Variations in serum vanadium levels during the treatment of mental depression.
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Biomedical subjects
Publications and source records attributed to B Fleury.
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Results of several surveys of variable complexity have provided confirmation that snoring is not only an overall sleep preventer but is mainly an unrecognized asphyxia. Comparison of groups of snorers and non-snorers, and evaluation of biologic and functional improvement following surgical treatment of snoring, have shown that this chronic nocturnal hypoxia is, with the snoring as such, the essential feature of a well individualized new disease for which the term chronic rhonchopathy is proposed. This affection is composed of different clinical aspects of several syndromes, notably the Pickwickian and sleep apnea syndromes. However, a latent form also exists in which snoring is the only symptom, as well as a decompensated form with multiple signs related to the underlying condition. Improvement follows suppression of the respiratory obstacle provoking snoring. The most frequent of these signs is drowsiness, particularly when driving, and is the one with the heaviest social consequences.
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In 11 spontaneously breathing patients with chronic obstructive pulmonary disease (COPD) in acute ventilatory failure, we measured the total inspiratory (WItot) and total resistive (WI + Eres) work rate of breathing, together with lung mechanics (dynamic pulmonary elastance and inspiratory and expiratory pulmonary flow resistance). All variables were markedly increased compared with those in normal subjects. No significant correlation was found between WItot and WI + Eres with lung mechanics data. However, when WItot and WI + Eres were expressed per liter of ventilation, a significant positive correlation was found with all lung mechanics data. These results indicate that although in patients acutely ill with COPD, work rate and work per liter of ventilation are increased, only the latter is related to the severity of pulmonary mechanical impairment, and it could be used as one of the criteria for extubation. In addition, our results indicate that at end-expiration the alveolar pressure was positive (range, 6 to 13 cm H2O) in all patients (intrinsic PEEP), a fact that must necessarily affect hemodynamics; furthermore, it imposes an extra burden on the inspiratory muscles.
During the course of chronic airflow obstruction the effect of the pathological process and compensatory mechanisms that take place in the lungs to limit these effects express themselves by easily indentifiable clinical signs. The limitations of expiratory flow is responsible for the prolongation of the duration of maximal expiration: Pursed lipped breathing is probably the method used by certain patients to limit airway collapse; the increase in the residual volume and functional residual capacity results in distortion of the thorax and a change in the configuration of the inspiratory muscles, reducing their capacity to generate pressures (Hoover's sign: respiratory pulse, hypertrophy of the accessory respiratory muscles, thoraco-abdominal asynchrony); the considerable increase in the inspiratory thoracic depression accounts for the inspiratory descent of the trachea and the sub-sternal "tug". Finally the ventilatory pattern is different, ventilation being rapid and superficial, probably in order to adapt to the constraints imposed by the pathological process.
The natural history and pathophysiology of chronic airflow obstruction (BPCO) remain poorly understood. Therapy cannot cure the disease but should be aimed at palliating its effects: to reduce dyspnoea, to improve the exercise performance, to minimise the complications, to stabilise the disease and improve the quality of life, to prevent by combatting those factors which favour the development of the disease e.g. pollutants, tobacco, infections etc. The pre-requisite of any therapeutic action should be to recognise those factors which contribute to the pathology and the compensatory phenomena with which the organ opposes them. According to whether the compensation is insufficient or inappropriate the therapy should be either increased or designed to combat it. The therapeutic perspective demands a better understanding of the relationship between the respiratory centre and effector muscles on the one hand and the relationship between ventilation and pulmonary perfusion on the other.
Clinicopathologic findings are reported of a woman with plane xanthomatosis, multiple myeloma (IgG kappa) and normolipemia. Plasma lipoproteins were bound to the monoclonal immunoglobulin. The complex was separated by ultracentrifugation, then the proteins were measured by radial immunodiffusion and laser immunonephelometry. Monoclonal IgG kappa interact with the low-density lipoproteins. The literature about the association between normolipemic or hyperlipemic xanthomatosis and myeloma was reviewed and the physiopathology of this association discussed. Several hypotheses are suggested but, at present, it is shown that lipoprotein-paraprotein complexing in some patients may be due to autoantibody activity of the myeloma protein against serum lipoprotein; immune complexes interfere with normal lipoprotein catabolism resulting in xanthomas and normolipemia or hyperlipemia.
