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Biomedical subjects

H Barry

Publications and source records attributed to H Barry.

At least 55 records · Page 3Linked to original sources
PubMed1976

Anticonvulsant activity of delta9-tetrahydrocannabinol compared with three other drugs.

Delta9-tetrahydrocannabinol (THC) was compared with diphenylhydantoin (DPH), phenobarbital (PB) and chlordiazepoxide (CDP) using several standard laboratory procedures to determine anticonvulsant activity in mice, i.e., the maximal electroshock test (MES), and seizures induced by pentylenetetrazol, strychnine and nicotine. In the MES test, THC was the least potent and DPH the most potent blocker of hind limb tonic extensor convulsions whereas THC was the most potent and DPH the least potent in increasing the latency to this response and in preventing mortality. Seizures and mortality induced by pentylenetetrazol or by strychnine were enhanced by THC and DPH and were blocked by PB and CDP. In the test with nicotine, none of the four anticonvulsant agents prevented seizures; DPH was the only one which failed to increase latency; THC and DPH were less potent than PB and CDP in preventing mortality. THC most closely resembled DPH in the tests with chemical convulsant agents, but a sedative action of THC, resembling that of PB and CDP, was indicated by low ED5 0 for increased latency and for prevention of mortality in the MES test.

Animals↗
PubMed1976

Discriminative pentobarbital stimulus in rats immediately after intravenous administration.

Rats with chronically implanted venous cannulas were trained to make differential active or passive shock-avoidance responses in a 2-compartment box at 15 sec after i.v. adminstration of pentobarbital (5 mg/kg) or saline. The discriminative pentobarbital stimulus persisted for several min after adminstration. The pentobarbital response also was elicited in tests at 15 sec after i.v. injection of chlordiazepoxide (2.5 and 5 mg/kg) or alcohol (500 mg/kg). Subsequent training at 10 min after i.p. injection of pentobarbital (10 mg/kg), followed by tests after i.p. administration of other drugs, indicated that the discriminative drug stimulus is qualitatively similar with this different route and time interval. A general preference for the passive over the active response developed only in the second stage of training, during i.p. injections.

Animals↗
PubMed1975

Differential effects of methylphenidate on reticular formation and thalamic neuronal activity.

Intravenous administration of methylphenidate (1 or 2 mg/kg) markedly attenuated the unit discharge rate in the mesencephalic reticular formation of rats and cats. Concurrently this drug enhanced the neural activity in the primary sensory nuclei of the thalamus. The differential effect of methylphenidate on these two neural systems suggest a possible mechanism by which it may improve attentive processes in hyperkinesis.

Acoustic Stimulation↗
PubMed1975

Sex of siblings of male alcoholics.

Research conducted with general population samples has demonstrated the importance of sex of siblings in the formation of sex-role identification and in the development of sex-role conflict. Information on early family structure was collected from 207 white male alcoholic inpatients. Among those reared in intact families with at least two older siblings, 65 had a second-older brother. This difference cannot be explained by variation in family size, differential sex ratios in birth rates, or greater availability of women in the sibships of the alcoholics. It is consistent with a model that postulates that alcoholism in men may express dependency conflict associated with sex-role identify problems.

Alcoholism↗
PubMed1974

Effect of ethanol on the oxidative metabolism of tryptamine by rat liver homogenate.

1 The effect of a wide range of ethanol concentrations (v/v) on indoleacetic acid (IAA) formation from the oxidative deamination of tryptamine was studied in vitro, in rat whole liver homogenate.2 IAA production was inhibited progressively by ethanol in concentrations between 0.01% to 0.2%, but the inhibition declined when the ethanol concentration was increased further to 6%.3 Ethanol-induced inhibition of IAA formation was only partially reversed by excess aldehyde dehydrogenase, whereas reductions in IAA formation were completely prevented by pyrazole or ethanol (6% and 10%) itself.4 Excess nicotinamide adenine dinucleotide failed to alter the inhibitory effect of ethanol and no evidence was obtained for inhibition of monoamine oxidase by ethanol or its metabolite, acetaldehyde.5 We conclude that ethanol indirectly inhibits IAA production as a result of oxidation of ethanol by alcohol dehydrogenase, during which the oxidative metabolism of tryptamine is shifted towards the reductive pathway, thus favouring the formation of tryptophol in place of IAA.

Acetaldehyde↗