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Biomedical subjects

Y Lecrubier

Publications and source records attributed to Y Lecrubier.

At least 109 records · Page 6Linked to original sources
PubMed1982

[Side effects and risks of benzodiazepines].

If benzodiazepines rank amongst the less harmful drugs, they are not completely safe. As all other drugs, they must be evaluated in relation with their risk/benefit ratio knowing that their side effects must be assessed for each patient and that they may vary according to indication, dosage, routes of administration and pharmacokinetic differences between the molecules. The authors mainly study: vigilance disorders and performance impairment, memory loss, behaviour disturbances, exceptional toxicomania risk, teratogen effects, not proved to this date, acute overdosage, interaction with other sedative psychotropic drugs (CNS depressors, imipramine). In conclusion, the authors underline the importance of the use of benzodiazepines and their success which is a social phenomenon.

Anti-Anxiety Agents↗
PubMed1982

[A qualitative study of clinical change in population of salbutamol-treated hospitalized depressives (author's transl)].

On the basis of pharmacological and clinical findings, salbutamol, a beta-adrenergic stimulant, is used in the treatment of depression. The day by day evolution of each of the most commonly evaluated symptoms in depressed patients is presented as observed during 10 days in 13 patients who were administered this treatment. Improvement appears to be global: it concerns all symptoms. However: - improvement of psychomotor retardation is early and is often observed before mood recovery; - and anxiety seems to variate independently from other factors. Responding patients were those who presented a frank depressive state with no associated psychiatric pathology. Tolerance was satisfactory in all cases.

Adult↗
PubMed1981

Effect of chronic lithium treatment on isolation-induced behavioral and biochemical effects in mice.

The following effects were induced in mice by a prolonged of isolation (6-7 weeks from weaning): (1) reduction in motor activity; (2) reduction in the effect of oxotremorine on rectal temperature; (3) increase in the response to salbutamol, a beta-adrenergic stimulant. Chronic lithium treatment (2 mg/ml in the drinking water during the last 3-4 weeks of isolation) prevented these phenomena. The number and affinity of beta-adrenergic receptors in the whole mouse brain (excluding the cerebellum) was unmodified by either isolation or by lithium. It is suggested that lithium blocks isolation-induced hypersensitivity, especially of the beta-adrenergic system; this mechanism may be involved in the therapeutic action of lithium.

Animals↗
PubMed1981

Beta-adrenergic stimulation and antidepressant activity.

The results presented here, together with the literature data, support the noradrenergic hypothesis of depressive states, and especially the involvement of beta-adrenergic receptors: --In animals, beta stimulants have the same spectrum of activity as other antidepressants. --These effects of both classical antidepressants and beta-adrenergic stimulants are antagonized by beta blockers. --Chronic administration of antidepressants results in a decrease of beta receptors. --Salbutamol, a beta-adrenergic stimulant had, in depressed patients, a clear and rapid antidepressant effect.

Adrenergic beta-Agonists↗
PubMed1980

Evidence for the role of noradrenaline in some effects of quipazine.

In mice, quipazine has shown several behavioral effects: It antagonizes hypothermia induced by a high dose of apomorphine without altering climbing or stereotyped behavior; it antagonizes oxotremorine-induced hypothermia without altering tremors or peripheral signs; and it increases the toxicity of yohimbine. These three responses are considered to be predictive of an antidepressive action; in these three tests the effects of quipazine are inhibited by D,L-propranolol but not by D-propranolol or methysergide. Quipazine, in mice pretreated with pargyline, induced head twitches which were inhibited by methysergide but not by D,L-propranolol. Quipazine, in addition to its well-known serotonergic effects, seems to have beta-adrenergic properties which should be kept in mind when this drug is used as a pharmacological tool and which suggest that the beta-adrenergic system is implied in depression.

Animals↗
PubMed1980

A beta adrenergic stimulant (salbutamol) versus clomipramine in depression: a controlled study.

A controlled study comparing salbutamol (6 mg/day) to clomipramine (150 mg/day), both given by intravenous infusion, was performed on depressed inpatients (10 per group). The symptomatology was evaluated by two blind observers at days 0, 5, and 15 using the Hamilton Rating Scale. Both treatments were effective on the overall symptomatology but the onset of action of salbutamol was more rapid.

Adolescent↗
PubMed1980

[Treatment of orthostatic hypotension induced by tricyclic antidepressants with yohimbine (author's transl)].

Following the observation that two patients with depression and essential orthostatic hypotension recovered from the latter affection after yohimbine administration, an open study was conducted to assess the activity of yohimbine in correcting orthostatic hypotension induced by tricyclic antidepressants. Results were conclusive in 10 of the 11 patients treated, and were confirmed in a further 12 cases during a double-blind study. Yohimbine appears to be the most effective treatment for orthostatic hypotension, either essential or induced by thymoanaleptic or neuroleptic therapy.

Blood Pressure↗
PubMed1979

Antagonism by d,1-propranolol of imipramine effects in mice.

Three agents with known or suspected antidepressant activity, imipramine, salbutamol and dexamphetamine, were active in animal tests predictive of an antidepressant effect in man: antagonism of the hypothermia induced by reserpine, by oxotremorine or by a high dose of apomorphine, and the potentiation of the yohimbine-induced toxicity. These effects were antagonized by d,1-propranolol, suggesting that the stimulation of beta-adrenergic receptors could be a common mechanism underlying their effects. These results agree with the noradrenergic hypothesis of the pathophysiology of affective disorders.

Albuterol↗
PubMed1979

[The role of norepinephrine in affective disorders (author's transl)].

The role of norepinephrine in affective disorders is supported by the following data. There is a decrease of activity of the noradrenergic system in depressive patients, evaluated by: --a decrease of the metabolism of noradrenaline; --an hyperreactivity of adrenergic receptors; --a decrease of the secretion of some hormones (melatonine, renine, corticosteroides) the liberation of which is mediated by stimulation of adrenoreceptors. The well recognized antidepressant drugs are able to activate by different mechanisms the noradrenergic system. Reciprocally, drugs well known to stimulate noradrenergic system are able to increase mood. Complementarily, antimaniac drugs are adrenolytic and adrenolytic drugs are antimaniac and depressogenic.

Antidepressive Agents↗
PubMed1977

[Study of a beta-adrenergic stimulant and its antidepressant activity in man].

In animals, the psychopharmacological profile of beta-adrenergic stimulants is very similar to that of tricyclic antidepressants. In patients, more particularly in endogenous depressive patients, the antidepressant effect of salbutamol was very clear. A definite improvement was observed in all of the 22 studied patients after 1 to 3 days of intermittent venous infusion. The place of salbutamol in the therapeutic armamentarium of depressive states has still to be defined exactly. It is speculated that the antidepressant effect of imipramine-like derivatives is related to the stimulation of central beta 2-adrenergic receptors.

Adrenergic Agonists↗