Search PubMed⌕ Search

Biomedical subjects

M Boucher

Publications and source records attributed to M Boucher.

At least 37 records · Page 2Linked to original sources

Phenotype of cultured fetal perivascular cells from human placenta studied by scanning electron microscopy.

The phenotype of perivascular placental cells has previously been studied using tissue sections from the fetal villi. The examination of these cells in culture by scanning electron microscopy gives us the opportunity to observe their three-dimensional phenotypes and associations outside their normal constraints. Human umbilical endothelial cells, which have a phenotype comparable to that observed in other studies, seem more flattened in culture than in their usual environment. Microvascular endothelial cells did not attain an epithelioid phenotype with close contacts between cells but formed a network of branched, elongated cells with phagocytotic activity. Some circular associations were observed when using a gelatinized matrix. Microvascular pericytes were large, flattened cells with an irregular border that pushed up nodular associations on a gelatin matrix. Chorioplacental myocytes adopted a network template comparable to that developed by microvascular endothelial cells. However, these elongated cells were thicker, without microvilli, and superficial filaments could be observed. In culture, confluent endothelial cells from the umbilical cord or microvascular pericytes associated as nodules reached a cell phenotype close to their in vivo counter-parts. This attainment of an in vivo phenotype remains questionable for chorioplacental myocytes. Microvascular endothelial cells, however, though there was sparse formation of circular associations, remained far from their in vivo phenotype.

Cell Differentiation↗

Cardiac vagal effects of rilmenidine in the dog: comparison with clonidine.

1. The cardiac vagal effects of rilmenidine (5 micrograms kg-1 min-1) and clonidine (0.5 micrograms kg-1 min-1) were studied in chloralose anaesthetized dogs. 2. Rilmenidine and clonidine progressively reduced the vagal stimulation-induced bradycardia. As indicated by the ED70, rilmenidine was about 23 times less potent than clonidine in this respect. Concomitantly, both drugs dose-relatedly decreased heart rate and mean blood pressure with potency ratios of rilmenidne to clonidine of about 1:23 and 1:12, respectively. 3. Importantly, the heart rate values observed under vagal stimulation during drug infusion never exceeded the values under basal vagal stimulation, and with both drugs large interindividual variations occurred under vagal stimulation. 4. These results show that the vagal bradycardia inhibition produced by rilmenidine and clonidine results from their true bradycardic effects and not from actual cardiac vagolytic properties.

Adrenergic alpha-Agonists↗

Cardiac electrophysiological effects of propafenone and its 5-hydroxylated metabolite in the conscious dog.

We studied the cardiac electrophysiological effects of propafenone and its 5-hydroxylated metabolite in conscious dogs. Sinus rate, corrected sinus recovery time and Wenckebach point were measured in 6 intact dogs. Atrial rate, ventricular rate and atrial effective refractory period were measured in 6 atrioventricular-blocked dogs. In both groups, we also determined blood pressure and plasma drug concentrations. Each dog received, with at least an 8-day interval, propafenone (hydrochloride) and 5-hydroxypropafenone (hydrochloride) in 4 successive intravenous injections, 30 min apart, at 0.5, 0.5, 1 and 2 mg kg(-1). Propafenone increased sinus rate and atrial rate more markedly than 5-hydroxypropafenone, and also transiently ventricular rate, whereas 5-hydroxypropafenone decreased it weakly. Propafenone shortened corrected sinus recovery time and increased Wenckebach point at the highest dose only, whereas 5-hydroxypropafenone did not modify corrected sinus recovery time and increased Wenckebach point less markedly than propafenone. Both drugs produced an identical atrial effective refractory period lengthening. Propafenone either increased mean blood pressure (in intact dogs) or decreased it (in atrioventricular-blocked dogs) at the highest dose only, whereas 5-hydroxypropafenone did not produce any effect on this parameter. Overall, these results show that propafenone and 5-hydroxypropafenone exhibit cardiac electrophysiological effects, reflecting (a) direct vagolytic action for both drugs associated with cardiodepressant effects for 5-hydroxypropafenone, and (b) marked atrial antiarrhythmic properties for 5-hydroxypropafenone probably involved in the therapeutic effect of propafenone.

Animals↗

Cardiac electrophysiological effects of falipamil in the conscious dog: comparison with alinidine.

