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B Housset

Publications and source records attributed to B Housset.

At least 91 records · Page 5Linked to original sources
PubMed1987

Effects of oxygen-derived free radicals on type II pneumocytes in primary culture.

After a brief review of oxygen-derived free radicals formation, cellular antioxidant equipment, and in vivo oxidant lung injury, the model of type II pneumocytes in primary culture is described with its characteristics and limitations. This model has been used to study either the in vivo or the in vitro effects of free radicals: the resistance of type II cells isolated from animals exposed to oxidants may be explained by their higher level of anti-oxidant enzymes. In contrast, type II cells isolated from control animals do not develop a resistance to the toxic effects on an in vitro exposure to free radicals. This discrepancy might be the result of a possible interaction of alveolar macrophages or fibroblasts with type II cells, which remains to be explored.

Adaptation, Physiological↗
PubMed1986

[Mechanisms of oxygen-induced lung injury].

Normobaric oxygen is responsible for pulmonary lesions which probably result from excessive production of free radicals derived from oxygen. The lung contains a number of enzymatic systems (superoxide dismutase, catalase, glutathione peroxidase) or non enzymatic systems (vitamins C and E, glutathione) capable of preventing lesions induced by these radicals. However the respective role of the various antioxidants in this tolerance to oxygen remains uncertain. The intra- or extracellular sites of overproduction of free radicals appear to involve different toxic mechanisms. Numerous aspects of pulmonary oxygen toxicity are still poorly understood, but studies in vitro show promises of forthcoming progress in this field of pathophysiology.

Animals↗
PubMed1985

[Physical signs reflecting mechanical changes in the respiratory system in chronic obstructive pneumopathy].

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.

Abdominal Muscles↗
PubMed1985

[Theoretical bases in the treatment of chronic obstructive bronchopneumopathies].

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.

Bronchi↗
PubMed1984

[Pulmonary toxicity of oxygen].

Prolonged breathing of normobaric oxygen can be responsible for pulmonary lesions which are frequently fatal. It is highly probable that this toxicity largely results from excessive production, by the alveolar cells, of free radicals derived from oxygen. The lung contains a number of enzymatic systems (superoxide dismutase, catalase, glutathione peroxidase) or non-enzymatic systems (vitamins C and E, glutathione) capable of preventing lesions induced by these radicals. However, the respective role of the various anti-oxidants in this tolerance to oxygen remains uncertain. Numerous aspects of pulmonary oxygen toxicity are still poorly understood, but in vivo and in vitro studies, now being vigorously pursued, show promises of forthcoming progress in the pathophysiology and treatment of pulmonary oxygen toxicity.

Animals↗
PubMed1984

[Spirometric modifications induced by bronchography. Effects of Salbutamol].

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.

Adult↗
PubMed1983

Effects of hyperoxia on biochemical indexes of pig aortic endothelial function.

To determine what biochemical indexes might be useful in measuring the endothelial response to hyperoxia in vitro we exposed endothelial cell monolayers (ECM) from pig aortas to either hyperoxic (95% O2:5% CO2, 1 atm) or control conditions (95% air:5% CO2) and made the following measurements: (a) DNA and protein contents remaining in the ECM; (b) lactate dehydrogenase (LDH) activity in the medium; (c) the net uptake of rubidium (Rb+), adenine, and adenosine; and (d) cellular ATP and medium lactate. Twelve hours of hyperoxic exposure did not cause significant changes. After 24 or 48 h of hyperoxia, DNA and protein contents were decreased; LDH activity and the protein-to-DNA ratio were increased; adenosine uptake was decreased per ECM but was unchanged when corrected for culture DNA and protein contents. Adenine uptake was unaltered as were cellular ATP content and medium lactate concentration. The net Rb+ uptake-to-DNA ratio was increased after 24 h but not after 48 h of hyperoxia. The extent of the DNA and LDH changes indicated that the cellular disturbance caused by hyperoxia was progressive from 12 to 48 h. Presence of superoxide dismutase (250 U/ml) prevented both the increase of LDH activity and the decrease of protein after 48 h but did not affect the decrease of DNA. These results suggest that the cells remaining in the ECM after hyperoxia have normal biochemical function and may represent a subpopulation of cells more resistant to oxygen toxicity than the damaged cells.

Adenine↗
PubMed1983

Oxygen toxicity in cultured aortic endothelium: selenium-induced partial protective effect.

