PubMed Health⌕ Search

Biomedical subjects

J M Senard

Publications and source records attributed to J M Senard.

121 records · Page 7Linked to original sources
PubMedDate not supplied

[Midodrine (Gutron) prescription practice at a University Hospital Center].

A historical study of the prescription of midodrine was carried out at the university hospital of Toulouse (France) between 1994 and 1998. The aim was to compare the observed prescriptions and the ideal prescriptions in accordance with the Summary of Product Characteristics (SPC). The analysis of 97 consecutive medical reports found discrepancies in prescription concerning the non-respect of contraindications and of potentially hazardous drug associations. Fifty-four (55.7 per cent) patients would have been excluded from prescription if the physicians had strictly respected the SPC. The inappropriate prescription of midodrine was associated with an increase in adverse drug reactions (ADRs). ADRs occurred in 34.0 per cent of cases overall and required drug discontinuation in 15.5 per cent.

Adrenergic alpha-1 Receptor Agonists↗
PubMedDate not supplied

[Biological factors of PTSD: neurotransmitters and neuromodulators].

Subjects with posttraumatic stress disorder exhibit abnormalities in many psychobiological systems. Studies of the effects of stress on learning and memory processes suggest that fear conditioning, behavioural sensitisation, and a failure of extinction may be important in the persistence and reexperiencing of traumatic memories and stress sensitivity. All these symptoms are supported by specific biological mechanisms including NMDA receptors, noradrenergic system, etc. Recent findings show that amino acid transmitters, glutamate and GABA, are intimately involved in the process of factual memory registration, and suggest that amine neurotransmitters, norepinephrine and serotonin, are involved in encoding emotional memory. In addition, research suggests that 5-HT neurones have directs effects on both adrenergic and HPA function. Such findings provide important information that should guide current pharmacological practice and the development of innovative biological therapeutics.

Adaptation, Psychological↗
PubMedDate not supplied

[Study of ventricular repolarization in an experimental model of arterial hypertension associated with obesity].

UNLABELLED: High fat diet (HFD) in dogs is associated with obesity and hypertension (HTN) but also with a significant and early decrease in heart rate variability (HRV). Decreased HRV has been shown to be a good predictor of sudden cardiac death due mainly to arrhythmic event. The aim of this work was to investigate the changes in ventricular repolarization through 24 hours EKG recordings in dogs with hypertension and rendered obese by 20 weeks of HFD. This was achieved through 24 hour EKG recording analysis of QT parameters. The aims of this work was i) feasibility of this method in dogs and ii) identification of potential arrhythmic risk factors that could explain overmortality during obesity. METHOD: Six dogs received a high fat diet (HFD) ad libitum during 20 weeks. A 24 hour EKG recording was realized just before and after 20 weeks of HFD. The following parameters studying QT interval were collected: QT interval lasting from the beginning of the Q wave to the apex (QTa) and to the end of the T wave (QTe), QT intervals plotted against RR intervals and two regression lines were calculated characterized by their slope and intersection with the Y axis, QT dispersion (longest minus shortest QT interval for each RR value) as well as the difference of QT interval between night and day at a fixed RR value considered as a marker of the sympathovagal balance. Our results show that HFD significantly increased body weight, blood pressure, heart rate, left ventricular mass and insulinemia. QT dispersion was increased in a non-significant manner both during day (+35%) and night (16%) for QTa and only during day for QTe (+27%). This increased dispersion of QT was not associated to any increase of QT interval. There was no effect of HFD on QT dynamicity parameter nor on the night-day difference at any RR interval from 300 to 1,300 ms. CONCLUSION: HFD tend increase QT dispersion without any effect on QT interval. These results are compatible with a heterogeneous repolarization probably related to abnormal autonomic nervous system tone. This study could partly explain occurrence of lethal arrhythmias during obesity which might lead to overmortality of obese patients. These results are different for QTa and QTe, but these two parameters are characterizing different type of ventricular cells. This study confirms the feasibility of this method in an experimental model, but results need to be validated in larger groups and in human.

Animals↗
PubMedDate not supplied

[Early atrial gene regulation of obesity-related arterial hypertension].

High fat diet (HFD) induces both arterial hypertension and tachycardia in dogs. Changes in heart rate occur early and are in part due to a decrease in the parasympathetic drive to the heart secondary to down-regulation of atrial muscarinic M2 receptors (Pelat et al. Hypertension 1999; 340: 1066-72). These data suggest that HFD is able to modify genic expression at atrial level. Thus, the aim of this work was to perform a systematic study of the genic expression profile in dogs made obese and hypertensive by 9 weeks of HFD. Blood pressure and heart rate were measured by telemetry implanted 15 days before starting regimen in 6 HFD and in 6 control dogs. HFD was the normal canine diet administered to controls but mixed with 300 g of beef fat. At the end of the experience, animals were sacrified and right atria were collected. Gene regulation was assessed in pooled tissue samples from both groups using suppressive substractive hybridization and microarray analysis. Genes with induction or repression rates of at least 20% when compared to controls were sequenced. As previously reported HFD induced a significant increase in body weight, blood pressure and heart rate when compared to controls. The results of SSH experiments led to the identification of 32 genes which are differentially regulated in atria from HFD dogs. Most are genes encoding proteins which have been previously shown to be regulated during various cardiopathies (MMP9, Na/K-ATPase 3...). These changes indicate the existence of early remodeling processes of atrial myocardium secondary to HFD. Other group of genes encodes proteins with no role identified in heart up today (lec-3, ERK-3, TRIP1, nucleophosmin...) or which function remains totally unknown. This work confirms that HFD is associated with early changes in gene expression in atrium. These changes are unlikely to be related to ventricular hypertrophy which is observed only during long-term HFD. Further studies are necessary to demonstrate the role of these modifications in the pathophysiological mechanisms leading to the increase in heart rate in this model of obesity-related arterial hypertension.

