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Biomedical subjects

A Denjean

Publications and source records attributed to A Denjean.

49 records · Page 3Linked to original sources
PubMed1985

Effects of nifedipine on responses to exercise in normal subjects.

The responses to sublingual nifedipine (20 mg) and placebo were compared in normal subjects during two studies on cycle ergometer [progressive exercise and constant work-load exercise at approximately 60% of maximal O2 consumption (VO2max)]. The use of nifedipine did not modify maximal power, ventilation (VE), VO2, and heart rate (HR) at the end of the multistage progressive exercise (30-W increments every 3 min). Over the 45 min of the constant-load exercise and the ensuing 30-min recovery we observed with nifedipine compared with placebo 1) no differences in VO2, VE, respiratory exchange ratio, and systolic arterial blood pressure; 2) a higher HR (P less than 0.001) and lower diastolic arterial blood pressure (P less than 0.01); 3) a greater and more prolonged rise in norepinephrine (P less than 0.01) and growth hormone (P less than 0.001); 4) no significant differences in epinephrine and insulin and a lesser increase in glucagon during recovery (P less than 0.01); and 5) a lesser fall in blood glucose (P less than 0.01) and greater increase in acetoacetate (P less than 0.001), beta-hydroxybutyrate (P less than 0.05), and blood lactate (P less than 0.001). Our data do not support the hypothesis that nifedipine reduces hormonal secretions in vivo and are best explained by an enhanced secretion of catecholamines compensating for the primary vasodilator effect of nifedipine.

3-Hydroxybutyric Acid↗
PubMed1983

Acute effects of intratracheal administration of platelet-activating factor in baboons.

The bronchomotor effect of intratracheal administration of PAF-acether (60 micrograms X kg -1) was investigated in 37 curarized baboons mechanically ventilated with constant volume and frequency. PAF-acether caused an immediate bronchoconstriction as assessed by a marked increase in peak inspiratory pressure with no change in static pulmonary compliance and chest X-rays. There was a concomitant fall in arterial PO2 and a significant increase in ventilated unperfused lung zones. A decrease of circulating platelets and leucocytes was also observed. Local anesthesia with lidocaine and atropine did not prevent PAF-acether-induced bronchoconstriction although both markedly reduced the bronchial response to histamine. Albuterol significantly reduced the bronchial response to PAF-acether. Pretreatment with aspirin (80 mg X kg -1 iv) did not prevent the bronchoconstriction caused by PAF-acether, and intravenous or intratracheal arachidonic acid caused no bronchial response. Thus the role of cyclooxygenase metabolites of arachidonic acid in PAF-acether-induced bronchoconstriction is unlikely. In conclusion, an acute bronchoconstriction probably not triggered by stimulation of irritant receptors of the airways and associated with aggregation of platelet takes place subsequent to intratracheal administration of PAF-acether. These data suggest that PAF-acether might play a role in the pathogenesis of human asthma.

Anesthesia, Local↗
PubMed1981

Bronchoconstriction induced by intratracheal administration of platelet-activating factor (PAF-acether) in baboons.

Intratracheal administration of PAF-acether (60 microgram.kg-1) was performed in six premedicated, curarized and mechanically ventilated baboons. Whereas intratracheal administration of an equal amount of solvent (200 microliter of 80 degrees alcohol in 2 ml of saline) caused no measurable changes in lung mechanics, administration of PAF-acether caused an almost immediate bronchoconstriction that was spontaneously reversible within about 30 min. The concomitant fall in platelet count in peripheral blood and reduction of perfusion of ventilated lung territories estimated from the alveolar-arterial difference in CO2 tension provide circumstantial evidence that PAF-acether also caused aggregation of platelets in the lung microcirculation. In keeping with the release of PAF-acether by human alveolar macrophages, our findings suggest that this mediator may play a role in human asthma.

Airway Resistance↗
PubMed1981

Inhibition of exercise-induced asthma by a calcium antagonist, nifedipine.

Contraction of bronchial smooth muscle and release of mediators by mast cells are involved in asthmatic attacks and are calcium dependent. Therefore, we investigated the effects of a calcium antagonist, nifedipine, in asthma. Ten patients with asthma and documented exercise-induced bronchoconstriction exercised on 2 separate days after single-blind sublingual administration of 20 mg of placebo or nifedipine. The exercise-induced decreases in forced vital capacity, peak expiratory flow, and maximal expiratory flow after exhalation of 50 and 75% of the forced vital capacity were not modified on placebo but were prevented by nifedipine. Ten other asymptomatic patients with asthma and documented exercise-induced bronchoconstriction were studied at rest before and 45 min after nifedipine. The forced vital capacity, peak expiratory flow, and maximal expiratory flows were initially reduced and did not increase after nifedipine. Thus, nifedipine does not modify the basal bronchial tone of patients with asthma but does prevent exercise-induced asthma.

Adolescent↗
PubMed1977

[Etiological diagnosis of acute pneumopathies. Evaluative study. 100 cases in a pneumologic center].

This study involved 100 patients with acute pneumonia and hospitalised in a specialised service: 12 bacterial pneumonia, 40 viral pneumonia (i.e. 52% of the total). Only precise viral and bactérial studies could improve these results. Given the poor results obtained using the microbiological techniques available here, the authors suggest the inclusion in all subsequent studies of aetiological diagnosis of a quantitative examination of sputum bacterial flora and examination for the detection of bacterial exoantigens.

Acute Disease↗
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

[Routine bedside measurement of arterio-alveolar CO2 difference (author's transl)].

Deficiencies in pulmonary circulation can economically be demonstrated at the patient's bedside by measuring the difference in CO2 between arterial blood and alveolar air, which reflects the air flow in non-perfused ventilated lung areas. The method does not inform on the cause of the deficiency, but normal values (i.e. lower than 10 %) indicate that pulmonary circulation is unimpaired, whereas high values suggest that it is reduced (emboli, capillary obstruction by leukocytes). That the method is valid is shown by the parallelism observed between the percentage air flow in non-perfused ventilated areas and the angiographic and anatomical findings.

Acute Disease↗
PubMedDate not supplied

Lung transfer factor for CO at rest in normal children by a steady-state method.

Lung transfer for CO (TLCO) was measured at rest in 94 normal children (47 boys and 47 girls) whose ages ranged from 3.5 to 16 years. A steady-state method, using a technique of alveolar sampling based on the equality of the mean expiratory and alveolar respiratory quotients, was employed. Highly significant correlations, statistically different for boys and girls, were fond between TLCO and standing height. TLCO was also linearly correlated with the functional residual capacity--the only pulmonary volume measurable in very young children--but without any sex difference. A multiple linear regression relates TLCO to FRC and height. Variance analysis shows the preponderant influence of FRC.

Adolescent↗