We studied the cardiac electrophysiological effects of falipamil, a specific bradycardic agent, in conscious dogs, in comparison with those of alinidine. Sinus rate, corrected sinus recovery time, and Wenckebach point were measured in six intact dogs. Atrial rate, ventricular rate, and atrial effective refractory period were measured in six atrioventricular-blocked dogs. In both groups, blood pressure was also monitored. Each dog received, with at least a three-day interval, falipamil (hydrochloride) and alinidine (hydrobromide) in four successive intravenous injections, 30 min apart, at 0.5, 0.5, 1, and 2 mg kg-1. Falipamil increased sinus rate and atrial rate, but decreased ventricular rate, whereas alinidine decreased sinus rate and ventricular rate, but increased atrial rate. Falipamil shortened corrected sinus recovery time and increased Wenckebach point, whereas alinidine lengthened corrected sinus recovery time and decreased Wenckebach point. Falipamil and alinidine increased atrial effective refractory period. Neither falipamil nor alinidine modified mean blood pressure in either group. Overall, these results show that (a) falipamil exhibits effects on the electrical activity of the heart, reflecting the predominant direct vagolytic effect of this drug, (b) alinidine exhibits effects reflecting the marked antiarrhythmic potential of this agent, and (c) thus indicate that two drugs with almost identical specific bradycardic properties can produce quite different electrophysiological effects in the conscious dog.

Animals↗

Does the use of a tocolytic agent affect the success rate of external cephalic version?

OBJECTIVE: Our purpose was to study the effect of ritodrine tocolysis on the success rate of external cephalic version at > or = 36 weeks' gestation. STUDY DESIGN: This was a prospective, double-blinded, randomized study. All patients were > or = 36 weeks' gestation, confirmed by early ultrasonography. External cephalic version assessment included nonstress testing before and after external cephalic version and ultrasonographic evaluation of type of breech, estimated fetal weight, position of placenta and fetal spine, and amniotic fluid index. Patients were excluded if the breech was not mobile or if they had any contraindications to tocolysis or external cephalic version. After randomization 283 patients received either ritodrine (111 micrograms/min) or identical placebo by intravenous infusion for > or = 20 minutes. Up to three attempts at external cephalic version under ultrasonographic surveillance were performed. With an alpha error of 0.05 and a beta of 0.2, 264 patients were required to complete this study. RESULTS: There were no differences between study groups in maternal age, body mass index, gestational age, amniotic fluid index, position of fetal spine, and placental location. Statistical analysis controlled for parity because parity had a major influence on success rates. There was a higher success rate in the group receiving ritodrine tocolysis (52% vs 42%, p = 0.028). Ritodrine improved success rates in nulliparous patients (43% vs 25%, p = 0.026) but not in parous subjects (66% vs 58%, p = 0.385). CONCLUSION: Ritodrine tocolysis improves the success rate of external cephalic version performed at > or = 36 weeks in nulliparous patients.

Adult↗

From Morvan's fibrillary chorea to the "mal des ardents".

The authors present a case of Morvan's fibrillary chorea. We compare this observation with cases in the past such as the "mal des ardents", the plague of Athens, acrodynia and the epidemic of Pont St Esprit which were all characterized clinically by pain, burning sensations, hallucinations and insomnia. Since aetiological aspects remain uncertain, the similarity in clinical observations establishes a close relationship between the "mal des ardents" and the clinical features of our patient.

Chorea↗

Hysteresis in atrial refractoriness in the conscious dog: influence of stimulation parameters and control by the autonomic nervous system.

This work (a) provides evidence for hysteresis in the atrial effective refractory period (AERP) in the conscious dog; (b) studies the main stimulation parameters that may affect this phenomenon; and (c) evaluates the influence of the autonomic nervous system. AERP was measured by the extrastimulus method in the conscious dog with chronic atrioventricular block (n = 6) during the increasing and decreasing phases of an S1S2 fixed protocol. AERP was longer during the increasing phase than during the decreasing phase, thus demonstrating hysteresis, calculated as the difference between the two values. Hysteresis was greater with an S1S1 basic cycle length of 300 ms than with a basic cycle length of 400 ms, 9 +/- 0.9, and 7 +/- 0.9 ms, respectively. It was also greater with trains of six basic cycles before each extrastimulus S2 than with trains of 12 basic cycles, 9 +/- 0.9 and 7 +/- 1.0 ms, respectively. Suppression of vagal tone with atropine reduced hysteresis from 8 +/- 0.6 to 4 +/- 0.6 ms, whereas suppression of cardioaccelerator tone with propranolol increased it from 9 +/- 0.9 to 14 +/- 1.2 ms. These data were confirmed by the neostigmine-induced increase in hysteresis from 8 +/- 0.8 to 11 +/- 0.8 ms and the isoproterenol-induced decrease in hysteresis from 9 +/- 0.6 to 4 +/- 0.4 ms. Overall, these results provide evidence for a hysteresis effect in the AERP in the conscious dog that is stimulation frequency-dependent and modulated by the autonomic nervous system with permanent increase by vagal tone and decrease by cardioaccelerator tone.

