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Biomedical subjects

D Bentue-Ferrer

Publications and source records attributed to D Bentue-Ferrer.

At least 19 recordsLinked to original sources
PubMed2004

[Mechanisms of chronic cough pathophysiology].

INTRODUCTION: In some situations such as post-virus or post whooping cough, a non productive subacute cough may occur without apparent local inflammation, epithelium abnormalities or bronchoconstriction. This subacute or chronic cough represents a real syndrome (cough disease) due to the central nervous system (CNS) and its ortho and parasympathic outputs. At the CNS level, functional disturbancies and neosynaptogenesis can be described, with the intervention of the NMDA-type glutamatergic receptors. STATE OF ART: The neurons located in the expiratory area of the breathing center (Pre-Boetzinger complex of the lower brainstem) present exagerated responses to stimuli, due to the repetitive stimulation of the NMDA receptors; this phenomenon is similar to long-term-potentiation (LTP), the molecular basis of learning, memory and neosynaptogenesis. The cough reflex is thus amplified and rapidly chronic and would justify any pharmacological intervention at the NMDA-receptors level. PERSPECTIVES: More recently 5TH4 receptors have been implied in the control of respiration; an overexpression of these receptors in the Pre-Boetzinger area could contribute to an increase of the cough reflex. CONCLUSION: The present review aims at summarizing the main rationale target to pharmacologically block the chronic cough.

Antitussive Agents↗
PubMed2002

[Mild Cognitive Impairment: potential therapeutics].

Mild Cognitive Impairment (MCI) is an emerging concept used to describe memory decline and probably attention disturbances in otherwise intellectually intact individuals. MCI may be considered in 12 to 15 p. 100 of the cases as announcing an Alzheimer's Disease (AD). Although still speculative, the debate concerning the drugs susceptible to normalize symptoms of MCI or to stop conversion to AD must be raised. For that purpose, several long term clinical trials are running (antioxidants, nootropics, anticholinesterasics.) and new molecules in the pipe-line should be assessed in patients with the diagnosis of MCI.

Aged↗
PubMed2001

Glucose tolerance during moderate prolonged exercise in women with oral contraceptives as compared to non-users.

BACKGROUND: The purpose of this study was to assess gluco-se tolerance during exercise in women on oral contraceptives. METHODS: To this end, we investigated the effects of glucose ingestion on glucose and hormonal responses in 7 women on oral contraceptives (OC(+); 21.3+/-1.3 yrs) and 7 normally menstruating (OC(-); 22.6+/-1.3 yrs) during an ergocycle test (30 min, 60% VO2max). Venous blood samples were withdrawn at 0, 3, 5, 10, 15 and 30 min exercise and at the 30th min postexercise. Glucose was ingested per os (0.5 g x kg(-1) b.w) between the 2nd and the 3rd min of the exercise. RESULTS: Under resting condition, plasma glucose and catecholamine concentrations were similar in both groups whereas plasma GH and insulin levels were greater in OC(+) (p<0.05). Glucose/insulin ratio (G/I), used as an indicator of insulin resistance, suggested a reduced insulin sensitivity at rest in the OC(+) (p<0.05). No significant differences were observed between OC(+) and OC(-) in plasma glucose, insulin, and catecholamine concentrations during exercise. Plasma GH values were greater in OC(+) from the 15th min of the exercise and during the recovery period (p<0.01). CONCLUSIONS: This study indicated that oral glucose ingestion at the onset of prolonged submaximal exercise induced similar glucose tolerance in women taking or not oral contraceptives.

Adult↗
PubMed2001

[Perspectives for drug treatment in Alzheimer's disease].

The last decade was very fruitful in neuropharmacology and notably in the therapeutic strategies of dementia and Alzheimer's disease (AD). The amount of data, information and breakthroughs is nevertheless difficult to apply in direct relationship with patients. The present review aims at classifying information according to their origins: epidemiology, clinical trials, neurosciences. A guide for drug prescription in Alzheimer's disease is thus warranted and becomes clearer, sure that, in the next future modifications and new strategies will appear. The main goal of the present review is to summarize the state-of-the-art for a non specialist in AD.

Alzheimer Disease↗
PubMed2000

Effects of glucose ingestion at the onset of moderate-intensity, prolonged exercise in women as compared to men.

