PubMed Health⌕ Search

Biomedical subjects

J M Senard

Publications and source records attributed to J M Senard.

At least 55 records · Page 3Linked to original sources
PubMed1997

Prevalence of orthostatic hypotension in Parkinson's disease.

OBJECTIVES: To investigate the prevalence of orthostatic hypotension and the nature of the postural events related to a fall in blood pressure in patients with Parkinson's disease. METHODS: Blood pressure was measured first in a supine position after a rest of at least 15 minutes and every minute during 10 minutes of an active standing up procedure. Orthostatic hypotension was considered as present when a fall of at least 20 mm Hg of systolic blood pressure was recorded. Postural events which occurred during the standing test were identified from a questionnaire and self reporting. Statistical analysis was performed to determine the relation between orthostatic hypotension and disease characteristics (duration, severity) and the use of antiparkinsonian drugs. Ninety one consecutive patients with Parkinson's disease (48 women, 43 men, mean age 66 (SD 9) years) participated to the study. RESULTS: A fall of at least 20 mm Hg of systolic blood pressure was found in 58.2% of the patients. Orthostatic hypotension was asymptomatic in 38.5% and associated with postural events in 19.8% of the patients. Symptomatic (but not asymptomatic) orthostatic hypotension was related to duration and severity of the disease and with the use of higher daily levodopa and bromocriptine doses. The analysis of the relation between the postural symptoms (and the need for standing test abortion) with the fall in systolic blood pressure allowed the identification of six clinical criteria specific of orthostatic hypotension. A direct relation between the postural changes in systolic blood pressure and the number of clinical events in this clinical scale was found. CONCLUSION: The frequency of orthostatic hypotension in Parkinson's disease is high and it is possible to establish a clinical rating scale which could be used to assess the effects of drugs employed in the management of orthostatic hypotension.

Aged↗
PubMed1997

[Left ventricular repercussion of obesity-induced arterial hypertension in the dog].

UNLABELLED: Obesity and hypertension are frequently associated. The aim of our study was to assess the effects of high fat diet on weight, blood pressure and left ventricule in dogs. We studied 6 male Beagle dogs before and after 7 weeks of hypercaloric hyperlipidic diet. Echocardiography was used to measure left ventricular wall thickness, volumes, ejection fraction and mass. Results are expressed as % of variation of initial values. After 20 weeks, dogs presented abdominal obesity with increased body weight (11.9 +/- 2.3 to 15.2 +/- 2 kg; p < 0.03) associated with an increasing of systolic (196.5 +/- 14.6 to 260.1 +/- 17.5 mmHg; p < 0.03), diastolic (76.6 +/- 9 to 110.6 +/- 10.2; p < 0.004) and mean blood pressure (128.8 +/- 7 to 152.7 +/- 7.6 mmHg; p < 0.004). There were non significant changes concerning diastolic thickness of septum and posterior wall. Left ventricular volumes increased in diastole (41.1 +/- 4.5 to 48.9 +/- 10.3 cm3; p < 0.03) and systole (12.2 +/- 1.7 to 14.9 +/- 3.2 cm3; p < 0.03). So, despite any changes in wall thickness, we observed an increased of ventricular mass (67 +/- 15 to 80 +/- 24.3 g; p < 0.03). Ejection fraction remained unchanged. CONCLUSION: it appears that hight fat diet induces obesity and hypertension in dogs; changes in left ventricule suggest a volodependent hypertension.

Animals↗
PubMed1997

[Autonomic nervous system abnormalities in the initial phase of insulin resistance syndrome. Value of the study of variability of cardiac rate and blood pressure on a model of nutritional obesity].

