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International audience; SETTING: Occupational asthma (OA) is most likely to develop in the very early years of exposure. OBJECTIVE: To describe the early incidence of OA among bakers/pastry-makers (BP) and hairdressers and to explore the role of atopy. DESIGN: Following a retrospective follow-up design, subjects were invited to undergo telephone interviews. Those who declared work-related respiratory or rhinitis symptoms and a sample group of others were offered a medical visit for OA investigations. Data from interviews and from medical visits were used to estimate the incidence of OA according to increasing durations of exposure. RESULTS: A total of 866 subjects were interviewed (mean age 25.3 years, 43.8% females), of whom 282 underwent a medical visit. Total estimated incidence rates of 'confirmed or probable' OA during the first 12 years of exposure were high in BP (2.63 per 100 person-years [py]) and in hairdressers (0.58/100 py), particularly in the first 4 years. Atopy is a strong risk factor for incidence among BP but, irrespective of the occupational sector, it does not influence the timing of OA symptoms. CONCLUSION: OA symptoms occur soon after the start of exposure. Our results suggest that atopy does not precipitate the occurrence of symptoms in two different allergen exposure settings.

Resume Introduction Une etude epidemiologique basee sur un questionnaire « sommeil/respiration » a ete realisee dans un echantillon de sujets de sexe masculin, en activite. Methodes Les 850 hommes, âges de 22 a 66 ans, ont repondu a un questionnaire de sommeil complete avec des informations sur leur mode de vie et leurs antecedents medicaux. Deux groupes ont ete compares : les « sedentaires » (sans aucun exercice) et les sujets faisant au moins cinq heures d’exercice de loisirs par semaine. Resultats Parmi les troubles respiratoires pendant le sommeil, seule la reponse a la question trop peu specifique « Vous a-t-on dit que vous avez ronfle ? » etait significativement plus frequente parmi les sedentaires. Par ailleurs, ces sujets declaraient plus souvent une hypertension arterielle sous traitement. Conclusions Cette enquete sur une population active ne met pas en evidence une difference significative de prevalence des symptomes de troubles respiratoires pendant le sommeil entre sujets sedentaires et les sujets pratiquant un exercice modere de loisirs. Le groupe sedentaire declare plus souvent hypertension arterielle sous traitement. Ce resultat peut s’expliquer par les limites d’une enquete par questionnaire et par le relativement faible contraste du niveau d’exercice de loisirs entre les temoins et les sedentaires.

Resumen Introduccion La disnea de esfuerzo (DE) es frecuente entre fumadores a pesar de una espirometria normal. Objetivos Determinar si el test de ejercicio y la observacion de posibles alteraciones del patron ventilatorio pueden reflejar una insuficiencia respiratoria precoz. Material y metodo Se ha comparado a 24 varones fumadores que presentaban DE con 31 varones fumadores sin DE. En ambos grupos se realizo espirometria, pletismografia, estudio del patron ventilatorio, gasometria arterial y test de ejercicio incremental (30 W/3 min), empezando por 40 W×10 min. La se evaluo mediante la escala de Borg. Resultados La espirometria era normal en ambos grupos. Los sujetos con DE presentaron un aumento de la frecuencia respiratoria (fB) y un volumen corriente (VT) significativamente reducido (p V ˙ O2pico y de la potencia maxima tolerada (Wmax) (p V ˙ A / V ˙ E ), la PaO2 y el pulso de O2 (p V ˙ E ), la relacion ventilacion (VE)/ventilacion maxima minuto (MVV), el espacio muerto (VD), la lactatemia (AL) y la frecuencia cardiaca (FC) fueron, para un mismo nivel de ejercicio, significativamente mayores (p Conclusiones Sujetos aparentemente sanos, cuya espirografia es normal, presentan DE, junto con una combinacion de efectos adversos durante el ejercicio (aumento de la demanda ventilatoria central, importantes alteraciones del patron ventilatorio, con hipoventilacion e importante reduccion de la maxima cantidad de ejercicio). Tales alteraciones frecuentemente no se exploran, pero se podrian corregir mediante un elaborado tratamiento fisioterapeutico y entrenamiento muscular.