To test glucose tolerance during exercise, the effects of oral glucose ingestion (0.5 g x kg(-1)) on plasma glucose and hormonal responses (insulin, catecholamines) were investigated in 11 women [mean (SEM) age 21.6 (1.3) years] and 10 men [22.0 (0.3) years] during cycle ergometer exercise (30 min at 60% maximum oxygen consumption, VO(2max)). The two groups exhibited similar VO(2max) values, when expressed per kg of lean body mass. Venous blood samples (5 ml) were withdrawn immediately before the exercise, during the exercise (at 3, 5, 10, 15 and 30 min) and at the 30th min of the recovery period. Glucose was ingested orally between the 2nd and the 3rd min of the exercise. As compared to men, plasma glucose concentrations were lower in women during exercise (P < 0.05 at 3, 15 and 30 min) and at the 30th min of the recovery period (P < 0. 001), while plasma insulin concentrations were higher in women during exercise (P < 0.05 at 3, 15 and 30 min). The ratio of the area under the curve for glucose over the area under the curve for insulin was lower in women during exercise (P < 0.0002). A linear relationship between glucose and insulin concentrations was found only for women during exercise (r = 0.615, P < 0.0001). No gender difference was observed for the catecholamine concentration during exercise. In conclusion, this study postulates that an oral glucose load given at the onset of a prolonged and moderate exercise bout induced lesser plasma glucose and greater insulin concentrations in women as compared to men. These data argue in favour of a greater glucose tolerance in women during exercise.

Administration, Oral↗
PubMed1999

Between 21 and 34 years of age, aging alters the catecholamine responses to supramaximal exercise in endurance trained athletes.

The purpose of this study was to determine the effect of aging and training on the adrenaline (A) and noradrenaline (NA) responses during the Wingate-test in three age groups of subjects: 21 year old untrained subjects (21U), 21 year old endurance trained (21T) (national elite runners), 34 year old endurance trained (34T) (national elite runners). Performances during the test were judged using the usual parameters of peak power (Wmax) and mean power (W) expressed in absolute or relative values. A and NA responses were measured at rest (A0 and NA0) immediately at the end of the exercise (Amax and NAmax) and after 5 minutes recovery (A5 and NA5). Plasma maximal lactate (La(max)) was determined 3 minutes after the end of the exercise. Wmax, W and La(max) were always significantly lower in 34T compared to 21T and 21U. The catecholamine responses were similar in 21T and 21U. Inversely, a significantly lower value of Amax was observed in 34T (2.01 +/- 0.5 nmol x l(-1)) compared to 21U (3.62 +/- 0.3 nmol x l(-1)) associated with a significantly higher value of NA(max) in 34T versus 21T and 21U. Thus, the Amax/NA(max) ratio was found to be significantly lower in the older subjects versus both 21T and 21U. All these findings indicated that endurance training did not affect the sympathoadrenergic responses to a supramaximal exercise and suggested that only one decade may reduce the capacity of the medulla to secrete adrenaline and therefore the adrenal medulla responsiveness to the sympathetic nervous activity.

Adrenal Medulla↗
PubMed1999

Comparative efficacies of antibiotics in a rat model of meningoencephalitis due to Listeria monocytogenes.

The antibacterial activities of amoxicillin-gentamicin, trovafloxacin, trimethoprim-sulfamethoxazole (TMP-SMX) and the combination of trovafloxacin with TMP-SMX were compared in a model of meningoencephalitis due to Listeria monocytogenes in infant rats. At 22 h after intracisternal infection, the cerebrospinal fluid was cultured to document meningitis, and the treatment was started. Treatment was instituted for 48 h, and efficacy was evaluated 24 h after administration of the last dose. All tested treatment regimens exhibited significant activities in brain, liver, and blood compared to infected rats receiving saline (P < 0.001). In the brain, amoxicillin plus gentamicin was more active than all of the other regimens, and trovafloxacin was more active than TMP-SMX (bacterial titers of 4.1 +/- 0.5 log10 CFU/ml for amoxicillin-gentamicin, 5.0 +/- 0.4 log10 CFU/ml for trovafloxacin, and 5.8 +/- 0.5 log10 CFU/ml for TMP-SMX; P < 0.05). In liver, amoxicillin-gentamicin and trovafloxacin were similarly active (2.8 +/- 0.8 and 2.7 +/- 0.8 log10 CFU/ml, respectively) but more active than TMP-SMX (4.4 +/- 0. 6 log10 CFU/ml; P < 0.05). The combination of trovafloxacin with TMP-SMX did not alter the antibacterial effect in the brain, but it did reduce the effect of trovafloxacin in the liver. Amoxicillin-gentamicin was the most active therapy in this study, but the activity of trovafloxacin suggests that further studies with this drug for the treatment of Listeria infections may be warranted.

