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Biomedical subjects

J Savoy

Publications and source records attributed to J Savoy.

At least 19 recordsLinked to original sources
PubMed2000

[Madelung disease and obstructive sleep apnea syndrome: apropos of a case].

Madelung's disease, or benign symmetric lipomatosis, is an uncommon disease. It is an unencapsulated fatty infiltration which in rare cases extends into the perilaryngeal space and mediastinum. The authors present a case complicated by an obstructive syndrome and sleep apnoea syndrome, which was successfully treated by continuous positive airway pressure. The literature is reviewed.

Humans↗
PubMed1995

[A brief plea against the use of guidelines in medicine].

The use of guidelines in medical practice may be dangerous since it limits the art of medicine to the mere observance of rules. Some aspects of guidelines do not rely on scientific knowledge, but on a democratic approach (panel of specialist!). Finally, guideline users expose themselves to the pressure of communities, health care systems or possible legal action. These are risks which cannot justifiably be incurred.

Attitude of Health Personnel↗
PubMed1994

[Is non-allergenic bronchial hyperreactivity a good diagnostic test for asthma?].

The measurement of non-allergic bronchial hyperreactivity brings limited information in the diagnosis of asthma, whether for epidemiological purposes or for an individual patient. Its sensitivity and specificity in the general population amount to 46 and 89% respectively. It follows that the positive and negative predictive values are of little use when the prevalence of asthma lies between 1 and 10%. The situation is different, more complex, but not necessarily more favorable when one deals with one given patient. The characteristics of the test may vary as a function of the severity of the disease (concept of spectrum bias). Furthermore, the differential diagnosis will be made for other diseases that can also be associated with bronchial hyperreactivity. The negative and positive predictive values of this test will therefore be sufficiently informative only when the diagnosis is already certain.

Asthma↗
PubMed1992

[Spirometry in the physician's office].

Spirometry is a valuable tool for the estimation of lung function in the daily practice. Some basic criteria for its use, its interpretation, as well as for the selection of a good spirometer are shortly discussed.

Family Practice↗
PubMed1991

[The effects of smoke on airways].

Among the numerous effects of tobacco smoke on airway mucosa, the best known and the most frequent are those leading to chronic bronchitis (CB) or chronic obstructive pulmonary disease (COPD). Recent studies suggest that inflammation is central to these disorders. If predominant in larger airways (diameter greater than 4 mm), inflammation is associated with CB. When predominant in small airways (diameter less than 2 mm), it can induce COPD. The exact mechanisms remain unknown. There is no useful way in early detecting evolution toward COPD in asymptomatic smokers.

Asthma↗
PubMed1990

[Motility of the bronchi].

Airway diameter depends on bronchial smooth muscle tone which is regulated via complex nervous influences including afferent and efferent vagal fibers, sympathetic agonists and the so called 'third nervous system' (non adrenergic non cholinergic), as recently described. Additionally, various mediators of inflammation and epithelium derived factors contribute to the regulation of bronchi motility in health and disease.

Bronchi↗
PubMed1988

[Nonspecific bronchial reactivity].

Nonspecific bronchial reactivity is defined as the ability of bronchial smooth muscles to contract in response to non-allergenic (nonspecific) stimuli. Recent techniques for its measurement in different experimental and clinical situations have opened up new avenues in the understanding of asthma, airway infection, cough, and effects of pollution. The most recent data suggest that airway inflammation is the central mechanism of bronchial hyperreactivity, but the cells and mediators involved remain to be discovered. Bronchial reactivity as a test for clinical purposes needs standardization, careful establishment of normal values and assessment of validity in terms of the decision-making process.

Asthma↗
PubMed1988

Respiratory response to histamine- and methylcholine-induced bronchospasm in nonsmokers and asymptomatic smokers.

