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Biomedical subjects

F Boismare

Publications and source records attributed to F Boismare.

At least 109 records · Page 6Linked to original sources

GABA transmission, but not benzodiazepine receptor stimulation, modulates ethanol intake by rats.

Adult male Long Evans were selected as ethanol preferring rats (DR) during 28 days. After this period, they were daily IP injected during 14 days with one of the next drugs: diazepam 1 mg.kg-1, alprazolam 1 mg.kg-1 (benzodiazepines), progabide 25 mg. kg-1 (GABA A and B agonist), nipecotic acid 150 mg.kg-1 (GABA uptake inhibitor), muscimol 0.2 mg.kg-1 (GABA A agonist), AOAA 10 mg.kg-1 (GABA decarboxylase inhibitor), baclofen 3 mg.kg-1 (GABA B agonist), or NaCl 0.9% (1 ml/200 g). During treatment, rats were isolated, had free access to food, and free choice between ethanol (12%) and water whose respective consumption were daily noted. Among treatments, only AOAA and baclofen were able to decrease significantly ethanol intake, without modifying total liquid intake. The action of these different drugs on GABA transmission and on ethanol intake was discussed. It was concluded that GABA A and benzodiazepine receptors were not implicated in ethanol intake, but that modulation of voluntary ethanol intake could be associated with a modification of GABA metabolism and/or stimulation of GABA B receptors. An intervention of GABA B receptors on noradrenergic pathways was also evoked.

Alcohol Drinking↗

Haemodynamic effects of nicergoline in man at rest and during exercise.

1. The intravenous administration of nicergoline (5 mg) was followed by a rapid and sustained lowering of blood pressure; less rapid effects were bradycardia and an elevation of cardiac output. These delayed effects are consistent with an indirect action on the alpha-adrenoreceptors of the central nervous system. 2. Following the oral administration of nicergoline (30 mg), a partial reduction of exercise-induced lactacidaemia was demonstrated, which is consistent with the haemodynamic changes shown at rest.

Administration, Oral↗

Interference between central dopaminergic stimulation, and adrenal secretion in normoxic or hypobaric hypoxic rats.

Previous data have established that postsynaptic stimulation of central dopaminergic receptors was mainly involved in the protective action of apomorphine against the comportmental consequences of hypobaric hypoxia in rats: disturbances in a conditioned avoidance response. We confirm this notion showing that domperidone (a peripheral dopaminergic blocking agent) does not antagonize the protective effect of apomorphine. Furthermore, we establish that the action of apomorphine is at least partially mediated by adrenal glands since it is no longer seen in adrenalectomized rats. In normal rats, apomorphine enhances the corticosterone increase which is observed during hypobaric hypoxia and decreases the hypoxia-induced elevation of the adrenaline level. It is therefore concluded that the anti-hypoxic activity of apomorphine is probably mediated by a centrally mediated dopaminergic modification of the adrenal response to hypobaric hypoxia.

Adrenal Glands↗

[Effects of nicergoline on artificially induced micturition in the rabbit with and without prostatic hypertrophy].

An original experimental model of prostatism is proposed: Prostatic hypertrophy was induced in rabbit by testosterone 5 mg/kg-1. Three days later an increased number of micturitions, a correlate decrease in volume and an increased premictionnal vesical pressure were observed during a perfusion of the bladder in situ by NaCl 1 ml min-1. Phenoxybenzamine was not deeply studied because a lack of satisfaisant dose action-curve. I.V. administration of low doses of nicergoline (50 to 250 mcg/kg-1) reduced the consequences of the induced prostatic hypertrophy on the micturitions. These results are considered as a confirmation of a greater number of alpha 1-adrenoceptors in the bladder than in detrusor and allow us to confirm the use of nicergoline as a medical treatment of urinary retention in prostatic hypertrophy.

Animals↗

[Absence of the antihypertensive effect of chronic treatment with prazosin in the spontaneously hypertensive rat (SHR) and their offspring].

Seven consanguine monogamous SHR couples (G 1) were treated from their 5th to their 39th week of age with prazosin, 100 micrograms/kg/day i.p. Male rats were treated without interruption. Treatment was withheld in female rats from delivery to weaning. They were compared to seven similar SHR couples who were only daily i.p. injected with the same volume of solvent. Second (G 2) generation rats (untreated were studied. In G 1 female rats only, prazosin induced a transient decrease in systolic blood pressure (SBP), 6 hours after the injection, at 25 weeks of age. SBP, heart weight/body weight ratio and plasma renin activity remained unchanged at 39 weeks of age. Gestational parameters were not changed by the treatment, and no parameter was changed in G 2 rats. A previous study in the same conditions with another alpha 1-adrenoreceptor blocking agent, nicergoline, showed an inhibition of hypertension development in G 1 rats together with a preventive effect on untreated G 2 SHR (Moore et al., 1983). Thus prazosin failed to produce similar antihypertensive effects both in the treated rats and in their offspring and one can therefore conclude that nicergoline's effects were not only due to alpha 1-adrenoceptor blockade.

Aging↗