Animals↗
PubMed1996

Noninterchangeability of specific radioimmunoassay and monoclonal antibody fluorescent polarization immunoassay in cyclosporine measurements.

This study compares cyclosporine (CsA) concentrations in whole blood from patients receiving bone marrow (n = 10), renal (n = 48), heart (n = 50) or liver (n = 50) transplants, as measured by monoclonal antibody flurorescence polarization immunoassay (FPIA) and specific 125I-radioimmunoassay (RIA). The FPIA overestimated CsA by an average of 25%. Results were higher for all indications: FPIA/RIA ratios were 1.17 for bone marrow, 1.23 for renal and 1.27 for both heart and liver transplants, and these values were significantly different from 1.0. The percentage of overestimation was higher at low CsA concentrations (< or = 100 micrograms/L) than at high CsA concentrations (> or = 400 micrograms/L). In all indications, results by both methods correlated well (r > 0.96) but slopes and intercepts were different from 1.0 and 0.0, respectively, and these parameters varied greatly between the grafted populations. These findings obtained with the two methods could not be attributed to matrix effect because the mean FPIA/RIA ratio for spiked control samples was 1.0. The discrepancy between the FPIA and RIA could be explained by the lower specificity of the monoclonal antibody contained in the FPIA kit. These results suggest that FPIA is not as accurate as RIA and that the two methods are not interchangeable in CsA level measurement.

Antibodies, Monoclonal↗
PubMed1996

The dopamine agonists lisuride and piribedil protect against behavioural and histological changes following 4-vessel occlusion in the rat.

The 4-vessel occlusion model of ischaemia in the rat was used to assess the effects of two dopaminergic agonists, lisuride and piribedil, on some behavioural and histological changes. Animals were either sham-operated, subjected to 20 min 4-vessel occlusion, or administered lisuride (0.5 mg/kg i.p.) or piribedil (10 mg/kg i.p.) 1 h before 20 min 4-vessel occlusion. Both drugs attenuated deficits in neurological testing, Morris water maze and 14-unit T-maze (p < 0.05). Extensive neuronal death was observed in the CA1, CA3 and CA4 regions of the hippocampus of 4-vessel-occluded animals. Pretreatment with both lisuride and piribedil provided protection against cell death in the hippocampal regions. These findings suggest dopamine may play a role in cerebral ischaemia and dopaminergic agonists may be beneficial in preventing ischaemia-induced neurodegeneration.

Animals↗
PubMed1995

[Delay in the effect of antidepressive agents: pharmacologic approach].

A paradox which is not resolved in the use of antidepressants (ATD) is that in pharmacological studies of animal models of depression and in neurochemical studies, the onset of activity of all drugs is extremely rapid, whereas in human clinical practice the onset is delayed (15 days). An attempt is made to explain this in 3 ways, involving the synapse, transduction mechanisms, and cognition. Analysis of the impact of all ATDs shows that we are confronted with slow adaptive processes which are correlated with the delay observed in clinical practice. The interest of such considerations is that they may give rise to alternative therapies which are able not only to accelerate response, but also to increase it.

Affect↗
PubMed1994

Inhibitor effects of diltiazem, nicardipine, nifedipine and verapamil on the norepinephrine-induced contractions of the canine saphenous vein in calcium-free medium.