The respiratory response to bronchospasms of the same magnitude induced by inhalation of histamine or methylcholine was measured non-invasively, using bellow pneumographs, in nonsmokers and asymptomatic smokers. In each subject, tidal volume (VT), breathing frequency (f) and inspiratory time (TI) were obtained on two different days, in a randomized crossover fashion, with the following sequence: basal conditions, after inhalation of buffered saline as a control and after histamine or methylcholine inhalation. Basal and control conditions did not differ from each other and were the same for both groups. The respiratory responses to both bronchoconstrictors did not differ from each other and were also the same in both groups: VT increased, f and TI remained unchanged. Thus, VT/TI, an index of respiratory drive, also increased. In nonsmokers the increased VT/TI and the associated increase in minute ventilation were both correlated to the decrease in FEV1. These correlations were not found in smokers. Although they have different effects on airway irritant receptors, inhaled histamine and methylcholine induce the same respiratory response in nonsmokers and smokers. Thus, the presumed smoking-related changes in airway mucosa permeability do not seem to influence the direct stimulating effect of histamine on these endings. The absence of correlation between FEV1 and VT/TI changes in smokers suggest that smoking might affect the respiratory drive in acute drug-induced bronchospasm.

Administration, Inhalation↗
PubMed1984

Ventilatory response to bronchospasm induced by methylcholine and histamine in man.

In 9 normal subjects, we compared mouth occlusion pressure (P0.1) and breathing pattern in bronchospasm of the same magnitude induced by inhalation of acetyl-beta-methylcholine (M) and histamine phosphate (H). The measurements were performed on two different days, in a single blind randomized crossover design, under basal conditions first, then after control inhalation of isotonic buffered saline and finally after inhalation of M or H. For a same mean decrease in FEV1 (+/- SD) by 22.2% (+/- 7.2) after M and 22.3% (+/- 9.4) after H (P less than 0.001), the increases in P0.1 were similar (P less than 0.01 for both drugs) and were correlated to the magnitude of the bronchospasm (r = 0.775, P less than 0.01 for M; r = 0.692, P less than 0.05 for H). However, the minute ventilation and breathing pattern parameters did not differ from each other and from basal or control conditions. Thus, although we can assume that both drugs have different effects on vagal airway receptors, they induce the same respiratory response. We conclude that only receptors indirectly stimulated via airway smooth muscle contraction contribute to the mediation of drive and breathing pattern in drug induced bronchospasm in humans.

Adult↗
PubMed1982

Inhaled lidocaine aerosol changes resting human breathing pattern.

We compared resting breathing patterns in twelve normal humans before and after administration of aerosols of normal saline and 4% lidocaine. Experiments were performed in random order on two consecutive days in single blind fashion. At the time of the experiments, neither the subjects nor the people who analyzed the results knew the purpose of the study. Neither saline nor lidocaine aerosols produced changes in FEV1.0 or end-tidal PCO2, or, in the six subjects in whom measurements were made, changes in functional residual capacity or airway resistance. Aerosols of normal saline produced no change of ventilation (VI), breathing frequency (f), tidal volume (VT), duration of inspiration (Ti), mean inspiratory flow (VT/Ti) or the fraction of the breathing cycle devoted to inspiration (Ti/Tt). Lidocaine aerosols, on the other hand, were associated with a decrease in f (P less than 0.01), an increase in Ti (P less than 0.01), an increase in VT (P less than 0.02) and a decrease in VI (P less than 0.05), while VT/Ti and Ti/Tt were unchanged. We conclude that lidocaine aerosols, by compromising the function of vagal airway receptors, altered breathing pattern in normal resting humans, indicating that these receptors play a role in regulating breathing pattern under these circumstances. Though the changes we observed are most simply explained as being due to decreased stretch receptor activity, we cannot be certain that such was the case.

Adult↗
PubMed1982

Response to external inspiratory resistive loading and bronchospasm in anesthetized dogs.

Mouth occlusion pressure (P0.1) and breathing-pattern responses to external inspiratory resistive loading and methacholine chloride-induced bronchospasm were assessed in six dogs under pentobarbital sodium anesthesia. There was no change in P0.1 with external loading, but, in response to bronchospasm, we observed a P0.1 increase proportional to the change in lung resistance. These results indicate that, unlike external loading, the ventilatory-drive adaptation to bronchospasm does not require consciousness of the animal. The breathing-pattern response to bronchospasm consisted of tachypnea associated with decreased tidal volume (VT), decreased inspiratory duration (TI), and unchanged mean inspiratory flow (VT/TI). In response to resistive loading there was no tachypnea, VT decreased, TI was unchanged, and VT/TI decreased. We suggest that in response to resistive loading there was no modification of vagal activity, whereas in bronchospasm there was an increase of vagal activity, which was responsible for the changes in breathing pattern and, at least in part, for the changes in P0.1.

Anesthesia, General↗