Changes in the activity of the sympathetic activity are often involved in the development of human insulin-resistance syndrome. However, the nature of changes in both the parasympathetic and orthosympathetic components are still controversial. We have recently developed an experimental model reproducing in dog this morbid triptyque (obesity, hypertension and hyperinsulinism), obtained by hypercaloric hyperlipidic diet. The aim of the present study was to characterize the changes in autonomic nervous system and spontaneous baroreflex in the initial period of obesity-hypertension syndrome. Ten male Beagle-Harrier dogs were used in this study. We investigated before and during 20 weeks after the beginning of the hypercaloric diet, plasma insulin, noradrenaline levels, spontaneous baroreflex efficiency (using the sequence method), arterial blood pressure, heart rate and their spectral analysis (fast Fourier Transformation) in both low (LF: 50-150 mHz, reflecting sympathetic activity) and high (HF: respiratory rate +/- 50 mHz, reflecting parasympathetic activity) frequency bands. Body weight (+20%), systolic (SBP: +23%) and diastolic (+16%) blood pressure and heart rate (+19%) increased during 6 weeks and then remained stable. Concomitantly, high frequency of HR (22.01 +/- 1.9 vs 14.15 +/- 1.04% at 7th week) and BF of systolic blood pressure (15.6 +/- 1.1 vs 19.2 +/- 1.2% at 4th week); p < 0.07, showed a rapid decrease in parasympathetic tone and a early increase in sympathetic activity. Nevertheless, in steady state of this syndrome, parasympathetic tone returned to initial values (18.43 +/- 3.25% at 20th week). Insulinemia significantly increased from the 4th week (14.2 +/- 0.9 vs 25.3 +/- 2.2 microUI/mL at 20th week), but noradrenaline remained not modify (400 +/- 85 vs 312 +/- 45 pg/mL at 20th week). Spontaneous baroreflex efficiency also decreased from the 2nd week (35.5 +/- 5.5 vs 16.7 +/- 4.9 mmHg/ms at 20th week). This study shows that an hyperlipidic hypercaloric diet induces a decrease in both parasympathetic tone and spontaneous baroreflex efficiency, which could be the physiopathological link between obesity, hypertension and hyperinsulinism.

Animals↗
PubMed1996

The discovery of vasomotor nerves.

The relative contribution of Claude Bernard and Charles Edouard Brown-Séquard to the discovery of vasomotor nerves is described and discussed. The controversy surrounding these two founding fathers of autonomic physiology and pharmacology is also summarized. In 1851, Bernard showed that section of the cervical sympathetic nerve unexpectedly elicited a marked and rapid increase in skin temperature. In 1852, Brown-Séquard extended these observations and established the relationship between blood vessels and the sympathetic nervous system. Thus, Brown-Séquard was the first to demonstrate the existence of sympathetic vasoconstrictor fibres. In contrast, Bernard discovered vasodilator nerves and is the founder of the modern concept of vasomotricity.

Anatomy↗
PubMed1996

Spectral analysis of blood pressure and heart rate, catecholamine and neuropeptide Y plasma levels in a new model of neurogenic orthostatic hypotension in dog.

The aim of the study was to compare changes in blood pressure (BP) and heart rate (HR) variability, catecholamine and neuropeptide Y (NPY) plasma levels induced by passive head-up tilt in normal and sino-aortic denervated (SAD) chloralose-anaesthetized dogs. In controls, 80 degrees head-up tilt test failed to change BP and increased HR. Plasma noradrenaline and NPY levels (but not adrenaline) significantly rose. In SAD dogs, head-up tilt test induced a marked and reproducible decrease in BP without any change in HR or noradrenaline and NPY plasma levels. In SAD dogs, spectral analysis in supine position was characterized by reduced variability in the high frequency (HF) band of the HR spectrum without changes in low frequency (LF) bands of both HR and systolic blood pressure (SBP). Head-up tilt test increased the LF component of SBP variability and decreased the HF component of HR variability in controls but failed to modify HR and BP variabilities in SAD dogs. In conclusion, sino-aortic denervation in dogs elicits a reproducible postural fall in BP with impaired adaptation of sympathetic nervous system activity. This model may be of value in evaluating the pharmacological effects of drugs for the management of orthostatic hypotension.

Adaptation, Physiological↗
PubMed1996

[Serotonin syndrome in acute poisoning with antidepressive agents].

We report a case of severe serotonin syndrome after self-poisoning with two antidepressant drugs, paroxetine (a selective inhibitor of serotonin reuptake) and moclobemide (a reversible inhibitor of MAO-A). The serotonin syndrome is characterized by neuromuscular, behavioural, and autonomic changes. It occurs with the use of drugs able to increase serotonergic transmission in brain by acting on biosynthesis, reuptake, catabolism or release of serotonin. Treatment is symptomatic. The incidence of severe cases seems to have increased, probably due to the use of new antidepressant "specific" inhibitors of the serotonin reuptake.

Adult↗
PubMed1996

Alniditan in the acute treatment of migraine attacks: a subcutaneous dose-finding study. Subcutaneous Alniditan Study Group.

