The Fate of Thiopental in Man and a Method for Its Estimation in Biological Material*

Brodie, Bernard B.; Mark, Lester C.; Papper, E. M.; Lief, Philip A.; Bernstein, Eleonore; Rovenstine, E. A.

doi:10.1097/00132586-196508000-00056

Cited by 49 publications

(65 citation statements)

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“…The dose required to protect the baboon brain from stroke, however, was larger than that shown to protect dogs from MCA occlusion. "-" The dose-response differences observed in our experiments, earlier with dogs and now with baboons, might be attributed to dissimilar cerebrovascular anatomy, 18 -1B to species-specific tolerance to barbiturates 20 or to other unknown factors. The pentobarbital dose (90 ± mg per kilogram) needed to reduce stroke commonly was accompanied by prolonged ventilatory insufficiency, intermittent cardiac arrhythmias, and systemic hypotension sufficient to require a continuous infusion of phenylephrine.…”

Section: Discussionmentioning

confidence: 48%

Barbiturate Protection From Cerebral Infarction in Primates

Hoff

Smith

Hankinson

et al. 1975

Stroke

208

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Barbiturate Protection From Cerebral Infarction in Primates• Baboons were anesthetized with halothane or pentobarbital prior to middle cerebral artery (MCA) occlusion to test the protective effect of barbiturates against stroke in primates. Significantly less infarction was found in animals that received 90 mg per kilogram pentobarbital or more than occurred in control animals. Because of cardiovascular and ventilatory complications at high doses of barbiturate, however, therapeutic trials to suppress stroke in the human must await further identification of an effective regimen which includes a safe barbiturate dose.

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Section: Discussionmentioning

confidence: 48%

Barbiturate Protection From Cerebral Infarction in Primates

Hoff

Smith

Hankinson

et al. 1975

Stroke

208

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“…The shorter duration of action of thiopental is believed to be derived from the faster redistribution to less well-perfused tissues of the body, mainly muscle and fat (7,8 (12) showed that the rabbit's atria in the presence of propranolol or pronethalol responded to isopropylnoradrenaline with a marked shortening of the total duration mainly caused by the acceleration of the repolarization phase of the potentials. Such an acetylcholine-like effect of isopropylnor adrenaline is likely to serve at least partly for the antagonism against the barbiturate depression.…”

Section: Discussionmentioning

confidence: 99%

Effects of Thiopental and Pentobarbital Sodium on the Transmembrane Potentials of the Rabbit’s Atria in Special Reference to Interaction With Catecholamine

Kiba

1966

Japanese Journal of Pharmacology

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“…Hepatic drug metabolism of various substrates was measured using the 105,000g,a, microsomal pellet as previously described (2,3). Substrates used were: hexobarbital, determined by the method of Brodie et al (4); ethylmorphine, assessed by determining the amount of formaldehyde formed using a modification of the method of Nash (5) as described by Anders and Mannering (6); and aniline, determined by the method of Imai et al (7). Unless stated otherwise enzyme activity was expressed as: hexobarbital, nmoles hexobarbital metabolized/mg microsomal protein/20 min; ethylmorphine, nmoles formaldehyde formed/mg microsomal protein/15 min; and aniline nmole p-aminophenol formed/mg microsomal protein/20 min.…”

Section: Methodsmentioning

confidence: 99%

Studies on Cadmium-Induced Inhibition of Hepatic Microsomal Drug Biotransformation in the Rat

Schnell¹,

Means²,

Roberts³

et al. 1979

Environmental Health Perspectives

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Cadmium is a potent inhibitor of hepatic microsomal drug biotransformation in the rat. Male rats receiving a single intraperitoneal dose of cadmium exhibit significant decreases in hepatic microsomal metabolism of a variety of substrates. The threshold cadmium dose is 0.84 mg Cd/kg, and the effect lasts at least 28 days. Mechanistically, the inhibitory effect results from decreased cytochrome P450 content since cadmium does not alter NADPH cytochrome c reductase activity. This effect is also observed following acute oral administration of cadmium in doses greater than 80 mg Cd/kg but is not observed following chronic administration of the metal via drinking water in concentrations of 5-200 ppm for periods ranging from 2 to 50 weeks. A tolerance to the inhibitory cadmium effect is observed if male rats are pretreated with subthreshold doses of the metal prior to the challenge cadmium dose. The degree of tolerance can be overcome by increasing the challenge dose of cadmium. Characterization of the tolerance phenomenon in terms of onset, duration, and intensity reveals a good correlation with the kinetics of metaliothionein production, suggesting that the underlying basis for the tolerance phenomenon is likely the induction of metallothionein. A sex-related difference in the inhibitory effect of cadmium was observed. Cadmium did not inhibit the metabolism of hexobarbital or ethylmorphine in female rats but did inhibit that of aniline or zoxazolamine. Cadmium did not lower cytochrome P-450 content in female rats.

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The Fate of Thiopental in Man and a Method for Its Estimation in Biological Material*

Cited by 49 publications

References 0 publications

Barbiturate Protection From Cerebral Infarction in Primates

Barbiturate Protection From Cerebral Infarction in Primates

Effects of Thiopental and Pentobarbital Sodium on the Transmembrane Potentials of the Rabbit’s Atria in Special Reference to Interaction With Catecholamine

Studies on Cadmium-Induced Inhibition of Hepatic Microsomal Drug Biotransformation in the Rat

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