105, 788–791.CrossRefGoogle Scholar
2 Brazier, M. A. B., and Finesinger, J. E. (1945). “Action of barbiturates on the cerebral cortex.” Arch. Neurol. Psychiat., 53, 51–58.CrossRefGoogle Scholar
3 Eilenberg, M. D., Lodge Patch, I., and Hare, E. H. (1960). “Comparative hypnotic efficacy of phenaglate.” J. Ment. Sci., 106, 675.CrossRefGoogle Scholar
4 Fox, R. (1962). “Safe sedation?: a controlled trial of ‘megimated’ amylobarbitone.” Ibid., 108, 731–734.Google Scholar
5 Louw, A., and Sonne, L. M. (1956). “‘Megimide’ in treatment of barbituric acid poisoning.” Lancet, ii, 961–965.CrossRefGoogle Scholar
6 McGuinness, B. W., and Roberts, F. J. (1960). “‘Megimated’ barbiturates.” Brit. med. J., ii, 996.CrossRefGoogle Scholar
7 Nymgaard, K. (1959). “Studies on the sedation threshold: A. Reproducibility and effect of drugs. B. Sedation threshold in neurotic and psychotic depression.” A.M.A. Arch. Gen. Psychiat., 1, 530–536.Google Scholar
8 Peacock, J. M. (1956). “Electroencephalographic examination of effects of Megimide and Daptazole in barbiturate narcosis.” EEG and Clin. Neurophysiol., 8, 289–298.CrossRefGoogle Scholar
9 Pederson, J. (1956). “Arousing effect of Megimide and amiphenazole in allylpropymal poisoning.” Lancet, ii, 965.CrossRefGoogle Scholar
10 Shagass, C. (1954). “The sedation threshold: a method for estimating tension in psychiatric patients.” EEG and Clin. Neurophysiol., 6, 221–233.CrossRefGoogle Scholar
11 Shaw, F. H., Simon, S. E., Cass, N., Shulman, A., Ansee, J. R., and Nelson, E. R. (1954). “Barbiturate antagonism.” Nature, 174, 402–403.CrossRefGoogle ScholarPubMed
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