Contractile responses to norepinephrine (noradrenaline, NE 10(-5) M) in the canine saphenous vein (SV) are significantly, although slightly, reduced (14%) when induced in a physiological medium depleted of calcium for 1 hour (+ EGTA). In contrast, they are inhibited by about 75% after 24 hr in calcium free physiological saline solution (P.S.S.). ED50 of norepinephrine in 1-hr calcium-free medium and in normal Ca++ P.S.S. are 6 x 10(-7)M and 4.2 x 10(-7)M, respectively. Two blockers of extracellular calcium entry have also been cited as inhibitors of intracellular calcium pool refilling. At concentrations of 10(-6)M, 10(-5)M and 10(-4)M, diltiazem and nicardipine inhibit the norepinephrine-induced contractions (NIC) in a concentration-dependent manner. At 10(-4)M, the two calcium blockers inhibit the NIC by 70% and by 72% respectively in Ca++ free (+ EGTA) P.S.S. Nifedipine and verapamil only begin to significantly inhibit NIC in Ca++ free (+ EGTA) P.S.S. at concentrations equal to or greater than 10(-5)M. At 10(-4)M concentration, control inhibition in Ca++ free P.S.S. was observed as 60% and 49%, respectively. Contrary to the other 3 calcium antagonists tested, diltiazem antagonises NIC significantly less in calcium-containing medium (45%) than in calcium-free medium (72%). Procaine at a concentration of 10(-3)M, described as sufficient to totally inhibit calcium release from its intracellular storage sites, only inhibits NIC by 52% in calcium free (+ EGTA) P.S.S. These results are consistent with the following conclusion: i) in the canine saphenous vein (SV), NIC is mainly mediated by calcium mobilization from its intracellular storage sites; ii) the calcium antagonists tested here and procaine are unable to totally inhibit, even at high concentrations, the contractions induced via intracellular calcium release; this characteristic is nonsignificant for nifedipine and verapamil at low concentrations (10(-6)M). iii) verapamil and nifedipine, like diltiazem and nicardipine at high concentrations, may not only possess the characteristics of extracellular calcium entry blockers, but also that of partial antagonist of NIC via non specific mechanisms; iv) diltiazem may relax the vascular smooth muscle of SV, not only by the above two properties, but also through another mechanism yet unknown; v) partial persistence of NIC on the SV under conditions of short or long extracellular calcium depletion may be due to a mechanism of intracellular Ca++ recycling, the smooth muscle cell partially retaining its intracellular Ca++.

Animals↗
PubMed1992

[Pharmacology of cellular ischemia].

Knowledge of cellular disturbances provoked by an ischemic aggression conditions the use of a pharmacologic strategy that could possibly protect the cell from necrosis. Whatever the type of cell, the basic mechanisms are very similar: energy failure, acidosis, loss of electrolytic homeostasis, particularly of calcium, formation of free radicals and, of more recent knowledge, genetic induction. Different molecules have been shown to be effective at each of these stages in one or other of the many experimental models available. The therapeutic approach is not very forthcoming at present but the field of applications is vast. Ischemic disease is not restricted to cerebral or cardiac ischemia and, although the lesions are mainly those of senescence, it is observed in other etiologic frameworks, if only in the perinatal period. Finally, the great increase in the use of organ transplants opens up another field of application with research on the best method for organ preservation and optimization of its acceptance by the host organism.

Animals↗
PubMed1991

Cardiac beta-adrenoceptor sensitivity and Parkinson's disease.

Certain clinical manifestations of Parkinson's disease (PD) (speech or/and balance disturbances) are not linked to brain dopamine deficiency. The purpose of the present study was to search for a possible relationship between those so-called "non-dopamine-dependent" extrapyramidal manifestations and the sensitivity of cardiac beta-adrenoceptors. Fourteen patients aged 51 to 69 were included in the study after having given their informed consent. Any factor or pathology susceptible to modify receptor sensitivity entailed exclusion. In the absence of a reference model for measuring the reactivity of central beta-adrenoceptors, a computation of the isoprenalin dose necessary to increase the resting heart rate by 20 bpm was used as an index for beta-adrenergic system reactivity. In addition to that test, other parameters were recorded: disease duration, motor status scale (Columbia), some cognitive functions (MMS and image differed recall). The cardiac beta-receptor decrease in reactivity to isoproterenol is correlated to PD duration (r = 0.8, P less than 0.001). Conversely, the sensitivity of these receptors appeared to be unrelated to the extrapyramidal severity of the disease, hence to the degree of the so-called "non dopamine-dependent" disturbances. Furthermore, such results raise the meaning of the impairment of peripheral aminergic receptors in the cognitive disturbances linked to ageing and/or PD.

Aged↗
PubMed1991

Comparison of three regimens of Parlodel-SRO in levodopa-treated parkinsonians: a randomized double-blind crossover study.