Alniditan is a new 5HT1D receptor agonist, belonging to a different chemical class from sumatriptan and other indole derivatives used or being developed for the treatment of acute migraine. In a multinational double-blind randomized parallel-groups dose-finding trial, alniditan was given subcutaneously in hospital to patients with migraine headache of moderate or severe intensity at doses of 0.8 mg (n = 44), 1.0 mg (n = 42), 1.2 mg (n = 46) and 1.4 mg (n = 39). Efficacy, tolerability and safety of each dose were compared with those of placebo (n = 41). At 2 h after injection, headache was absent or mild in 83% and 82% of patients receiving alniditan 1.2 and 1.4 mg respectively compared with 39% for placebo (p < or = 0.002). Complete relief from headache was achieved in 72% (1.4 mg). Time to onset of relief decreased with increasing alniditan dose, and there was a dose-dependent reduction in headache recurrence rate: 25% of patients receiving 1.4 mg had responded by 15 min and headache recurred within 24 h in only 16% of the patients who initially responded to alniditan 1.4 mg, significantly less than for placebo (p = 0.018). Alniditan was superior to placebo in reducing the associated symptoms of nausea, phonophobia and photophobia, and in increasing patients' functional ability. The use of rescue medication was reduced when compared with placebo, and up to 87% of patients said that they would use the drug again if available. No clinically relevant cardiovascular effects were seen, nor consistent changes in clinical laboratory findings. Adverse effects, mainly head pressure, paraesthesia, and hot flushes, were reported by 34% of placebo-treated patients and up to 70% of patients receiving alniditan, but all doses were very well tolerated and no clear relationship with dose was established. Comparison with published findings suggests that alniditan 1.4 mg sc may have advantages over sumatriptan 6 mg sc in providing complete relief from acute migraine headache, and may be associated with fewer headache recurrences within 24 h. Both of these suggestions warrant further and larger trials of alniditan in acute migraine.

Adult↗
PubMed1996

Ropinirole in the treatment of levodopa-induced motor fluctuations in patients with Parkinson's disease.

Forty-six patients with Parkinson's disease experiencing motor fluctuations and not optimally controlled on levodopa received as adjunct therapy a new nonergoline dopamine agonist, ropinirole, in a 3-month randomized placebo-controlled trial. Ropinirole significantly reduced the duration of off periods as assessed by self-scoring diary cards. There were more nonserious dopaminergic adverse events in the ropinirole group. More patients withdrew because of adverse events or insufficient therapeutic effect in the placebo group. Ropinirole has beneficial adjuvant effects in parkinsonian patients with moderate motor disability and motor fluctuations.

Adult↗
PubMed1996

A study of dopaminergic sensitivity in Parkinson's disease: comparison in "de novo" and levodopa-treated patients.

The present study investigates dopaminergic sensitivity in Parkinson's disease (PD) through the measurement of neuroendocrine (growth hormone: GH, prolactin: PRL) and cardiovascular (blood pressure: BP, heart rate: HR) responses to low doses of apomorphine (5 micrograms/kg s.c.) in three groups of subjects: 13 normal volunteers (controls), 19 "de novo" never-treated PD patients, and 14 levodopa-treated PD patients. Apomorphine did not change BP and HR but significantly decreased PRL plasma levels in controls as well as in the two groups of PD patients. GH plasma levels significantly increased after apomorphine. There was no significant difference in the changes in neuroendocrine (GH, PRL) parameters in the two groups of PD patients in comparison with controls. However, "de novo" patients exhibited a significantly higher number of apomorphine-induced orthostatic symptoms (7 of 19) than did controls (0 of 13) or treated PD patients (2 of 14). These results show that hypothalamic dopaminergic sensitivity (studied through GH and PRL responses to apomorphine) is normal in PD. In contrast, because apomorphine-induced orthostatic hypotension is mainly due to the stimulation of peripheral dopaminergic receptors, our study suggests a peripheral dopaminergic hypersensitivity in some "de novo" never treated (but not in treated) PD patients.

Adult↗
PubMed1996

Which drug for which orthostatic hypotension?

This review focuses on the actual limits of the clinical pharmacology of drugs used for the treatment of orthostatic hypotension. The evidences for heterogeneity of the pathophysiological mechanisms of primary orthostatic hypotension and autonomic failure are discussed. The available data on the efficacy of some drugs used in orthostatic hypotension are also discussed.

Antihypertensive Agents↗
PubMed1996

Effects of pentobarbital and etomidate on plasma catecholamine levels and spectral analysis of blood pressure and heart rate in dogs.