Ventilatory and mouth occlusion pressure (P0.1) responses to progressive isocapnic-hypoxia and hyperoxic-hypercapnia were compared in eleven healthy sleeping men during the same night. Hypoxic and hypercapnic responses were determined during wakefulness, non-rapid and rapid-eye-movement sleep. The following parameters were measured: minute ventilation (VE), tidal volume (VT), 'duty cycle' (TI/TT), mean inspiratory flow rate (VT/TI) and P0.1, an index of the neuromuscular inspiratory drive. To allow a direct comparison between the two types of chemostimuli, responses were characterized by the value of the different parameters at 'equivalent' levels of hypoxia and hypercapnia, i.e., at levels which produced the same P0.1 during wakefulness: an oxyhaemoglobin saturation (Sao2) of 94% during the isocapnic-hypoxic tests (PETCO2 = 42.5 +/- 1.2 mmHg) was found to be equivalent to a PETCO2 of 47.4 +/- 3.7 mmHg during hypoxic-hypercapnic tests. For both tests, the arousal levels of the stimulus and of P0.1 were similar in all sleep stages. Sleep did not significantly modify P0.1 or breathing pattern responses to hypoxia (Sao2 = 94%). In contrast, at the 'equivalent' level of hypercapnic stimulation, P0.1 (P less than 0.05) and VE (P less than 0.01) responses were significantly impaired, particularly in REM sleep, with a decrease in VT (P less than 0.01) and VT/TI (P less than 0.05) responses. The results suggest that CO2 intracranial receptor mechanisms are more affected by sleep than the O2 peripheral receptor activity.

Resume Introduction Cette etude a evalue l’hypothese de la presence de troubles respiratoires du sommeil chez des sujets exposes a des faibles concentrations de CO sur leur lieu de travail. Methodes Deux cent trente sujets exposes a des concentrations moyennes de 1 a 5 ppm de CO a leur travail et 116 sujets temoins non exposes ont ete etudies avec un protocole comprenant un questionnaire de sommeil auto rempli et des mesures anthropometriques. Resultats Les deux groupes avaient des donnees anthropometriques et des habitudes de vie similaires, a l’exception d’un âge legerement plus bas pour les sujets exposes. Aucune difference n’a ete trouvee pour les antecedents medicaux, pour les troubles respiratoires pendant le sommeil ou les alterations du sommeil. Conclusions L’exposition professionnelle a des basses concentrations de CO ne semble pas affecter la motricite pharyngienne pendant le sommeil, Il faut souligner que ce resultat est obtenu avec une approche relativement peu sensible (questionnaire) ; un protocole comprenant des enregistrements polysomnographiques, applique a des sujets exposes a des concentrations CO plus elevees pourrait arriver a d’autres conclusions.

Resume Introduction Nous avons analyse la prevalence et les facteurs de risque du ronflement habituel dans un echantillon de sujets masculins de la population active de Lorraine. Methodes Les 850 sujets, âges de 22 et 66 ans, ont repondu a un questionnaire sur la frequence du ronflement, leur mode de vie, leurs antecedents personnels et familiaux. Des mesures anthropometriques ont ete completees par un examen non invasif de permeabilite de voies aeriennes superieures. Resultats La prevalence du ronflement habituel etait de 34,6 % ; augmentant avec l’âge, le poids et ses indices derives. Nous avons identifie (par regression logistique) les variables independamment associees au ronflement habituel : l’âge, le poids, l’obstruction nasale nocturne, le diagnostic d’apnees du sommeil par un medecin, et l’hypertrophie du voile du palais et de la luette. Le resultat original a ete la mise en evidence d’un effet « protecteur » d’une grande taille ; l’exercice de loisir n’apparait significatif qu’a l’analyse univariee. Conclusions Cette etude rapporte une prevalence du ronflement habituel similaire a d’autres etudes utilisant les memes methodes. Elle confirme le risque lie a l’âge, au poids, a l’obstruction nasale, et aux modifications nasopharyngees. Un effet protecteur d’une haute taille apparait comme element original, jamais signale par les enquetes precedentes.

