Convulsions in cats following withdrawal of barbital sodium

Essig, Carl F.; Flanary, Harold G.

doi:10.1016/0014-4886(59)90015-9

Cited by 21 publications

(4 citation statements)

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“…Thus there is a reasonably good correlation between the occurrence of withdrawal excitability as indicated in the present experiments and the published results of other workers, for both animal and man. Withdrawal phenomena or CNS tolerance have been reported to occur in laboratory animals after administration of barbiturates (Essig & Flanary, 1959;Ebert, Yim & Miya, 1964;Jaffe & Sharpless, 1965;Leonard, 1968), ethanol (Le Blanc, Kalant, Gibbins & Berman, 1969Ratcliffe, 1972), meprobamate (Kato, 1961) and chlorpromazine (Boyd, 1960) and in man after withdrawal of chlordiazepoxide (Hollister, Motzenbecker & Degan, 1961), methyprylon (Berger, 1961), meprobamate (Essig, 1964), nitrazepam (Oswald & Priest, 1965) and diazepam (Isbell & Chruschiel, 1970). However, no evidence was found in our experiments for a withdrawal excitability following methyprylon or diazepam administration.…”

Section: Discussionmentioning

confidence: 99%

“…Other methods which have been adopted to detect and quantitate the hyperexcitability produced by withdrawal from CNS depressant drugs have been estimation of the threshold to chemically or electrically induced seizures (Jaffe & Sharpless, 1965;Leonard, 1968); determination of the amount of intravenously infused hexobarbitone required to produce a burst suppression of 1 s or more on the electroencephalogram (Wahlstrom, 1968); correlation of drug effect with serum or brain concentrations (Kato, 1967;Stevenson & Turnbull, 1970); a scoring of the abstinence symptoms (Yanagita & Takahashi, 1970) or observation of the occurrence of spontaneous (Essig & Flanary, 1959) or sound induced convulsions (Crossland & Leonard, 1963). We suggest that determination of the duration of anaesthesia following an intracerebroventricular injection of pentobarbitone is another method which could be usefully added to this list, being especially applicable when the drugs administered are thought to affect the activity of hepatic drug-metabolizing enzymes.…”

Section: Discussionmentioning

confidence: 99%

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A Study of the Factors Affecting the Sleeping Time Following Intracerebroventricular Administration of Pentobarbitone Sodium: Effect of Prior Administration of Centrally Active Drugs

Stevenson

Bull

1974

British J Pharmacology

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1 Injection of pentobarbitone sodium into a lateral cerebral ventricle of rats produced a loss of righting reflex. The duration of anaesthesia was dose-dependent. 2 The optimum dose of pentobarbitone to allow study of the factors affecting the sleeping time was considered to be 650 ,ug injected in 25 M water. 3 In a study of the effect of age and sex on the sleeping time, the youngest rats used (88 g body weight) were found to be the most sensitive to barbiturate. Female rats were more sensitive than male animals. 4 The duration of anaesthesia was not affected by induction or inhibition of hepatic drug-metabolizing enzyme activity. 5 Prior administration (acute) of central nervous system depressant drugs shortened the latent period and prolonged the duration of sleep. Prior administration of stimulant drugs antagonized the effect of pentobarbitone. 6 Animals withdrawn following chronic administration of a number of drugs, barbitone, barbitone/bemegride mixture, Mandrax (methaqualone: diphenhydramine; 10: 1), chlordiazepoxide, nitrazepam, chlorpromazine or ethanol, exhibited a significant tolerance to intracerebroventricularly administered pentobarbitone. 7 Withdrawal of amphetamine, morphine, methyprylon or diazepam did not result in tolerance to intracerebroventricularly administered pentobarbitone. 8 Chronic administration of all drugs except amphetamine and morphine induced a tolerance to intraperitoneally administered hexobarbitone (100 mg/kg). 9 The usefulness of sleeping time determination following intracerebroventricular administration of pentobarbitone as an assessment of central nervous system excitability is discussed. It is concluded that this method gives a valid indication of the sensitivity of the central nervous system to barbiturate and of the level of excitability in general. The method is particularly applicable in situations where the activity of hepatic drug-metabolizing enzyme activity may be altered.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A Study of the Factors Affecting the Sleeping Time Following Intracerebroventricular Administration of Pentobarbitone Sodium: Effect of Prior Administration of Centrally Active Drugs

Stevenson

Bull

1974

British J Pharmacology

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“…Generalized convulsions occurred in more than 90% of cats attaining a final daily dosage of sodium barbital in excess of 173 mg/kg. The final dose of drug was more highly correlated with the occurrence of withdrawal convulsions than the total duration of chronic intoxication (11).…”

Section: Investigations On Barbiturate Withdrawal Convulsions In Aninwlsmentioning

confidence: 93%

“…Convulsive and other behavioral manifestations of barbiturate withdrawal have been produced in rats, cats and dogs (2,8,11,18,27). Crossland and Leonard (2) reported that the white rat develops physical dependence on sodium barbital if fluid intake is restricted to increasingly concentrated solutions of that drug.…”

Section: Investigations On Barbiturate Withdrawal Convulsions In Aninwlsmentioning

confidence: 99%

Clinical and Experimental Aspects of Barbiturate Withdrawal Convulsions

Essig

1967

Epilepsia

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SUMMARY Clinical and experimental data concerning mechanisms underlying barbiturate withdrawal convulsions have been reviewed. Such abstinence seizures have occurred in decorticate and decerebellate dogs. The possible role of the reticular activating system in the origin of this convulsive process was discussed. An increase in neuronal excitability probably develops during barbiturate withdrawal, but a biochemical basis for this has not been proven. RÉASUMÉA Les donneAes cliniques et expeArimentalesconcernant les meAcanismes responsables des convulsions secondaires au sevrage barbiturique sont passeAes en revue. Des crises de ce type peuvent s'observer chez des chiens deAcortiqueAs et deAceAreAbelleAs. Le roCle possible du systeGme reAticuleA activateur aG l'origine de ces crises est discuteA. Une augmentation de l'excitabiliteA neuronique se deAveloppe probablement pendant le sevrage barbiturique mais une base biochimique n'a pas eAteA deAmontreAe aG l'origine de cette hyperexcitabiliteA.

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Convulsive and Sham Rage Behaviors in Decorticate Dogs During Barbiturate Withdrawal

Essig¹

1962

Archives of Neurology

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Convulsions in cats following withdrawal of barbital sodium

Cited by 21 publications

References 4 publications

A Study of the Factors Affecting the Sleeping Time Following Intracerebroventricular Administration of Pentobarbitone Sodium: Effect of Prior Administration of Centrally Active Drugs

A Study of the Factors Affecting the Sleeping Time Following Intracerebroventricular Administration of Pentobarbitone Sodium: Effect of Prior Administration of Centrally Active Drugs

Clinical and Experimental Aspects of Barbiturate Withdrawal Convulsions

Convulsive and Sham Rage Behaviors in Decorticate Dogs During Barbiturate Withdrawal

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