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Biomedical subjects

F Boismare

Publications and source records attributed to F Boismare.

At least 19 recordsLinked to original sources
PubMed1990

Acamprosate appears to decrease alcohol intake in weaned alcoholics.

Five hundred and sixty-nine alcoholics were included in a double-blind placebo-controlled randomized multicenter study of the effects of Acamprosate (calcium acetylhomotaurinate (CA), 1.3 g/day) on indicators of alcoholic relapse after withdrawal. One hundred and eighty-one patients in the CA group versus 175 in the placebo group completed the three-month study. The major efficacy criterion was plasma gamma-glutamyl transpeptidase (GGT), as an indicator of recent alcohol ingestion. This analysis was completed by criteria concordance analysis on a number of indicators of alcohol intake. Patients in both groups were similar initially. After 3 months of treatment, the patients in the CA group had significantly lower GGT (1.4 +/- 1.56 versus 2.0 +/- 3.19 times normal, P = 0.016). All significant differences (P less than 0.05) or trends (0.10 greater than P greater than 0.05) were in favor of a superior effect of CA over placebo. The major side-effect of CA was diarrhea (present in 13% of CA patients versus 7% of placebo, P = 0.04). CA proved superior to placebo on the evolution of markers of alcohol ingestion at three months, in this large-scale multicenter study. It could be a new modality in the drug therapy of alcoholism, not involving an antabuse effect, an antidepressant action, or conditioning.

Acamprosate↗
PubMed1990

Alcohol and GABA: ethanol intake modifies hippocampal nipecotic acid binding in ethanol-preferring and non-preferring rats.

3H-nipecotic acid (3H-NIP) binding to GABA uptake recognition sites was studied in the hippocampus of 3 groups of male, Long Evans rats: Group 1: ethanol-naive rats (ENR); Group II: ethanol-preferring rats (DR) and non-preferring rats (NDR), which had consumed about 5 g.kg-1.d-1 and 1 g-1.d-1 of alcohol respectively in the form of a 12% ethanol solution prior to 3H-NIP binding analysis; Group III: DR and NDR who had had no access to ethanol for 21 d after the initial exposure of ethanol solution (28 d). Binding studies showed that ethanol drunk by both DR and NDR in Group II decreased 3H-NIP binding (Bmax decreased) with an enhancement of affinity (KD decreased). In rats subjected to withdrawal of ethanol (Group III), affinity of 3H-NIP for GABA uptake sites was higher than in controls (Group I), but lower than in Group II, Bmax in this group being higher than in the 2 other groups. In Group III, KD was higher in DR than in NDR. These results showed that ethanol intake, in a free-choice paradigm, altered 3H-NIP binding, and that differences in ethanol intake between DR and NDR were associated with differences in sensitivity of hippocampal GABA uptake sites. These differences in 3H-NIP binding could either precede ethanol intake, or be a direct result from it. The results, together with data from other laboratories suggest that: 1), 3H-NIP binding sites are involved in the regulation of ethanol intake; 2), 1 factor responsible for individual differences in ethanol response is reflected by the GABA uptake system.

Animals↗
PubMed1990

Influence of an alpha-1-adrenoceptor antagonist, nicergoline, on placental prostanoid production in streptozotocin-induced diabetic pregnant rats.

The aim of this study was to determine if placental prostanoids could mediate the vasodilating action of an alpha-1-adrenoceptor antagonist, nicergoline (400 micrograms/kg i.p.), during late pregnancy in streptozotocin-induced diabetic rats (40 mg/kg i.v.). Placental prostanoid concentrations were evaluated by radioimmunoassay. Prostaglandin E2 levels showed a highly significant increase in diabetic and nondiabetic rats treated with nicergoline (p less than 0.001). 6-Keto-PGF1 alpha concentrations were slightly increased in diabetic rats compared to controls, and this increase was reversed by both nicergoline and insulin treatments. In all groups studied thromboxane B2 levels were comparable. It is concluded that prostaglandin E2 could mediate the vasodilating action of nicergoline on the placental irrigation and, therefore, improved the hemodynamic state of this organ in diabetic rats.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Increase in uterine prostaglandin E2, F2 alpha, prostacyclin and stability in thromboxane A2 production during late pregnancy in streptozotocin-induced diabetic rats.

This experiment was conducted to determine the effect of diabetes on uterine prostanoids production in near-term rats. The incidence of an insulin therapy was also studied. On the 21st day of pregnancy, uterine PGE2, PGF2 alpha and PGI2 levels showed a significant increase (respectively p less than 0.05, p less than 0.01 and p less than 0.05) in diabetic rats compared to controls whereas TxA2 production remained unchanged. The insulin therapy restored PGE2 levels, the most potent stimulatory factor of the myometrial fiber at control values, whereas it enhanced significantly PGI2 concentrations (p less than 0.05) and had no effect on PGF2 alpha production; TxA2 levels remaining always unchanged. It is suggested that the increase in uterine protanolds production during diabetes could induce a myometrial hypertonicity and play a role in the disturbances of the fetal development. The maintenance of PGE2 levels to control values by the insulin therapy might contribute to a normal delivery.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Application of an analytical method to calcium acetylhomotaurinate determination in urine.

After urine purification, plasma and urine concentrations of calcium acetylhomotaurinate (Acamprosate, CaAOTA) were determined with a high-performance liquid chromatography method following i.v. administration of the drug in two dogs. Results obtained in serum were in good agreement with those found previously. The CaAOTA urine determination is a promising method to be used in healthy volunteers.