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Following acute intoxication with alcohol, 8 patients developed 16 episodes of arrhythmia, including 15 supraventricular tachycardias and one torsade de pointe. Seven of the 8 patients were chronically abusing of alcoholic drinks. None of the patients had clinically obvious cardiac pathology nor echocardiographic evidence of myocardiopathy. In 7 of them, however, baseline electrocardiograms disclosed disorders of intra-atrial conduction. The role of the different factors which might determine the occurrence of arrhythmia (notably alcohol, the autonomic nervous system, associated metabolic abnormalities and absorption of medicines) is discussed.
Moderate alcohol consumption is associated with lower cardiovascular mortality. The effect of moderate alcohol intake during 5 weeks on lipoproteins, especially on the high density lipoprotein (HDL) cholesterol total (of which the levels are inversely predictive of coronary heart disease) and apoproteins A, A1 and B, was studied in 7 normal men. HDL cholesterol total appreciated by the heparin manganese precipitation method and phosphotungstate magnesium method increased (p less than 0.01) during alcohol consumption. The composition of HDL was modified by alcohol consumption: increase of the esterified/total cholesterol ratio (p less than 0.05) and phospholipids (p less than 0.05) without significant modification of triglycerides. Low density lipoprotein and very low density lipoprotein did not vary significantly. Apoprotein A1 increased during alcohol consumption (p less than 0.05) with a transitory increase of apoprotein A. There was no significant modification of apoprotein B.
The effects of aminophylline on diaphragmatic fatigue and recovery in the face of hypoxemia and hypercapnic acidosis were studied in anesthetized, spontaneously breathing, dogs. The phrenic nerves were stimulated supramaximally at 10, 20, 50, and 100 Hz during 2 s with electrodes placed around the fifth roots, and the resulting transdiaphragmatic pressure (Pdi) was measured with balloon catheters. The dogs were occluded before the stimulations at functional residual capacity. The latter was monitored by measuring the end-expiratory transpulmonary pressure, which remained constant throughout the experiment. Diaphragmatic fatigue was produced by resistive loaded breathing. At the end of the runs, which lasted 15 +/- 2 min, all the dogs were severely hypoxemic (30 +/- 5 mmHg), hypercapnic (65 +/- 4 mmHg), and acidotic (7.1 +/- 0.05). During the fatigue runs, phrenic stimulation resulted in a marked decrease in Pdi, which amounted at 20 Hz to 70 +/- 8% and 45 +/- 12% of the control values 5 min after the onset of the fatigue runs and at the end, respectively. After recovery (3 h), Pdi and arterial blood gas determinations returned to control values. Identical fatigue runs were repeated with aminophylline infusion (loading dose, 6 mg/kg in 10 min and maintenance dose, 1 mg/kg/h), leading to a plasmatic concentration of 16.4 +/- 2 mg/l. Aminophylline protected the diaphragm against fatigue, and despite the presence of hypoxemia and hypercapnic acidosis, the Pdi generated for a 20 Hz stimulation of the phrenic nerves at identical times of the preceding run amounting to 100 +/- 15% and 85 +/- 10% of control values, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
The pattern of gammaglutamyl transpeptidase levels was studied in the sera of 25 subjects with hyperthyroidism and 11 subjects with hypothyroidism, before and after treatment, and in 14 age- and sex-matched control subjects. Gammaglutamyl transpeptidase levels were significantly increased in hyperthyroidism (65 +/- 59 U/l) (p less than 0.01) and significantly decreased under treatment (40 +/- 27 U/l) (p less than 0.001). Before treatment, gammaglutamyl transpeptidase levels correlated with alkaline phosphatase levels and 5'-nucleotidase levels, the correlation persisting after treatment with 5'-nucleotidase. Alkaline phosphatase levels significantly increased under treatment (p less than 0.01). The percentages of gammaglutamyl transpeptidase variation correlated with thyroxine (r = 0.44, p less than 0.03), triiodothyronine (r = 0.47, p less than 0.02) and latent fixation capacity (r = 0.44, p less than 0.03) variations. Subjects with hypothyroidism had significantly decreased gammaglutamyl transpeptidase levels before treatment (18 +/- 9 U/l, p less than 0.01). Alkaline phosphatase levels were significantly decreased before treatment, and significantly increased after treatment. For all subjects with hyperthyroidism of hypothyroidism, the percentages of gammaglutamyl transpeptidase variations correlated with thyroxine (r = 0.48, p less than 0.003) and triiodothyronine (r = 0.39, p less than 0.016) variations. These results suggest that variations in gammaglutamyl transpeptidase levels in hyperthyroidism and hypothyroidism are, at least in part, in relation with variations in thyroid hormone levels.