The time course of biochemical changes related to cell loss and damage during exposure to 95% O2 [DNA and protein content of dishes, lactate dehydrogenase (LDH) release] was studied in postconfluent endothelial cells isolated from pig aorta, cultured in standard medium and in medium supplemented with 2 X 10(-7) M selenomethionine (Se-Met). A fourfold increase in glutathione peroxidase (G-Px) was the only major enzymatic Se-related effect under both normoxic and hyperoxic conditions, the other antioxidant enzymes being little or not at all affected by this treatment. The addition of Se-Met had a clearcut protective action against the cytotoxic effect of O2 as shown by measurements of DNA and protein content of Petri dishes and of LDH release. On the other hand, the most sensitive O2-related effect, namely the decrease in [3H]thymidine incorporation into DNA, was not affected by Se-Met addition. These experiments suggest that some of the O2-related toxic effects (but not the inhibition of DNA synthesis) could be mediated by lipid peroxides, since they were, at least partly, prevented by a Se-Met-induced increase in G-Px activity.

Animals↗
PubMed1983

[Pulmonary toxicity of free radicals of oxygen].

Free oxygen radicals result from aerobic cellular metabolism; their toxicity is prevented by immediate degradation due to an endless variety of biochemical systems. The nature of these radicals, their cellular production as well as the defence mechanism which oppose their toxic effects are successively and briefly analysed. The potential role of these radicals in the genesis of different lung diseases is still poorly understood. However, certain toxic agents (oxygen, gas pollutants, ionising radiation, toxic products) can act as a whole or at least in part by their intermediaries. The experimental arguments in favour of this hypothesis are reviewed in passing. If the relative importance of the toxic mechanism is still imprecise, free radicals are certainly implicated in pulmonary disease and constitute a new aspect of respiratory patho-physiology.

Animals↗
PubMed1983

[Respiratory physiotherapy and respiratory mechanics of chronic respiratory insufficiency].

The effect of short, medium and long term physiotherapy remain controversial. The theoretical objectives of the method are to reduce dyspnoea and respiratory disability while improving exercise performance and expectation of life. As regards respiratory mechanics, the goals are to reduce bronchial obstruction and the mechanical properties of the chest wall. A rise in expiratory flow might result in an increased drainage of secretions, a reduction in transmural bronchial pressure and a raised level of ventilation at end-tidal volume. The correction of parietal distortions by physiotherapy has as an objective a diminution of thoracic elastance. Muscular training, a new aspect of respiratory physiotherapy, consists of increased both the endurance and the force of contraction of the respiratory muscles. The beneficial effects of these recent methods require confirmation with long term clinical studies. The correct indications for the diverse techniques proposed require a better understanding of the mechanism of action of respiratory physiotherapy, an essential complement to effective treatment of chronic airflow obstruction.

Biomechanical Phenomena↗
PubMed1982

Effects of culture conditions and hyperoxia on antioxidant enzymes in pig pulmonary artery and aortic endothelium.

Because hyperoxia induces early injury to lung endothelial cells and since tolerance to hyperoxia is correlated with increased lung antioxidant enzyme activity, we measured superoxide dismutase, catalase and glutathione peroxidase in both fresh isolates and primary cultures of endothelial cells from pig pulmonary artery and aorta. Cultured endothelial cells were studied at confluency and up to 5 days thereafter under control or hyperoxic conditions. In both types of confluent cell, total and cyanide-insensitive superoxide dismutase increased when compared to fresh cells. The most conspicuous postconfluency change in both types of endothelial cell was a marked decrease in glutathione peroxidase, which could be prevented by the addition of selenomethionine to culture media. A 5-day exposure to hyperoxia resulted in a 2-fold increase in cyanide-insensitive superoxide dismutase in both aortic and pulmonary artery endothelial cells. In view of a similar decrease in DNA in both types of cells despite some differences in enzyme levels, oxygen cytotoxicity could not be related to a particular antioxidant enzyme profile.

Aerobiosis↗
PubMed1977

[The cyclines].

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Drug Resistance, Microbial↗
PubMedDate not supplied

Decreased phosphatidyl choline content in bronchoalveolar lavage fluids of children with bronchopulmonary dysplasia: a preliminary investigation.

Bronchoalveolar lavage (BAL) was performed on 12 infants who had recovered from neonatal acute respiratory failure and on 12 patients with bronchopulmonary dysplasia (BPD) in order to evaluate the concentration of phosphatidyl choline (PC) in BAL fluid. These two groups were similar at birth (mean birth weight: 1,980 and 1,750 g, respectively; mean gestational age: 33.4 and 32.1 weeks respectively). Mechanical ventilation based on oxygen requirement lasted longer in the group with BPD. BAL was performed at the end of the first year of life (at 8.5 and 10.3 months, respectively) and the results were compared to control values (from infants of the same age without neonatal disease). Whereas the protein concentration in BAL fluid was similar in the two groups, a dramatic decrease of the BAL PC was found in BPD: The mean values of BAL-PC over protein ratio were 0.9 in the group without pulmonary sequelae and 0.3 in the group with BPD. These preliminary results suggest an impairment of the pulmonary surfactant metabolism in this chronic lung disease following neonatal acute respiratory failure.

Bronchopulmonary Dysplasia↗