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M Bourin

Publications and source records attributed to M Bourin.

196 records · Page 11Linked to original sources
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[Unexpected interactions of some psychotropic drugs with barbital and pentobarbital effects in mice (author's transl)].

Some of the substances studied modified the effects of the two barbiturates as expected and in the same direction: --chlorpromazine and diazepam increased the effects; --amphetamine and caffeine decreased them. Barbital, unlike pentobarbital, undergoes almost no metabolic transformation. This explains why pentobarbital is potentiated in the presence of proadifen, an inhibitor of liver microsomial enzymes, whereas the effect of barbital is unchanged, and probably explains similar results obtained with iproniazide and imipramine. For the same reason, rifampicine, an enzyme inducer, antagonizes the effect of pentobarbital without affecting that of barbital. The dissociated effects obtained with other substances are more difficult to explain: --increased effects of barbital without modification of the effects of pentobarbital (sulpiride); --decreased effects of barbital without modification of the effects of pentobarbital (methylphenidate, nomifensine, amineptine, oxolinic acid, methysergide); --decreased effects of barbital with increased effects of pentobarbital (viloxazine). Two hypotheses may be considered: 1. The study of barbital and pentobarbital concentrations in blood and brain would allow to exclude a pharmacokinetic interaction; 2. Barbital does not act through the same mechanism as pentobarbital.

Amphetamine↗
PubMedDate not supplied

[Isoniazid and rifampicin in the rabbit. Effect on hepatic microsomal enzyme activity].

1. Enzymatic induction or inhibition induced by isoniazid (10 mg/kg) and/or rifampicin (13 mg/kg) oral treatment of 13 days in the rabbit, is evaluated with the following parameters: --variation of antipyrine half-life measured before treatment and 24 h after the end of treatment, --cytochrome P450 content, aniline hydroxylase and aminopyrine N-demethylase activities in hepatic microsomes. Isoniazid half-life is evaluated before treatment, in order to obtain an homogeneous repartition of animals in each group: isoniazid, rifampicin, isoniazid + rifampicin and control. 2. Rifampicin treatment gives a variable enzyme induction of antipyrine metabolism, cytochrome P450 and aniline hydroxylase activity; aminopyrine N-demethylase activity is significantly inhibited. Isoniazid treatment inhibits antipyrine metabolism and increases the cytochrome P450 content.

Animals↗
PubMedDate not supplied

Provocative agents in panic disorder.

The pharmacological challenge strategy involves giving a provoking agent under controlled rules to clarify some aspect of behavioural or biological function. Various agents such as sodium lactate, carbon dioxide, caffeine, yohimbine, isoprenaline and now cholecystokinin have been used as provoking agents in healthy volunteers as well as in panic patients. Results obtained in this field are updated, with emphasis on the potential mechanisms of action. It is concluded that there may be a final pathway between carbon dioxide, sodium lactate, and cholecystokinin inducing panic attacks.

Caffeine↗
PubMedDate not supplied

[The future of pharmacological models].

Do pharmacological models have a future? This was the question that had to be answered during seminar n.3 of the annual clinical pharmacology meeting in GIENS. The concept of 'model' is very extensive: it comprises both simple physiological testing and the replication in animals of human diseases. The main problems of pharmacological models are their predictive value and their validity in relation to the pragmatic target of finding new active molecules. Among numerous models proposed by the participants, three types have been selected as examples in this paper: a human model (cholecystokinin inducing panic attacks), the goal of which is to discover new molecules active in panic disorders. an animal model close to clinical features (coronary restenosis) which was to date unable to help in identifying molecules acting in human pathology transgenic animals as tools in drug development. The guidelines are very clear: models, however far they are from human pathology, are useful in predicting new molecular developments. Models are necessary steps to go from receptors to ill patients.

Animals↗
PubMedDate not supplied

[Iprindole: a functional link between serotonin and noradrenaline systems?].

Iprindole is an active antidepressant in clinical practice but its mechanism of action has never been clearly defined. Serotoninergic regulation of noradrenergic neurons of locus coeruleus depends on 5-HT2 receptors. This regulatory action of the 5-HT system appears to facilitate the down-regulation of beta receptors. In behavioural tests involving the noradrenergic system, the role of iprindole, administered in subactive doses, was evaluated in the presence of subactive doses of fluvoxamine, a serotonin uptake inhibitor. Yohimbine is an alpha2 antagonist, inducing a dose-dependent toxicity. This test allows a rapid and selective screening of antidepressants with direct and indirect beta-agonist properties. Administration of iprindole displayed a toxicity of fluvoxamine in the presence of yohimbine. A 5-day pre-treatment of iprindole antagonized this potentiation unmasked after acute administration of iprindole. The down-regulation of beta receptors induced by a chronic treatment by iprindole could prevent the adrenergic expression of yohimbine's toxicity. But the down-regulation of 5-HT2 receptors also obtained with chronic treatment by iprindole, can explain this antagonism preventing fluvoxamine's action. Hypothermia induced by a high dose of apomorphine, depends on an activation of the noradrenergic system. During the interaction with fluvoxamine, iprindole unmasked an antagonism of this hypothermia due to apomorphine. The activity of a subactive dose of salbutamol, a direct beta-agonist, was evaluated in the presence of fluvoxamine on hypothermia induced by a high dose of apomorphine. The aim of this interaction was to define the beta-adrenergic property of iprindole more precisely.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Reviewing the initial plans for the teaching of pharmacology: quality vs. quantity of knowledge, hesitation is no longer possible].