SummaryThe aim of the study was to evaluate the prevalence, the covariates and determinants of respiratory pauses during sleep in a sample of French middle-aged males.Study subjects were 850 active males, aged 22–66 years; 88.4% of them answered the question on breathing pauses during sleep from a structured, validated sleep questionnaire.Forty-one (=5.4%) subjects reported breathing pauses at least once a week; these “positive responders” were older, heavier and had larger neck- and waist girths as compared to subjects with negative answers. Loud habitual snoring, various sleep disturbances, excessive daytime sleepiness, a doctor diagnosis of sleep apnoea, history of stroke and hypertension were significantly more frequent among subjects with breathing pauses during sleep.The prevalence found in this survey was close to that reported from the UK (5.2%). However, by logistic regression, we identified novel determinants of breathing pauses i.e. habitual snoring, loud snoring, and excessive sleepiness, factors well known in clinical setting, but never previously reported in epidemiologic studies.

Background: No data on snoring prevalence obtained with a standard questionnaire exist for France. Major nose-throat abnormalities have been demonstrated in cases with obstructive sleep apnea; evidence of ‘minor’ abnormalities in community studies is scarce. Objectives: The fist objective of our study was to estimate the prevalence of habitual snoring in a sample of middle-aged active males in France. The second objective was to test the hypothesis that ‘minor’ nose-throat abnormalities could be associated with habitual snoring in a field survey. Methods: Three hundred thirty-four male employees of a local university volunteered for the study (93.6% of those contacted by mail); 300 returned a sleep questionnaire. The protocol also included anthropometry and a noninvasive nose-throat examination. Results: Complete data were obtained in 299 subjects aged 23–63 years. When ‘habitual snorers’ (= 32%) were compared with never-snorers, significant differences were found for all anthropometric variables, except height. In univariate analysis, habitual snoring was associated with a large number of variables, including a large soft palate, a large uvula, and altered nose patency. A logistic regression model retained 8 factors independently associated with snoring: age, neck circumference, tobacco consumption, breathing pauses during sleep, not feeling rested during the day, need for coffee to stay awake, blocked or running nose at night and a large soft palate. Conclusions: The prevalence of habitual snoring in this sample of middle-aged French males was 32%. We confirmed the significant association of habitual snoring with age, weight excess, and tobacco smoking, and identified two further factors: blocked nose at night and a large soft palate.

Sleep-disordered breathing (SDB) and lower socio-professional status have in common a series of risk factors for ill health such as sedentary lifestyle, weight excess, heavy alcohol and tobacco consumption. We hypothesised that SDB will be more prevalent in lower socio-professional groups. A total of 496 male middle aged subjects (23–66 years) were tested with a protocol including a self-completed structured sleep questionnaire (translation of the Madison sleep cohort study form), anthropometry (including neck, waist and hip girth) and a simple, non-invasive nose–throat examination by a specialist physician. The subjects were classified according to the 10 major groups of the ISCO-88 classification (International Labour Office). Our sampling base did not contain subjects in the major groups 1 (senior officials, legislators), 6 (fishery and agricultural workers), and zero (armed forces), thus these groups were not represented in the analysis. To improve the power of the statistical analysis, groups 3 and 4, 5 and 7, 8 and 9 were merged, the analysis thus including four categories. The differences in demographic data were negligible; as expected, smoking was more prevalent in low socio-occupational groups (difference non-significant). A history of chronic bronchitis was more frequent in low socio-occupational groups, while a low physical job labour was more frequent in higher occupational groups. We did not find any differences in the prevalence of sleep-related respiratory disturbances (snoring, sleep apnoeas). This first study of the possible association between socio-occupational factors and sleep disordered breathing was negative, but we believe further studies, on larger samples, with a more homogeneous distribution of social groups are warranted.

Hypotension is known to affect the rate of carotid chemosensory activity in the adult cat, but the relationship between arterial blood pressure and carotid sinus nerve discharge has not been established in the kitten. The purpose of this study was to determine the response of carotid chemosensory afferents to hypotension induced in normoxia and in hyperoxia in eight kittens aged 1 to 25 days. Hypotension was obtained by a gradual decrease in blood volume. The activity of a few chemosensory fibres was recorded from one carotid sinus nerve. Baseline steady-state mean arterial blood pressure and carotid chemosensory activity were, respectively, 70.0 +/- 4.3 mmHg and 7.6 +/- 1.9 impulse/s (mean +/- SEM) in normoxia and 56.3 +/- 6.7 mmHg and 0.58 +/- 0.2 impulse/s in hyperoxia. Lowering arterial blood pressure below 37.5 +/- 3.5 mmHg in normoxia and 26.8 +/- 2.3 mmHg in hyperoxia was associated with a consistent increase in the rate of chemosensory discharge. Above this threshold, blood pressure variations had little effect on carotid chemoreceptor activity. These data are qualitatively similar to those of adult cats and provide evidence that, in newborn kittens, changes in arterial blood pressure will not influence carotid chemosensory discharge unless these changes are out of the physiological range.