Adrenergic beta-Antagonists↗

Interactions of the cardiac chronotropic effects of rilmenidine with the autonomic nervous system in conscious dogs: comparison with clonidine.

1. The cardiac chronotropic effects of rilmenidine (10-100 micrograms kg-1) and clonidine (1-10 micrograms kg-1) were studied in conscious dogs with chronic atrioventricular block. 2. Rilmenidine and clonidine initially (< 3 min) decreased atrial rate, although the effect was not related to dose. More lastingly, ventricular rate was decreased in a dose-related manner (ratio, 1:21). Rilmenidine lowered mean blood pressure only at 100 micrograms kg-1, while clonidine had the same effect at doses of 5 micrograms kg-1 upward (ratio, 1:15). 3. When administered after atropine and pindolol, rilmenidine (50 micrograms kg-1) produced a decrease in atrial rate, with an identical intensity but longer duration than under basal conditions. When clonidine (2.5 micrograms kg-1) was given after atropine, no chronotropic atrial effect was observed. However, when clonidine (2.5 micrograms kg-1) was given after pindolol, it produced a decrease in atrial rate that was more marked, both in intensity and duration, than under basal conditions. After phenoxybenzamine, rilmenidine decreased atrial rate with a more marked and lasting effect than observed under basal conditions. Clonidine produced a bradycardic atrial effect identical to the basal effect. After yohimbine, rilmenidine and clonidine decreased atrial rate with an intensity similar to that under basal conditions, although the time course was totally different. 4. When given after atropine, rilmenidine (50 micrograms kg-1) and clonidine (2.5 micrograms kg-1) decreased ventricular rate as under basal conditions, whereas after pindolol and phenoxybenzamine, both drugs decreased ventricular rate less markedly than under basal conditions, both in intensity and duration. After yohimbine, rilmenidine and clonidine produced no chronotropic ventricular effect. 5. These results show that (a) the initial atrial bradycardia caused by rilmenidine results from both a decrease in sympathetic tone and an increase in cholinergic activity; while the effect of clonidine is caused mainly by the enhancement of cholinergic activity. For both drugs, alpha 2-adrenoceptors are involved at least in the initiation of the effect; (b) the very short duration of atrial bradycardia may result from reflex buffering in response to ventricular bradycardia. This buffering is less effective when heart rate was high; and (c) the ventricular bradycardia caused by both drugs is mainly the result of a decrease in sympathetic tone in response to the stimulation of alpha 2-adrenoceptors. The results also suggest that negative chronotropic postsynaptic alpha 2-adrenoceptors could be involved in the ventricular bradycardia.

Adrenergic beta-Antagonists↗

[Paul F. Girard, neurologist and historian of medicine].

The authors pay tribute to their master, Pr Paul Girard, former President of the "French Society of Neurology", Head of the Neurology Department at the Antiquaille Hospital and later at the Lyons Neurological Hospital. He was the instigator of important research on cervical and lumbar discopathy, infantile encephalopathy and Gayet-Wernicke encephalopath;y now called Gayet-Wernicke-Girard disease. In psychiatry, his particular interests were cerebral diminance and the corpus callosum. He was also a great historian of medicine and published works on the history of Neurology and Psychiatry in Lyons and also on the "Mal des ardents" (burning or fiery disease).

France↗

Cardiac electrophysiologic effects of alinidine, a specific bradycardic agent, in the conscious dog: plasma concentration-response relations.