Animals↗
PubMedDate not supplied

[Extrapyramidal syndromes caused by flunarizine. Apropos of 6 cases].

The ability of flunarizine in inducing or worsening extrapyramidal symptoms is well documented. The relation with age or dose of such symptoms as their clinical characteristics remain controversial. We report 6 cases of extrapyramidal syndromes induced by flunarizine in five women and one man (mean age 71.5 +/- 5 years). The daily dose was 10 mg in five cases (as recommended by the marketing laboratory) and 20 mg in one patient. These observations allow to discuss the dose-dependent occurrence of this adverse reaction. In only three cases the reason for treatment was compatible with the official french indication. These side effects appeared after 7.0 +/- 1.6 months and disappeared after 2.2 +/- 0.5 months respectively. Flunarizine-induced extrapyramidal symptoms are mainly characterized by tremor (which was the main symptom in 4 cases and the only one in 2 cases).

Aged↗
PubMedDate not supplied

Verapamil interacts in vitro with alpha 2-adrenoceptors but does not modify alpha 2-receptivity in vivo.

The kind of interaction of two structurally different calcium channel blockers (verapamil and nicardipine) with both alpha 2-adrenergic agonist and antagonist binding on human platelets was investigated. Only verapamil, but not nicardipine, interacted in vitro with platelet alpha 2-adrenoceptors on [3H]-yohimbine or [3H]-UK 14,304 binding. Verapamil behaves as a weak antagonist competitor for alpha 2-adrenoceptors. In patients with mild essential arterial hypertension, the number of platelet alpha 2-adrenoceptors as well as velocity of aggregatory response to adrenaline, are significantly decreased: -21 and -25%, respectively (p less than 0.05). Verapamil (120 mg t.i.d. orally during 1 month) failed to modify the platelet alpha 2-adrenoceptor number or the adrenaline-induced platelet aggregation in hypertensive patients. These results show that, although interacting in vitro, verapamil does not modify the alpha 2-adrenergic receptivity after 1 month treatment in humans.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

[Physiological mechanisms of cardiovascular adaptation to orthostatism. Role of the sympathetic nervous system and pharmacological implications].

The main physiological adaptative systems occurring during orthostatism are discussed. The nervous mechanisms and especially baroreceptor pathways allow a rapid adaptation to the new hemodynamic conditions whereas hormones (mainly vasopressin) are involved later. The role of baroreflex and cardiocirculatory mechanisms is explained by the description of adaptative mechanisms in giraffe, an animal with its brain so far above the ground. The changes in adrenoceptor receptivity and the adaptative homeostatic mechanisms of the autonomic nervous system during orthostatism in human are discussed. Their characterization might allow to propose new pharmacological approaches for the treatment of orthostatic hypotension.

Animals↗
PubMedDate not supplied

[Movement disorders induced by drugs: experience at a pharmaco-vigilance center over five years].

The present retrospective study investigates the characteristics of drug-induced movement disorders notified to a Regional Drug Surveillance Centre. Among 4000 general side effects spontaneously reported to the Centre between 1989 and 1993, 122 were drug-induced movement disorders. Drug-induced parkinsonism (40 per cent) was mainly due to antidopaminergic agents (neuroleptics but also antiemetics or calcium channel blockers). Acute dyskinesia and dystonia (25 per cent) as well as tardive dyskinesia (14 per cent) involved mainly neuroleptics or antiemetics. Non-parkinsonian tremors (11 per cent) were related mostly to tricyclic antidepressants. Involvement of other less often suspected drugs (non-imipramine antidepressants, cardiac or hypolipidaemic drugs, etc) is discussed.

Adult↗
PubMedDate not supplied

[Pharmacologic approach to autonomic failure].

Four different forms of primary autonomic failure (multiple system atrophy, pure autonomic failure, Parkinson's disease and dopamine beta-hydroxylase deficiency) have been described. The first part of the article will focus on the interest to pharmacology of elucidating pathophysiological mechanisms underlying autonomic involvement at the central level (growth hormone response to clonidine acute challenge), presynaptic level (plasma catecholamine levels after yohimbine administration) and on post-synaptic receptors (binding studies, pressor responses to noradrenaline). The second part will discuss efficacy and side-effects of some of the many drugs which are currently proposed for the treatment of one of the most disabling symptoms related to autonomic failure, orthostatic hypotension. Special attention will be paid to drugs acting on blood composition (fludrocortisone, erythropoietin), on post-synaptic alpha-adrenoceptors (midodrine and clonidine) and on noradrenaline spill-over (yohimbine and L-Threo-DOPS).

Adrenergic Agonists↗