In a previous study, it has been shown that bolus injections of dopamine could either stimulate or inhibit the carotid chemosensory discharge in the kitten (Marchal et al., 1992a). To further characterize dopaminergic mechanisms in the carotid body during development, the effects of a continuous infusion of dopamine on carotid chemosensory activity in air, hypoxia (8% O2 in N2) and hyperoxia (100% O2) were studied in ten anesthetized, paralyzed and artificially ventilated kittens, aged 1 to 21 days and in three adult cats. One carotid sinus nerve was prepared for recording the activity of a single or a few chemosensory afferents. In the kittens, the immediate effect of dopamine at the onset of infusion (10 micrograms/kg/min) was an inhibition of the discharge in five kittens, a progressive excitation in four and no change in one. Four minutes after the onset of dopamine infusion, there was a significant increase in chemosensory activity both in room air (from 4.5 +/- 0.8 impulse/sec to 8.8 +/- 1.4 impulse/sec, mean +/- SEM, P0.05) and in hypoxia (from 24.6 +/- 3.7 impulse/sec to 33.4 +/- 5.3 impulse/sec, P0.05) but not in hyperoxia (0.5 +/- 0.2 impulse/sec vs 0.7 +/- 0.3 impulse/sec). The adult cats received four successive dopamine infusions at the rate of 2.5, 5, 7.5 and 10 micrograms/kg/min, in an attempt to establish a dose-response relationship. The effects of dopamine infusions were consistent within, but variable between, cats. The onset of dopamine infusion was associated with an inhibition of the discharge in two cats, at all infusion rates. In one of them, chemosensory activity returned quickly to control and the response to hypoxia was enhanced. In the other cat, the inhibition of the discharge persisted for the duration of the infusion, and the response to hypoxia was inhibited. In the third cat, dopamine had no effect on the chemosensory discharge. The patterns of chemosensory responses evoked by dopamine are qualitatively similar in kittens and cats, but the excitatory type of response appear to be more readily elicited in the kitten.

BackgroundOccupational asthma is a common type of asthma caused by a specific agent in the workplace. The basic alteration of occupational asthma is airways inflammation. Although most patients with occupational asthma are mature adults, there is evidence that airways inflammation starts soon after inception of exposure, including during apprenticeship. Airways hyper responsiveness to methacholine is a valid surrogate marker of airways inflammation, which has proved useful in occupational epidemiology. But it is time-consuming, requires active subject's cooperation and is not readily feasible. Other non-invasive and potentially more useful tests include the forced oscillation technique, measurement of fraction exhaled nitric oxide, and eosinophils count in nasal lavage fluid.Methods and designThis study aims to investigate early development of airways inflammation and asthma-like symptoms in apprentice bakers, pastry-makers and hairdressers, three populations at risk of occupational asthma whose work-related exposures involve agents of different nature. The objectives are to (i) examine the performance of the non-invasive tests cited above in detecting early airways inflammation that might eventually develop into occupational asthma; and (ii) evaluate whether, and how, constitutional (e.g. atopy) and behavioural (e.g. smoking) risk factors for occupational asthma modulate the effects of allergenic and/or irritative substances involved in these occupations. This paper presents the study rationale and detailed protocol.DiscussionAmong 441 volunteers included at the first visit, 354 attended the fourth one. Drop outs were investigated and showed unrelated to the study outcome. Sample size and follow-up participation rates suggest that the data collected in this study will allow it to meet its objectives.