We studied the cardiac electrophysiologic effects of alinidine in conscious dogs. Sinus rate, corrected sinus recovery time (CSRT), and Wenckebach point (WP) were determined in 6 intact dogs. Atrial and ventricular rates, and atrial effective refractory period (AERP) were determined in 6 atrioventricular (AV)-blocked dogs. In both groups, we also measured blood pressure (BP) and plasma alinidine concentrations. Each dog received four intravenous (i.v.) injections of 0.5, 0.5, 1, and 2 mg/kg alinidine (hydrobromide) 30 min apart. At all doses, alinidine decreased sinus rate (< or = 43%) and ventricular rate (< or = 44%), but increased atrial rate (< or = 31%). It lengthened CSRT (< or = 71%) at the two highest doses and increased AERP (< or = 33%) and decreased WP (< or = 33%) at all doses. Alinidine did not modify mean BP at any dose in either group. Overall, these results indicate that alinidine exhibits electrophysiologic effects in conscious dogs that reflect antiarrhythmic potentials of this drug apart from its assumed antiischemic properties.

Animals↗

Chronotropic cardiac effects of NPY in conscious dogs: interactions with the autonomic nervous system and putative NPY receptors.

The chronotropic cardiac effects of neuropeptide Y (NPY) were studied in the conscious dog with chronic atrioventricular block. NPY (0.2-5 micrograms/kg i.v.) produced no effect on atrial cycle length (ACL), and increased ventricular cycle length (VCL) and mean arterial blood pressure (MBP). After atropine, NPY produced no effect on ACL and increased MBP. At 0.2 microgram/kg, it shortened VCL, whereas at 1 and 5 micrograms/kg, it lengthened this parameter. After pindolol, NPY produced no effect on ACL, shortened VCL and increased MBP. These results indicate that in the conscious dog, NPY (0.2-5 microgram/kg i.v.) does not exert any chronotropic effect on the sinoatrial node, most likely because of competition between opposite chronotropic effects and/or absence of specific NPY receptors in the sinoatrial node. They also suggest that the ventricular bradycardic effects produced by NPY result mainly from a reflex withdrawal of beta-adrenergic tone and that its ventricular tachycardic effects result from a direct action of NPY on specific receptors located in the His bundle.

Animals↗

Randomised comparison of amoxycillin and erythromycin in treatment of genital chlamydial infection in pregnancy.

Erythromycin, the standard treatment for chlamydial infection in pregnant women, commonly causes side-effects, which limits its efficacy. In a randomised, double-blind study, we compared amoxycillin with erythromycin in this setting. 210 pregnant women with Chlamydia trachomatis infection were randomly assigned 7 days' treatment with amoxycillin (500 mg three times daily) or erythromycin (500 mg four times daily). Control cultures were obtained 21 days after treatment, during late pregnancy, and from the infant within a week of birth. Treatment was judged a failure if any post-treatment culture was positive or if the patient had to stop therapy because of severe side-effects. 11 women (5.2%) were lost to follow-up. 1 (of 100) amoxycillin-treated women had to stop treatment because of severe side-effects compared with 12 (of 99) erythromycin-treated women (p = 0.002). 1 woman in the amoxycillin group had a positive culture at the third-trimester examination. No positive post-treatment culture was found in the erythromycin group. Severe gastrointestinal side-effects were more common in women who received erythromycin (31 vs 6%, p < 0.001). The overall failure rate was therefore 2% in the amoxycillin group and 12% in the erythromycin group (p = 0.005). These results suggest that amoxycillin is an acceptable alternative to erythromycin for C trachomatis infection in pregnant women.

Adult↗

Cardiac electrophysiological effects of rilmenidine, a novel antihypertensive agent, in the conscious dog: comparison with clonidine.

