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Biomedical subjects

B Angrist

Publications and source records attributed to B Angrist.

At least 91 records · Page 5Linked to original sources
PubMed1979

Behavioral and neuroendocrine effects of low dose ET-495: antagonism by haloperidol.

Low doses of the dopamine agonist ET-495 were administered to nonpsychotic volunteer subjects by slow intravenous infusion, followed by a bolus of 1.5--2.5 mg haloperidol. ET-495 caused progressive dysphoria and sedation (in some cases, light sleep), effects believed to be mediated by dopaminergic inhibition. However, ET-495 also elevated growth hormone and suppressed prolactin, typical responses to dopamine agonist activity. Haloperidol reversed both the sedation and prolactin suppression induced by ET-495. These findings suggest: (1) that the sedation and hormonal responses were produced by stimulation of dopamine receptors; (2) that neurotransmitter systems mediating behavioral and neuroendocrine regulation may have differential neuropharmacological characteristics.

Adult↗
PubMed1979

Variable attenuation of amphetamine effects by lithium.

In an open study of 8 subjects, approximately half showed some attenuation of CNS stimulant effects of amphetamine after pretreatment with lithium. Two showed specific blockade of euphoria, with persistence of some CNS stimulant effects. In 3 subjects lithium did not appear to affect the response to amphetamine. Lithium caused significant attenuation of the amphetamine-induced increase in systolic blood pressure for the group as a whole.

Adult↗
PubMed1979

Neuroendocrine effects of apomorphine: characterization of response patterns and application to schizophrenia research.

Apomorphine, a direct-acting dopamine agonist, stimulates release of growth hormone (hGH) and suppresses release of prolactin (PRL) from the anterior pituitary. Previous studies comparing the magnitude of these responses in schizophrenics and controls suggest that many acute (and some chronic) schizophrenics have exaggerated hGH responses; many chronic schizophrenics (and patients with tardive dyskinesia) have blunted hGH responses to apomorphine, and possibly blunted PRL responses. The present studies extend and confirm these findings in chronic schizophrenics; in addition, several studies were undertaken to further characterize these apomorphine-induced endocrine responses. Studies in which apomorphine was given on 2 or 3 separate occasions to each of five subjects indicate that the hGH response is a highly reproducible individual index, but PRL suppression is a less satisfactory measure. hGH responses to apomorphine were consistently antagonized by pretreatment with haloperidol, supporting the concept that the hGH-releasing effect of apomorphine is mediated by its action on dopamine receptors. Cyproheptadine pretreatment was associated with erratic increases or decreases in the hGH response to apomorphine, but did not alter PRL levels or apomorphine-induced PRL suppression. The relationship of these findings to biological hypotheses of schizophrenia and to neuroleptic-induced receptor changes is discussed.

Adult↗
PubMed1978

Suppression of prolactin by dopamine agonists in schizophrenics and controls.

Prolactin levels were determined in plasma samples obtained before and after administration of apomorphine or L-dopa to otherwise unmedicated chronic schizophrenic patients or control subjects. Basal prolactin levels did not differ in these two groups. Suppression of prolactin levels after each dopamine agonist was highly significant. Suppression in schizophrenics was slightly less than in controls following apomorphine and slightly greater following L-dopa. The authors discuss the implications of these findings as well as the limitations of the prolactin regulatory system as an index of dopamine agonist sensitivity.

Adult↗
PubMed1977

Dopaminergic agonist properties of ephedrine--theoretical implications.

Reports of ephedrine-induced psychoses resembling amphetamine psychosis prompted studies of this classic sympathomimetic agent in systems that indicate central dopaminergic actions. Ephedrine induced dose-related stereotyped behavior in rats. This behavior was antagonized by haloperidol, but not by alpha- or beta-adrenergic blockers. Pretreatment with AMPT, but not reserpine, attenuated the stereotypy induced by ephedrine under one of two sets of conditions. Consistent prolactin suppression in humans was not seen. These findings are discussed in the context of clinical and pharmacologic data regarding other dopamine agonist drugs (the central nervous system stimulants, apomorphine, ET 495). These data suggest the possibility that synergistic noradrenergic and dopaminergic facilitation may be important in the induction of the stimulant psychoses.

Animals↗
PubMed1976

Dimethyltryptamine levels in blood of schizophrenic patients and control subjects.

A gas chromatographic-mass spectrometric determination of blood N,N-dimethyltryptamine in normal controls and schizophrenic patients was carried out with a sensitivity limit of 0.05 ng/ml whole blood. Although the results appear to suggest that the mean DMT level was higher in the total patient group, those patients with acute psychosis, female patients and patients with suspiciousness scores on the BPRS of 4 or over, the differences were not statistically significant.

Female↗
PubMed1975

Clinical studies with dopamine-receptor stimulants.

Oral administration of ET-495 was found to cause worsening of psychiatric status in 4 out of 7 schizophrenic patients, and to induce a paranoid state and a syndrome of auditory hallucinosis in 2 non-schizophrenics. These observations were compatible with the hypothesized role of dopamine in schizophrenia. However, these psychotogenic effects were far less dramatic than those noted in other studies with amphetamine, methylphenidate or L-Dopa. Possible explanations for this differing psychotogenic potency of receptor stimulators versus presynaptic agonists are presented. Intravenous ET-495 and apomorphine did not show psychotogenic effects.

Adult↗