Two sets of seven pulse oximeters (Criticare CSI-502; Nellcor-N200; Datex-Satlite; Physio-Control-Lifestat 1600; Critikon-Oxyshuttle; Ohmeda-Biox 3700; Ohmeda-Biox 3740; Radiometer-Oxi; Spectramed-Pulsat; Kontron-7840; Biochem-Ox2000; Invivo-4500; Engstrom-EOS; Novametrix-505) were studied in two groups of eight healthy subjects, aged 26-50 yrs. The transcutaneous oxygen saturation (SpO2) was compared with arterial oxygen saturation (SaO2) measured in simultaneously with drawn blood samples (OSM2 Radiometer) at four 20 min steady-state levels of inspired oxygen fraction (FIO2) (0.21, 0.10, 0.08 and 0.07; SaO2 99-55%) in a conditioned chamber. Both the error in accuracy (mean SpO2-SaO2 difference), and the error in precision (SD of the differences) remained less than 3% for the two highest FIO2 levels (SaO2 greater than 83%) but, during deeper hypoxia, they were increased to 8% and 5%, respectively. An instrumental systematic bias affected accuracy in particular. We concluded that a good agreement between SpO2 and SaO2, as reflected by the Bartko's intraclass coefficient, was observed in nine instruments.

Pregnancy increases ventilatory and carotid body neural output (CBNO) responsiveness to hypoxia in cats (J. Appl. Physiol. 67: 797-803, 1989). To determine whether progesterone and estrogen stimulated hypoxic ventilatory and CBNO responsiveness, we studied 24 castrated male cats before and after 1 wk of placebo, estrogen, progesterone, or estrogen plus progesterone treatment. Estrogen plus progesterone treatment decreased end-tidal PCO2 (-3.8 +/- 0.8 Torr) and increased hypoxic ventilatory responsiveness, whereas estrogen or progesterone alone had no effect. Animals receiving progesterone alone or in combination with estrogen had higher CBNO responsiveness than placebo or estrogen-treated animals (shape parameter A = 45 +/- 7 vs. 27 +/- 4, P less than 0.05). However, the group treated with estrogen plus progesterone did not have greater CBNO responsiveness to hypoxia than the group receiving progesterone alone. The cross plot of the simultaneously measured CBNO and ventilation during progressive hypoxia revealed a greater slope in the estrogen-treated than in the placebo animals, suggesting that estrogen treatment increased central nervous system transduction of CBNO into ventilation. Thus the data taken together suggested that progesterone and estrogen had a combination of peripheral (carotid body) and central sites of action such that the administration of both hormones together had a more consistent stimulatory effect on hypoxic ventilatory responsiveness than either hormone alone.

The aim of the present study was to test the hypothesis that unmarried (single) men have more sleep-disordered breathing symptoms due to a higher prevalence of obesity and a less healthy lifestyle than men living with a partner. Men (499) aged 23–66 years completed a structured questionnaire, had standard anthropometric measurements and a simple, noninvasive nose-throat examination. Of the 499, 496 subjects answered the question concerning their marital status; 86% of them were married or lived with a partner (reference group) and the other 14% had never been married, divorced, or widowed (“single” group, considered at risk). Single subjects were younger, included slightly more smokers (30 vs. 23%) and more subjects with a history of chronic bronchitis, and less frequently had a large soft palate. The prevalence of sleep-disordered symptoms was not significantly different between the two groups. However, a study involving a larger number of subjects with information regarding alcoholic consumption may be needed to further evaluate this question.

Background: Most studies on habitual snoring have focused on its prevalence. However, from the clinical point of view, the intensity of snoring is of upmost importance, as it suggests the existence of sleep apnoeas. Objectives: The aim of the study was to assess the prevalence of loud snoring using a standard questionnaire and to evaluate the anthropometric and sleep characteristic differences between loud and light snorers in a sample of middle-aged males. Methods: The subjects were middle-aged active male employees. They completed a structured sleep questionnaire and had standard anthropometric measurements. Subjects reporting habitual snoring (≧3 nights/week) were further classified as loud or light snorers. Results: Of the 850 male subjects volunteering, 149 (17.5%) were habitual loud snorers. Loud snorers were older and had a greater waist-to-hip ratio as compared with light snorers. In univariate analysis, loud snoring was associated with gasping/snorting during sleep, breathing stops during sleep, waking up too early, excessive daytime sleepiness and falling asleep while watching TV. Logistic regression identified four independent associates of loud snoring: gasping during sleep, excessive daytime sleepiness, falling asleep watching TV and age. Conclusions: Loud snoring is present in a significant proportion of middle-aged men and is associated with central obesity and age. It disturbs sleep and elicits significant daytime sleepiness. Its association with breathing pauses (univariate) and its independent association with gasping during sleep suggests that loud snoring could be considered a clinical correlate of obstructive sleep apnoeas.