Bronchography enables an appreciation of the morphology and dynamics of the bronchi inaccessible to the fibroscope. However, this examination may aggravate pulmonary function in patients with chronic airflow obstruction. We have studied the effects of bronchography on forced expiration in order to identify and quantify possible spirometric changes. Thus spirometric tests were done at different times during the examination (V.C., F.E.V., flow-volume curves): before and after anaesthetizing the upper airways with xylocaine, after the introduction of contrast to the bronchi and finally after a Salbutamol aerosol. Spirometric values were unaffected by anaesthesia of the upper airways. On the other hand, the introduction of contrast led to a clear and constant fall in maximum expiratory flow, associated with a fall in forced vital capacity. These changes could not be reversed either after inhalation of Salbutamol or sub-cutaneous Terbutaline. The mechanisms producing the spirometric changes which we report does not seem to involve either the adrenergic system or the irritant receptors. Bronchial obstruction produced by the contrast does not alone appear to explain the changes induced by bronchography. Other mechanisms, not yet identified, probably contribute to the decrease in maximum expiratory flow.
Peripheral lymphocyte subpopulations have been quantified by a direct and indirect, immunofluorescence technique, using monoclonal antibodies, in 22 patients with continued heavy drinking, hepatocellular dysfunction (spider angiomata, ascites, and factor V decrease) (group I), in 16 patients with a history of heavy drinking and abstinence maintained for at least 6 months and hepatocellular dysfunction (group II) and in 28 patients admitted for continued heavy drinking, without hepatocellular dysfunction (group III). Sixteen normal subjects were studied as controls. The total number of lymphocytes and T lymphocytes (OKT3+) were significantly reduced (p less than 0.001) in groups I and II. A significant decrease of B lymphocytes was observed in group II (p less than 0.02). The OKT8+ lymphocytes were significantly reduced in group I (p less than 0.01) and in group II (p less than 0.001); the decrease of the OKT4+ lymphocytes was significant in group II (p less than 0.01) only. The OKT4/OKT8 ratio was higher in group I (p less than 0.05) and group II (p less than 0.01) than in the control group. Normal values of total lymphocytes, B lymphocytes, T lymphocytes subsets and OKT4/OKT8 ratio were observed in group III. In group III, the lymphocyte subpopulations and OKT4/OKT8 ratio were similar in patients with or without abnormalities of liver function tests. In group I and II, no correlation was found between the lymphocyte subpopulations or the OKT4/OKT8 ratio and factor V or nutritional status assessed by anthropometrical and biological tests. T-cell imbalance in alcoholic liver disease does not seem to be related to alcohol consumption, factor V decrease or malnutrition.
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Ethanol metabolism was studied in ten male non-alcoholic subjects following the constant intravenous infusion of ethanol (1.2 g/kg) administered during three hours with and without cimetidine. Pharmacokinetic analysis was performed on the pseudolinear portion of the elimination curve. The mean peak ethanol concentrations were not significantly different with and without cimetidine. There was no acceleration of ethanol metabolism at high concentrations: the ethanol elimination rate was similar above and under 17 mM, with and without cimetidine. Cimetidine administration had no effect on pharmacokinetic parameters of ethanol (area under the curve, Km and Vm). The fact that the ethanol elimination rate is similar whatever be its concentration and the absence of modifications of the pharmacokinetic parameters by cimetidine are not in favor of an important role of the microsomal ethanol oxidizing system (MEOS) in the ethanol metabolism of nonalcoholic subjects. The data do not allow to examine the role of MEOS in ethanol metabolism after chronic alcohol consumption.