The present paper investigates the effects of two anaesthetic drugs (pentobarbital and etomidate) on both short-term variabilities of systolic blood pressure (SBP) and heart rate (HR) using fast Fourier transformation and catecholamine plasma levels. HR and BP were continuously recorded through an arterial catheter and blood samples were taken from the jugular vein. Spectral analysis was performed first in the conscious state and six minutes after induction of anaesthesia on a series of 256 consecutive BP and HR values (delta t: 2 Hz). The area under the curve (AUC) was determined in the low-frequency component of the SBP (LF: 40-150 mHz), in the high-frequency band of HR (HF: respiratory frequency +/- 50 mHz) and in the total frequency spectra. Results were normalized by calculation of the ratio between AUC of LF and HF and the total AUC of the corresponding spectrum (TS). Etomidate (2 mg/kg i.v.) induced a significant increase in TS and LF without changing the LF/TS ratio or the HR variability when compared with the awake period. Catecholamine plasma levels did not change. In contrast, pentobarbital (30 mg/kg i.v.) decreased the values of LF, HF, LF/TS and HF/TS and catecholamine plasma levels. These results suggest that pentobarbital decreases the activity of the two components of the autonomic nervous system whereas etomidate induces only minimal changes.

Adjuvants, Anesthesia↗
PubMed1996

A study of tolerance to apomorphine.

1. The present study was designed to investigate tolerance to several pharmacological effects of apomorphine. 2. Changes in blood pressure, heart rate, plasma noradrenaline levels, rectal temperature, respiratory rate and retching plus vomiting were compared after administration of apomorphine (200 micrograms kg-1, i.v. as a bolus) or saline at different time intervals (30, 120 and 720 min) in four groups of chloralose-anaesthetized dogs. 3. The first administration of apomorphine induced a significant decrease in blood pressure and rectal temperature, a marked rise in heart rate with no change in noradrenaline plasma levels or respiratory rate. Emesis occurred in 71% of the animals. 4. A second administration of apomorphine 30 min later failed to modify blood pressure or heart rate. In contrast, the magnitude of apomorphine-induced changes in blood pressure and heart rate was similar to that observed after the first administration when apomorphine was given 120 or 720 min later. 5. The apomorphine-induced decrease in rectal temperature evoked by a second dose of apomorphine was less marked when given 30 and 120 min after the first dose and unchanged when given 720 min later. 6. The number of animals exhibiting retching and vomiting was lower when apomorphine was reinjected after 30 min than when the time between two successive injections of apomorphine was 120 or 720 min. 7. These results show that tolerance to apomorphine involves its cardiovascular, hypothermic and emetic effects. The time course of tolerance to repeated injections of apomorphine is longer for its hypothermic than for its hypotensive or emetic effects. This suggests a tissue-specific regulation of D2 dopamine receptors to repeated injections of apomorphine.

Animals↗
PubMed1996

New directions in the drug treatment of Parkinson's disease.

Parkinson's disease, a clinical syndrome with 4 cardinal features (bradykinesia, resting tremor, increased muscular rigidity and impaired postural balance), is mainly caused by the loss of dopaminergic neurons in the substantia nigra pars compacta. Although levodopa remains the 'gold standard' in the treatment of the disease, several emerging strategies are currently being developed. The first concerns new symptomatic drugs that either potentiate the effects of levodopa (e.g. slow-release preparations of levodopa, catechol-O-methyltransferase inhibitors and new dopamine agonists) or target clinical symptoms resistant to dopaminergic drugs (e.g. glutamate antagonists). The second strategy is to find drugs that are able to prevent or delay the neuronal death observed in Parkinson's disease. Several neuroprotective drugs are now in development in experimental research, but clinical trials in this area are still lacking. The development of these new drugs also depends on the validation of new clinical methodologies.

Antiparkinson Agents↗
PubMed1995

Abnormal vestibuloocular reflex cancellation in multiple system atrophy and progressive supranuclear palsy but not in Parkinson's disease.

We have measured the gain of the vestibuloocular reflex (VOR) in darkness and its cancellation by fixation in 37 patients with Parkinson's disease (PD), 26 patients with multiple system atrophy (MSA), 11 patients with progressive supranuclear palsy (PSP), and 19 normal volunteers. The capacity to cancel the VOR by fixation (VOR cancellation) was significantly reduced in the MSA and PSP patients compared with the PD and normal subjects (p < 10(-4)). A VOR cancellation < 90% (i.e., the mean VOR cancellation of the normals--2 SD) was present in four PD patients, 23 MSA patients, and 11 PSP patients. This criteria distinguished PD and MSA with a 89% sensitivity and a 89% specificity. Our results demonstrate that the VOR cancellation is impaired in most patients with MSA and PSP but not with PD. In MSA patients, the abnormal VOR cancellation is probably not related to the nigrostriatal dopaminergic deficit and more likely reflects a cerebellar dysfunction. Impaired VOR cancellation is a clinical criteria to differentiate MSA and PSP from PD.

Age Factors↗