Study objectives: To assess the prevalence of occasional snoring in a group of middle-aged men, and to compare anthropometric variables and prevalence of sleep-related symptoms of subjects who occasionally snore with those of other snoring categories. Design: A field survey of a sample of middle-aged men in France. Participants: Male employees of a local university and subjects from the community attending a preventive medicine center. Participation rate was 93.5%. Measurements: Anthropometric variables were recorded in 499 subjects aged 23 to 66 years (mean, 44.3 years). The subjects completed a standard sleep questionnaire and were classified according to the snoring frequency as never, rarely, sometimes, occasional, several nights per week, and every night. The subjects who snore occasionally represented 8.6% of the total. Results: The anthropometric data of subjects who snore occasionally were similar to those of subjects who habitually snore. When compared with subjects who do not snore, older age and a larger neck girth were significant. Subjects who snore occasionally were also significantly more often subjects who snore loudly, and tended more frequently to have breathing stops during sleep. Conclusions: Our epidemiologic study shows that approximately 9% of a sample of middle-aged men snore occasionally. Subjects who snore occasionally have anthropometric characteristics close to those of subjects who snore habitually. The prevalence of the main sleep-related symptoms is between that of subjects who do not snore and of subjects who snore habitually. In an epidemiologic setting, inclusion of subjects who snore occasionally as subjects who do not snore or subjects who snore habitually will lead to bias. The present results suggest they should be identified and considered as a separate category. (CHEST 2002; 122:562–568)

Asthma has a tendency, to destabilize and get worse at night, probably due to a nocturnal increase in airiway inflammation and bronchial responsiveness. Nocturnal airway narrowing in asthma is often associated with sleep disorders, such as episodes of nocturnal and early morning awakening, difficulty in maintaining sleep, and day time sleepiness. On the other hand, an association has been documented between nocturnal sleep-disordered breathing and asthma. This review highlights the causes of nocturnal worsening of asthma and examines the evidence pointing toward a causal relationship between nocturnal asthma and sleep-disordered breathing.

Sleep-disordered breathing (SDB) and lower socio-professional status have in common a series of risk factors for ill health such as sedentary lifestyle, weight excess, heavy alcohol and tobacco consumption. We hypothesised that SDB will be more prevalent in lower socio-professional groups. A total of 496 male middle aged subjects (23-66 years) were tested with a protocol including a self-completed structured sleep questionnaire (translation of the Madison sleep cohort study form), anthropometry (including neck, waist and hip girth) and a simple, non-invasive nose-throat examination by a specialist physician. The subjects were classified according to the 10 major groups of the ISCO-88 classification (International Labour Office). Our sampling base did not contain subjects in the major groups 1 (senior officials, legislators), 6 (fishery and agricultural workers), and zero (armed forces), thus these groups were not represented in the analysis. To improve the power of the statistical analysis, groups 3 and 4, 5 and 7, 8 and 9 were merged, the analysis thus including four categories. The differences in demographic data were negligible; as expected, smoking was more prevalent in low socio-occupational groups (difference non-significant). A history of chronic bronchitis was more frequent in low socio-occupational groups, while a low physical job labour was more frequent in higher occupational groups. We did not find any differences in the prevalence of sleep-related respiratory disturbances (snoring, sleep apnoeas). This first study of the possible association between socio-occupational factors and sleep disordered breathing was negative, but we believe further studies, on larger samples, with a more homogeneous distribution of social groups are warranted.

In patients with obstructive sleep apnoea (OSA) anatomic and functional upper airway abnormalities are frequent and severe. Invasive methods are used to identify and quantitate the obstruction, to precisely locate its site, etc. as part of pre-treatment or of preoperative evaluations. These methods (lateral skull radiographs, computerized tomography, MRI, fibroscopies, etc) are too expensive and too invasive to be utilized in field surveys. To the classical sleep questionnaires and anthropometric measurements, some simple nose-throat examinations, easily accepted by the volunteers in a population study, could add useful information for the identification of the subjects at risk for sleep-disordered breathing. The present paper is a review of these examinations and of their utility.

