[Early diagnosis of malignant bone tumours].
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Animals↗
Biomedical subjects
R Bordet
Publications and source records attributed to R Bordet.
Study of circadian melatonin secretion pattern at different stages of Parkinson's disease.
To explore changes in melatonin secretion patterns and biologic rhythms in Parkinson's disease patients with or without levodopa-related motor complications (LDRMCs), the authors investigated, in an observational study, circadian rhythms of central temperature, motor activity, plasma cortisol, and melatonin in three groups: de novo untreated patients (group I), patients treated with levodopa + dopamine agonist and without LDRMCs (group II), and patients treated with levodopa + dopamine agonist and with LDRMCs (group III). There were no differences among the three groups for the rhythm of temperature, motor activity, or plasma cortisol. There was a significant (p < 0.05) phase advance in plasma melatonin secretion in patients receiving a dopaminergic treatment compared with untreated patients. The daytime area under the curve (AUC) was increased significantly in group III, and the nighttime AUC-to-daytime AUC ratio of melatonin secretion decreased significantly in group III, suggesting that the nychthemeral pattern of melatonin secretion was changed in patients with LDRMCs. Comparison of the three groups suggests a slight but insignificant phase advance and amplitude decrease of circadian melatonin secretion related to both evolution and treatment of Parkinson's disease. Despite the lack of a global desynchronization in other circadian biologic rhythms, the circadian secretion pattern of melatonin is modified in patients with LDRMCs.
Aged↗
Susceptibility to provoked cerebral infarction is not increased in a rat model of pharmacologically-induced hypertension despite endothelial dysfunction.
An increase in susceptibility to provoked stroke has been described in a genetically-determined rat model of hypertension. We investigated whether the susceptibility to provoked cerebral ischaemia was also increased in a rat model of pharmacologically-induced hypertension with endothelial dysfunction. Chronic inhibition of nitric oxide synthase induced by N(omega)-nitro-L-arginine methyl ester (L-NAME) administration (50 or 75 mg.kg(-1) x day(-1)) in drinking water for 6 weeks caused a sustained hypertension, comparable in the two groups. Endothelium-dependent relaxation induced by acetylcholine or A23187 was significantly, and dose-dependently, impaired in rats receiving L-NAME, as proven by a decrease in maximal relaxation and increase of EC50, as compared to control. Endothelium-independent relaxation induced by sodium nitroprusside was not different in the three groups. Aortic media area was significantly, and dose-dependently, increased following chronic nitric oxide inhibition. Cerebral infarct volumes were not increased in L-NAME-treated groups independently of the level of endothelial dysfunction induced by chronic L-NAME administration. These data demonstrate that susceptibility to cerebral infarction was not increased in a non-genetically determined hypertension model in spite of the development of endothelial dysfunction and vascular structure alterations.
Animals↗
[Preventive neuroprotection: from experimental data to therapeutic strategies].
The concept of preventive neuroprotection is based on experimental concept of brain ischemic tolerance in which a cerebral resistance against ischemia consequences is induced prior to its occurrence. Pharmacological agents mimicking the biological mechanisms observed in brain ischemic tolerance might increase the resistance of patients with high stroke risk to the deleterious effects of brain ischemia. Activation of cytoprotective proteins or regulation of deleterious molecular pathways could constitute the main pharmacological targets to induce preventive neuroprotection. Several pharmacological agents such as statins or fibrates have been demonstrated experimentally to induce a preventive neuroprotection related to their pleïotropic anti-inflammatory and antioxidant properties. In future, the prevention treatment of stroke occurrence may be completed by preventive neuroprotective treatment. Moreover, some drugs could have potentially both preventive and neuroprotective properties, which are likely linked.
Animals↗
[Vascular effects of dihydropyridines].