Acamprosate↗
PubMed1986

Dynamic characteristics of dopamine, norepinephrine and serotonin metabolism in axonal endings of the rat hypothalamus and striatum during hypoxia: a study using HPLC with electrochemical detection.

The metabolism of dopamine, norepinephrine and serotonin was studied in normoxic or hypobaric hypoxic rats, using HPLC with electrochemical detection. The changes in serotonin and its metabolite 5 hydroxy indolacetic acid (5 HIAA) levels in the hypoxic striatum and hypothalamus suggest an inhibition of 5 HIAA formation and a complex interaction between synthesis, release and uptake. Hypoxia caused a decrease of the striatal levels of homovanillic acid (HVA), dihydroxy 3-4 phenylacetic acid (DOPAC) [inhibition of tyrosine hydroxylase (TH) and monoamine oxidase (MAO)] and 3-methoxytyramine (3 MT) (inhibition of release). Striatal dopamine levels were increased, suggesting an increase in granular dopamine storage, with an impaired release. Hypothalamic levels of norepinephrine were decreased during hypoxia [(inhibition of TH, MAO, and dopamine beta-hydroxylase (DBH)].

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

[Hemodynamic effects of nicergolin in man at rest and during exertion (author's transl)].

In 10 healthy subjects the injection of 10-methyl-1,6-diemthyl-ergoline-8 beta-methanol-(5-bromonicotinate (nicergoline, Sermion) (5 mg i.v.) caused a permanent decrease in blood pressure. This decrease in blood pressure is due to a rapidly occurring alpha-blocking effect and a secondary central alpha-stimulating effect which did not affect the postural regulating mechanisms of the arterial blood pressure in their function. The bradycardia and the elevation of the systolic volume and of the cardiac output are based on this central effect. After oral administration of 30 mg nicergoline the same modifications appeared but to a lesser extent. If nicergoline was administered in a dosage of 30 mg p.o. 1 h before bicyle exercise (100 W for 5 min), the cardiac output and blood flow in the lower extremities increased and the elevation of the systolic pressure was limited. However, the reactive tachycardia remained at the same level. The metabolic consequences of this administration resulted in an inhibited increase in the concentration of lactic acid in the blood, which is normally caused by this exertion. This favourable metabolic effect can be explained by 1. the initial bradycardia and the decrease in the total peripheral resistance whereby the oxygen consumption of the myocardium is reduced; 2. the peripheral vasodilation.

Adult↗
PubMed1978

Action of cytidine diphosphocholine on functional and hemodynamic effects of cerebral ischemia in cats.

The depression of evoked cortical potentials caused by brief periods of cerebral ischemia is attenuated by prior intracarotid injection of cytidoline (2, 4 or 8 mg/kg). Studies performed in hypercapnic cats suggest that the protection afforded by cytidoline is of metabolic rather than hemodynamic origin. The participation of the central dopaminergic structures by the drug is suggested according to the previous data.

Animals↗
PubMed1978

Biochemical and behavioural effects of hypoxic hypoxia in rats: study of the protection afforded by ergot alkaloids.

The conditioned avoidance response and the cerebral levels of dopamine and noradrenaline have been studied in control rats and in rats submitted to a hypobaric hypoxia. A protection against the effects of hypoxia was induced by both dihydroergocornine (20 microgram/kg) and dihydroergocryptine (100 microgram/kg), and the noradrenaline level did not decrease. This stabilization of cerebral noradrenaline level seems to be the main protection factor observed.

Animals↗
PubMed1978

[Effect of citidoline on hemodynamics in the normobaric hypoxic dog].

In dogs submitted to a normobaric hypoxia, we found an elevation of the arterial blood pressure, of the heart rate, of the cardiac output and of the regional blood flows, the total peripheral resistance remaining unchanged. Treatment with citidoline abolishes these hemodynamic responses and the authors hypothetize that this effect is correlated with the agonist dopaminergic effect of the drug.

Animals↗
PubMed1978

[Depressive states: clinical symptoms and monoaminergic hypothesis].

Twenty somatic symptoms are listed, that are often met in depressive states but that are presently neglected by clinicians and by the various depression rating scales. Thanks to the data provided by animal pharmacology and clinical studies, an attempt to correlate the clinical studies with the biochemical results is proposed between those symptoms and eventual monoaminergic dysfunctions. This study leads to a clinical observation scale. In the future, the authors envisage a multifactorial analysis of the data obtained by the use of the scale. Symptomatic groupings could help establish a new classification for depressive states. They could also guide the choice of the medication according to the monoaminergic dysfunctions that are pointed out.

Depression↗
PubMed1977

[Memorization and central catecholamines after a craniocervical injury carried out in rats: influence of imipramine administration (author's transl)].

A craniocervical injury has been carried out in rats (with head free to move) so that they get through a whiplash without any coma. Two days after the whiplash, comparable with a postcommotional syndrome, the acquisition of a labyrinth behavior is disturbed and, 7 days later, the retention is still disturbed. This disturbance of retention is not observed when the acquisition is performed before the whiplash. These data agree with the clinical observations, and we hypothesize a possible causal relation between the disturbance of learning behavior and the decrease of noradrenaline cerebral level induced by the whiplash. Treatment with imipramine (1 mg/kg) after the whiplash is able to remove these behavioral and biochemical disturbances.

Animals↗