But Rechercher les troubles du sommeil chez des patients ayant un diabete de type 2 (DT 2) connu. Patients et methodes Un groupe de 261 diabetiques (D) de type 2 (130 femmes et 131 hommes), âges de 57,7 ± 11,1 ans, avec un diabete ancien de 1 a 40 ans, a rempli 3 auto-questionnaires pour determiner un score de qualite du sommeil (Score de Pittsburgh), une echelle de somnolence diurne (Echelle d’Epworth) et 2 scores physique et mental de qualite de vie (SF36). Les D ont ete compares a 183 temoins (T) obeses non diabetiques, d’IMC comparable (D : 37,1 ± 7,1 vs T : 37,3 ± 5,6 kg. m −2 ; NS) mais legerement moins âges (50 ± 9,8 ans ; p vs T : 39,9 ± 4,6 cm ; p Resultats L’echelle d’Epworth est globalement similaire chez les T (D : 8,0 ± 4,6 vs T : 8,2 ± 4,8 ; NS) ainsi que le score de qualite de vie, legerement abaisse dans les 2 groupes (Score perturbe vs T : 6,8 ± 3,8 ; p 8,5 % sont plus de 80 % a declarer des perturbations nocturnes ( p p Conclusion Le diabete de type 2, surtout mal equilibre, s’accompagne de troubles respiratoires du sommeil sans somnolence diurne excessive. La qualite de vie en est affectee. Chez les D plus que chez les T, les perturbations du sommeil existent independamment des facteurs favorisants, evoquant un effet propre de l’hyperglycemie chronique sur la qualite du sommeil. Tout DT2 doit faire suspecter des troubles du sommeil et ceux-ci faire rechercher un DT2.

The accuracy and precision of transcutaneous pressure measurements of oxygen (Ptc,O2) and carbon dioxide (Ptc,CO2) in the monitoring of nocturnal assisted ventilation in adult patients were evaluated. Transcutaneous measurements obtained with two analysers, Radiometer TINATCM3 (R) and Kontron MicroGas-7650 (K), were compared with arterial blood gases analysed in blood samples withdrawn simultaneously in 10 patients. Sensors were heated to 43 degrees C. Measurements of transcutaneous blood gases and arterial blood gases were collected six times at 1-h intervals. The data obtained with both instruments were similar and did not significantly change over the 5 h test period. Measurement of Ptc,O2 underestimated arterial oxygen tension (Pa,O2) and this underestimation increased with the level of Pa,O2 (p

Catecholamines, dopamine and norepinephrine, are present in a significant amount in the carotid body of many animal species (Fidone et al, 1980; Fitzgerald et al, 1983). Dopamine is synthesized in glomus cells since the presence of the rate limiting enzyme in catecholamine synthesis, tyrosine-hydroxylase (TH), has been clearly demonstrated. Moreover, hypoxia is known to increase dopamine release (Fidone et al, 1982), norepinephrine content (Hanbauer et al, 1981; Verna et al, 1993), and activity of TH in carotid body, and to induce the expression of TH-mRNA (Czyzyk-Krzeska et al, 1992). However, the presence of epinephrine in the carotid chemoreceptors remains controversial probably because of the difficulty in detecting small amounts of this substance.

Summary We compared the effects of the laryngeal mask and tracheal tube on total respiratory resistance in 10 anaesthetised, mechanically ventilated patients undergoing otological microsurgery. The subjects were randomly divided into two groups. In the first group, the tracheal tube (Rusch) was inserted for the first series of measurements. This was then replaced by a laryngeal mask (Intavent) and a second series of measurements was made during the first hour of operation. In the second group, the same protocol was applied with inverse order in the use of the devices. From the measurement of respiratory flow and pressure at the airway opening, total respiratory resistance was calculated by multiple linear regression. The data were corrected to eliminate the previously determined nonlinear resistance of the two devices. Arterial blood pressure, electrocardiogram, oxygen saturation and end-tidal carbon dioxide concentration were continuously monitored. With the laryngeal mask and the tracheal tube, mean (SE) minute ventilation was 9.4(0.9)l.min-1 and 8.1 (0.9)l.min-l, respectively for end-tidal carbon dioxide concentrations between 3.6 and 4.1%. Although the glottic resistance was included in the measurement performed with the laryngeal mask but not with the tracheal tube, mean (SE) total respiratory resistance was not significantly different with the two devices (0.61(0.32) and 0.69(0.35) kPa.l-1.s, respectively). Leakage was avoided with the laryngeal mask because the insufflation pressure never exceeded 1.7 kPa except in one patient suffering from severe chronic obstructive pulmonary disease who had a total respiratory resistance of 1.45kPa.l-1.s. During the first hour of the operation all respiratory variables remained stable irrespective of the device used.

