PubMed Health⌕ Search

Biomedical subjects

M Mathieu

Publications and source records attributed to M Mathieu.

351 records · Page 20Linked to original sources
PubMedDate not supplied

Bronchial response to hyperventilation of dry air at room temperature in normals and asthmatics.

The bronchial effects of three levels (25, 40 and 60 1 X min-1) of voluntary isocapnic hyperventilation of dry air at room temperature (20-22 degrees C) have been studied in 18 normal, non-atopic subjects and in 25 nonperennial asthmatics who were asymptomatic and whose airway obstruction at the time of the study was mild, with a peak expiratory flow rate of 6.1 +/- 1.5 (SD) 1 X s-1 vs a predicted 8.4 +/- 1.3 1 X s-1. The bronchial response was assessed by use of maximal expiratory flow-volume curves obtained before and 1, 5, 10 and 15 min after the 5 min hyperventilation challenge. In normal subjects, there was a minimal though significant (p less than 0.001; two-way analysis of variance) fall in maximal expiratory flows which did not increase with the level of hyperventilation and was not accompanied by a fall in forced vital capacity. The bronchial response of asthmatics differed from that in normal: the fall in maximal expiratory flows was significantly greater, associated with a significant fall in forced vital capacity and increased with the level of hyperventilation. Results in 10 asthmatics studied on two different study days were highly reproducible. Sensitivity and specificity are excellent (approximately equal to 1) for the 40 1 X min-1 hyperventilation challenge. Our results suggest that isocapnic voluntary hyperventilation of dry air at room temperature (20-22 degrees C) is a highly satisfactory screening test to detect bronchial hyperreactivity.

Adolescent↗
PubMedDate not supplied

[Glucocorticoid receptor anomalies in asthma].

Asthma is an inflammatory disease sensitive to glucocorticoids as has been demonstrated by several studies on the mechanisms of action of these drugs both in vitro and in vivo. The cellular and molecular targets of glucocorticoids have however not been identified. The best candidates are lymphocytes and the glucocorticoid receptors, although other cells and other transcription factors which interact with glucocorticoids may also be involved. Qualitative and quantitative abnormalities in glucocorticoid receptor binding to glucocorticoids and desoxyribonucleic acid have been described in the lymphocytes of patients with corticosteroid-resistant asthma. The chances of observing an abnormality in the mechanism of action of glucocorticoids would be greatest in these patients. Indeed, such deficits might also participate in the pathogenesis of corticosteroid-dependent asthma or in asthma in general. We recall here the mechanisms of action of glucocorticoids and their effect in asthma.

Asthma↗