The cardiac electrophysiological effects of rilmenidine, a novel antihypertensive agent, and clonidine were studied in the conscious dog. Sinus rate, corrected sinus recovery time (CSRT) and Wenckebach point (WP) were measured in seven intact dogs. Atrial rate and atrial effective refractory period (AERP) were measured in six atrioventricular (AV)-blocked dogs with ventricular pacing. In both groups, blood pressure was also monitored. Each dog received with at least a three-day interval rilmenidine as dihydrogen phosphate and clonidine as hydrochloride in four successive intravenous injections, 30 min apart. In intact dogs, rilmenidine was administered at 50, 50, 100 and 200 micrograms/kg and clonidine at 2.5, 2.5, 5 and 10 micrograms/kg. In AV-blocked dogs, doses of rilmenidine were 25, 25, 50 and 100 micrograms/kg, those of clonidine 5, 5, 10 and 20 micrograms/kg. Rilmenidine and clonidine decreased sinus rate and atrial rate from the first dose. In this regard, rilmenidine was respectively 24 and 23 times less potent than clonidine. A lengthening of CSRT was observed at all doses with rilmenidine and at the last three doses with clonidine (ratio: 17) and a lowering of WP at all doses with rilmenidine and clonidine (ratio: 22). A shortening of AERP was also seen with rilmenidine and clonidine from the second dose (ratio: 6). All these effects may at least partly be explained by a cholinergic activation mechanism. In intact dogs both drugs produced a lowering of mean blood pressure (ratio: 17), whereas in AV-blocked dogs, in which ventricular rate was kept constant by pacing, pressure effects were more complex, being the resultant of hypotensive and hypertensive effects, the latter due to alpha vascular stimulation. Taken together, these results indicate that in the conscious dog, rilmenidine and clonidine exert qualitatively identical electrophysiological effects, but with different potency ratios.

Animals↗

Chronotropic cardiac effects of falipamil in conscious dogs: interactions with the autonomic nervous system and various ionic conductances.

The chronotropic cardiac effects of falipamil were studied in conscious dogs with chronic atrioventricular (AV) block. Falipamil (0.5-2 mg/kg) initially increased atrial rate dose dependently. After atropine and atropine-pindolol, falipamil (2 mg/kg) decreased atrial rate, but after pindolol, it did not modify atrial rate. After atropine-pindolol-phenoxybenzamine, atropine-pindolol-yohimbine, atropine-pindolol-verapamil, and atropine-pindolol-quinidine pretreatment, falipamil produced atrial bradycardia. Falipamil dose-relatedly decreased ventricular rate. Falipamil (2 mg/kg) decreased ventricular rate after atropine, pindolol, and atropine-pindolol more than under basal conditions. After the other four pretreatments, it also produced ventricular bradycardia. Falipamil did not affect mean blood pressure (MBP) at any dose. These results (a) show that the initial atrial cardio-acceleration produced by falipamil results from its direct vagolytic action; (b) show that absence of atrial bradycardia results from buffering by the vagolytic effect and/or a relatively low basal atrial rate; (c) suggest that the falipamil ventricular bradycardia is partly buffered by the vagolytic effect, norepinephrine (NE) release, and involvement of alpha 2-adrenoceptors; (d) exclude involvement of postsynaptic muscarinic, alpha- and beta-adrenoceptors, and of the slow calcium current in the mechanism(s) by which falipamil decreases cardiac automaticity; and (e) suggest possible involvement of a quinidine-sensitive current in this (these) mechanism(s).

Animals↗

[The causes of intracranial hemorrhagic complications induced by antivitamins K].

Cerebral haemorrhage is the main life-threatening complication of oral anticoagulant therapy. In order to identify a means of prevention, the authors undertook a retrospective study of 68 consecutive cases of anticoagulant-related intracerebral haemorrhage. The mortality was 38.5%. The respective frequency of intracerebral haemorrhage, subarachnoid haemorrhage, acute and chronic subdural haematomas was 63.2, 16.2, 10.3 and 10.3%, respectively. On admission, nearly half the patients (53%) had prothrombin ratios inferior to 25%. A predisposing factor was found in 58% of cases: hypertension (30.6%), head injury (14.5%), alcoholism or drug interaction (11.2%), and one case of intracerebral aneurysm. A history of a transient ischaemic attack or of a cerebrovascular accident was found in 10.2% of cases and 11.7% had a previous anticoagulant related extracranial haemorrhage. The initial indications for oral anticoagulation were ischaemic heart disease (32%), atrial fibrillation (20.5%), secondary prevention of venous thromboembolic disease (17.6%) and primary prevention of venous thrombosis (11.7%). The duration of treatment for isolated ischaemic heart disease was over 6 months in all cases: the average duration of treatment was 12.4 months in phlebitis and pulmonary embolism. A critical review of the indications of treatment in the light of recent recommendations showed that if inappropriate indications were rare, the sometimes unnecessary prolongation of treatment was more common. Nearly half of these cases were receiving anticoagulants when the potential benefits were questionable at the time of the haemorrhagic complication. Clinical and biological follow-up is necessary for patients on anticoagulants; minor bleeding complications may be the prelude to major haemorrhage. Biological follow-up is based on control of the international normalised ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Hydroxycoumarins↗