Pharmacology is located at the intersection of several branches of medical education. This position and the exponential development of medical knowledge, constrains university professors of pharmacology to make teaching choices, since time-limited education is imposed in this subject. Thus, it is necessary to list specific educational objectives within a frame of well defined and clear hierarchized pharmacological concepts. General and practical pharmacology teaching is to be preferred since it provides the knowledge base for further acquisition of specialized pharmacology. The necessary data can be easily and rapidly taught by means of clinical observations and case reports in connection with basic pharmacological concepts and therapeutic strategy. The medical student has to acquire rational guidelines for proper drug monitoring. He also has to learn how to assess the efficacy of the prescribed treatment and how to supervise the compliance. When an adverse effect is observed, the future physician must be able to evaluate the benefit-risk ratio. Initiation into the analysis of published clinical trials is the best way to develop a critical sense. Concurrently, pharmacology teachers should make available technical and practical resources to facilitate access to updated scientific data.

Drug Prescriptions↗
PubMedDate not supplied

[Study methods of drugs in Alzheimer disease].

The availability of new drugs for Alzheimer's disease, with different pharmacological profiles, leads to a redefinition the relevant methodology for developing drugs in this indication, including the inclusion/exclusion criteria, the duration of the studies, and therefore, the relevant guidelines. This was the purpose of the Giens Round-table devoted to the new methodology for drug development in Alzheimer disease.

Alzheimer Disease↗
PubMedDate not supplied

[Methodology of preparing a list of educational objectives: example of application to pharmacology. Groupe Objectifs Pédagogiques de L'Association des Enseignants de Pharmacologie].

Using a structured approach to categorize pharmacological knowledge and a systemic analysis of prescribing practice, we identified the knowledge needed to optimally prescribe and manage treatments with drugs. The approach consisted in finding the branched chains of knowledge beginning with each operation required to solve each problem which arises in prescribing and managing drugs at the most elementary level. This elementary knowledge is then transformed into educational objectives. The next step is to share the educational objectives between basic medical training, continuing medical education and acquisition of therapeutic knowledge. The method could be applied in other medical teaching domains.

Educational Technology↗
PubMedDate not supplied

Animal models of anxiety: are they suitable for predicting drug action in humans?

Currently there are numerous animal models of anxiety. A major concern with these models is their relevance with regard to predicting drug activity in humans. In the present review we try to make a parallel between the DSM IV classification of anxiety disorders and different models of anxiety in animals. These tests often measure more than one factor, so probably most of them are suitable as models of generalized anxiety disorder. Yet panic disorder appears to be more closely related to the elevated plus maze and to aversion in the rat, phobia to electric shock, posttraumatic stress to uncontrolled shock, and obsessive compulsive disorder to ultrasonic vocalization. But all these tests have to be revised using antidepressants active in these kinds of anxiety disorders.

Animals↗
PubMedDate not supplied

[Uroselectivity of alpha-1 antagonism in the treatment of benign prostatic hypertrophy: on the pharmacologic concept of the clinical approach].

Benign prostatic hyperplasia is the most common cause of voiding dysfunction in men. It becomes symptomatic from the fifth decade of life and needs treatment in 50 per cent of patients. Hyperplastic prostatic tissue and the smooth involuntary sphincter have a high density of alpha 1-adrenoceptors, thus alpha 1-blockers can decrease sphincter tone and reduce the tension exerted by the prostatic muscular component. Attempts have been made to find alpha 1-antagonists that have a selective effect on the prostate (alfuzosin), are long acting (tamsulosin, terazosin, doxazosin) or present specificity on the alpha 1A prostatic adrenoceptors (tamsulosin), in order to maintain efficacy without affecting blood pressure. Finasteride, a 5 alpha-reductase inhibitor without hypotensive side-effect may be more effective in men with a predominantly glandular component to their benign hyperplasia or with very large prostate glands, but has a longer onset of action and produces more adverse sexual effects. Thus, alpha-1 antagonists can be considered as an appropriate treatment option in patients with troublesome symptoms of BPH and who have not developed serious complications indicating surgery.

Adrenergic alpha-1 Receptor Antagonists↗