Parlodel-SRO is a newly developed slow-release formulation of bromocriptine, which prevents initial plasma peak--a known source of adverse events--and extends the half-life of the compound, an interesting feature for the management of motor symptoms in Parkinsonians. This study was designed to determine the best daily administration schedule for 30 mg Parlodel-SRO in 18 parkinsonians previously treated with levodopa and standard Bromocriptine (Br). The 30 mg dose was replaced from one day to the next, in a randomized, double-blind latin square design trial. Three consecutive 7-day courses were implemented, during which a total daily dose of 30 mg P-SRO was administered in one dose, two intakes (b.i.d.) and three intakes, (t.i.d.) respectively. The b.i.d. schedule produced the best improvement in UPDRS scores, especially as to postural stability, walking, bradykinesia; it also provided greater pharmacological stability throughout the assessment day. Adverse event analysis was not in favor of a single daily dose. It appeared that P-SRO administered in two 15 mg intakes (morning and evening) produces the best benefit-risk ratio in Parkinsonians who were already being treated with levodopa.

Adult↗
PubMed1990

[Development of memory-improving drugs].

Knowledge on the diverse processes involved in memory has been gained from multiple approaches, all necessary for the development of molecules aimed at enhancing memory. However, the neurobiological aspects of apprenticeship and memory remain to be fully elucidated. Long-term storage of information in the nervous system is under the control of glycoprotein synthesis. The chemistry of storage has been extensively studied in mollusks because of their simple neuroarchitecture. In mammals, the phenomenon of hippocampic long-term potentialization (HLTP), to a large extent linked to modification of glutamatergic transmissions, has been demonstrated. Stimulation of N-methyl-DL-aspartase (NMDA) receptors induces an influx of calcium, which is needed for HLTP maintenance, as are the activation of protein kinase C (PKC) and the synthesis of new proteins, for example calmodulin. At the molecular level, a cascade of biochemical events leads to modifications of neuronal connections, thus constituting the basis of memory. Memory-improving substances can be classified according to their theoretical mechanism of action: molecular pharmacology (agents inducing phenomena that mimic HLTP), neurotransmission (molecules acting on the cholinergic, noradrenergic, serotoninergic, GABAergic or dopaminergic systems), pathophysiology (substances antagonizing or correcting anomalies responsible for the memory deficiency, i.e., the cognitive enhancers). The development of memory-enhancing drugs has encountered many obstacles, notably the difficulty in evaluating the effectiveness of a medication in improving memory. It is imperative that guidelines be established for the clinical and experimental development of such substances as well as the standardization of tests in animals and man.

Animals↗
PubMed1989

[Experimental verification of the favorable activity of synthetic corticostimulin on brain edema induced by ischemia in rats].

The anti-oedematous effect of tetracosactide (Synacthene Immediate) was studied on a rat brain transient global ischaemia model. Brain oedema was evaluated by proton nuclear magnetic resonance, with measurement of T1 and T2 relaxation times in the cortex and white matter. The effective kinetic dose of tetracosactide was 0.4 mg/kg, and a comparison of the results obtained with those observed after treatment with dexamethasone 13 mg/kg confirmed that both drugs may be regarded as potent anti-oedematous agents, but there was nothing in this study to suggest that the mechanism of action of tetracosactide was different from that of corticosteroids.

Animals↗
PubMed1989

Clinical neuropharmacology of calcium antagonists.

Experimental and clinical data clearly demonstrate that calcium antagonists (CA) may have an action on the central nervous system (CNS). The cerebrovascular action of CA justifies their use in cerebral ischaemia, vasospasm and hypoxia. Several clinical trials have demonstrated such beneficial effects. On the other hand a number of reports indicate that CA may have a direct neuronal effect, although most of such trials have not been verified or are mere case reports. In addition, the large number of conditions susceptible to being corrected by CA is impressive: epilepsy, pain, dystonia, dyskinesia, psychiatric conditions, etc. Other papers are disconcerting that report extrapyramidal disorders induced by flunarizine and cinnarizine in the elderly, whereas nicardipine does not produce such side effects and may even alleviate some parkinsonian symptoms. In various experimental models (e.g. stroke, oedema), pharmacological effects have been shown to vary from one compound to the other. Two main questions are yet to be answered: 1) has the direct neuronal effect of CA been clearly established? 2) are the multiple clinical effects on the CNS really linked to calcium antagonism?

Aging↗