Dihydropyridines are the most numerous available calcium antagonists. While belonging to the same group these drugs have physical, chemical, pharmacokinetic or pharmacodynamic properties which are sometimes specific and can explain differences in the targets and the vascular selectivity. These properties can be related to lipophilic or hydrophilic characteristics, existence or lack of 'use-dependence', possible liaison to membrane phospholipids, and differences in elimination half lives. Selectivity of dihydropyridines also depends on the nature of the target structure (amount of intra-cellular calcium storage and mechanism of its release, electrophysiological properties of these cells) and of its pathological state (atherosclerosis and/or hypertension). Some of these properties could explain the anti-atherogenic effects, myocardial impact, cerebral and renal vascular flow and action in some pathological situations (Raynaud's syndrome, chronic arteriopathy, migraine...). A better knowledge of these different properties could lead to a more accurate choice of the drugs and to a decrease in the incidence of their side effects.
Blood Vessels↗
[Progressive muscular dystrophies and drug risks].
Many therapeutic agents are necessary during the evolution of progressive muscular dystrophy to cure intercurrent diseases. Some of them may impair muscular structure and induce rhabdomyolysis, toxic or inflammatory myopathy. Other treatments may produce metabolic and functional alterations or impair cardiac and respiratory functions, yet endanged in progressive muscular dystrophy. They must be contra-indicated or used carefully during progressive muscular dystrophy.
Humans↗
[Methods of antiarrhythmic drug evaluation in man].
Antiarrhythmic drugs (AA) are useful in some critical situations but their use remains questionable. Evaluation of their efficacy and possible side effects required accurate knowledge of various methods. ECG gives relevant informations on the conduction intervals alterations caused by AA. Holter monitoring allows evaluation of the efficacy and/or proarrhythmic effects throughout 24-48 hour periods provided that spontaneous variability is taken into account. Ambulatory sequential loop ECG allows a longer monitoring of treatment in patients with symptomatic arrhythmias. Provocative electrophysiological testings give good evaluation of AA efficacy in some supraventricular or ventricular arrhythymias but predictivity of efficacy or proarrhythmic effects is sometimes problematical. Use of effort testing is limited to evaluation of antiarrhythmic effects of drugs in major dysrythmias and in some frequency-dependent dysrythmias, but this technique allows also detection of proarrhythmic incidence in those extremely altered autonomic nervous system tone. Other techniques of evaluation (Signal averaged ECG, automatic implantable cardiovecter defibrillator with holter monitoring, drug plasma concentration monitoring) are still under discussion.
Anti-Arrhythmia Agents↗
[Acute catatonia and neuroleptic malignant syndrome. A case of infantile psychosis].
Similar clinical and biological features in lethal catatonia (LC) and neuroleptic malignant syndrome (NMS) suggest a relationship between both affections and common physiopathologic mechanisms. Pharmacological effects of several drugs--dopaminergic agonists, benzodiazepines, carbamazepine--suggest an impairment of several systems of neurotransmitters. We report the case of a young woman with infantile psychosis who developed catatonic syndrome worsened by neuroleptic treatment, arising the problem of the chronology of both affections. The evolution with treatment may partially explain the physiopathology. A 18-year old woman with an history of infantile psychosis, experienced insomnia, anorexia, paradoxical agitation developed after affective traumatism (mother's hospitalization). Chlorazepate (150 mg) remained inefficient and hospitalization was necessary. The patient was dumb, prostate in bed. She presented negativism, rigidity of the four limbs, catalepsia and hyperpyrexia (38.5 degrees C). Hepatic transaminases were increased (SGOT: 71 UI/l; N < 30). After cumulated dose of levomepromazine (100 mg) profuse sudation, thermic and cardiovascular instability, alteration of consciousness, major rigidity of limbs appeared. (Blood) hepatic transaminases and muscular enzymes increased. Bacteriological samples, cerebrospinal fluid analysis, CT-scan and EEG were normal. Within 48 hours after rehydratation and bromocriptine (30 mg per day) alteration of consciousness and autonomic disorders decreased but hyperpyrexia (38 degrees C) persisted. Biological parameters were normalized 10 days later. Negativism and psychomotor inertia remained. Lorazepam (3 mg per day) failed to be clinically beneficial. On carbamazepine (600 mg per day) she started speaking and moving spontaneously. Catalepsia disappeared but rigidity and anorexia persisted. Electroconvulsivotherapy (ECT) was necessary. After 2 shocks she started standing up, walking, taking food and speaking fluently.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