Doxapram is a respiratory stimulant which acts on peripheral chemoreceptors and central respiratory neurons in a dose-dependent fashion in the adult cat. In the newborn, the mechanisms of action of doxapram are still unclear. To evaluate the effects of doxapram on the carotid chemosensory discharge and its relationship with dopaminergic mechanisms in the carotid body, two groups of kittens less than 13 days old, anesthetized, artificially ventilated and paralyzed, were prepared for the recording of a single or a few chemosensory afferents of the carotid sinus nerve. The chemosensory activity was recorded under five conditions of inspired gas mixtures (21 and 8% O2 in N2, 100% O2, 5 and 10% CO2 in O2). Group 1 (n = 9) received only doxapram and group 2 (n = 8) was pretreated with haloperidol (1 mg/kg), a dopamine D2-receptor blocker, before receiving doxapram. Doxapram significantly stimulated the discharge rate of the carotid chemoafferents under all conditions of inspired gas. The chemosensory discharge was increased by haloperidol, and was raised further after doxapram by an amount similar to group 1. For instance, in normoxia, the activity increased from 2.9 +/- 0.4 to 7.5 +/- 0.9 impulse/s (mean +/- SEM, p < 0.01) in group 1 and from 3.8 +/- 0.6 to 9.1 +/- 1.0 impulse/s (p < 0.01) in group 2. These results indicate that the mechanisms of response of carotid chemoreceptor to doxapram are developed in the newborn kitten and doxapram acts independent of the dopaminergic mechanisms in the carotid body.

In adult cats, peripheral chemoreceptors respond to a step increase in PCO2 by a rise in activity to a maximum and then adapt to a lower steady level within one minute. It has been shown that the transient peak response is entirely dependent on the catalyzed CO2 hydration and disappears after carbonic anhydrase inhibition (Black et al., 1971). In newborn kittens, the dynamics of response of peripheral chemoreceptors are different from that observed in adult cats (Marchal et al., 1992). It is known that neither the chemosensory activity (Hanson, 1986) nor the carbonic anhydrase activity (Maren, 1967) is mature at birth. However, the dynamics of the hypercapnic response of the peripheral chemoreceptors in newborns remains unknown.

Doxapram stimulates ventilation by acting on peripheral chemoreceptors and medullary respiratory neurons in a dose-dependent fashion (Hirsh and Wang, 1974; Mitchell and Herbert, 1975). In adult cats, doxapram has been found to increase the chemosensory response to hypoxia and hypercapnia (Mitchell and Herbert, 1975; Nishino et al., 1982). Several studies have shown that bilateral section of the carotid sinus nerves abolishes or decreases the ventilatory effect of doxapram in adult animals (Hirsh and Wang, 1974; Mitchell and Herbert, 1975; Folgering et al., 1981; Nishino et al., 1982). Despite a frequent use of this drug in the treatment of neonatal apnea (Bairam and Vert, 1986; Barrington et a1.,1986; Tay-Uyboco et al., 1991), its action on carotid chemoreceptor activity is still unclear. We studied the effects of doxapram on carotid chemosensory responses to hypoxia and hypercapnia in newborn kittens. We found that doxapram stimulates the discharge rate of the carotid chemoreceptor afferents at all levels of FiCO2 and FiCO2 tested. In hypoxia, the effect of doxapram is more variable and this variability is not dependent on age.

The carotid body chemoreceptors are the main sensors for the level of arterial PO2 involved in the ventilatory control. It is well recognized that they also contribute to the ventilatory response to changes in PaCO2. Electrophysiological recordings of carotid chemoreceptor activity in adult animals show that they present a rapid response to sudden step rise of PCO2 in the arterial blood (Dutton et al., 1967; Fitzgerald et al., 1969; Black et al.,1971). It is still appreciable during hyperoxia and is enhanced by hypoxia (Fitzgerald and Parks, 1971;Lahiri et al., 1975, 1982). On the other hand, it has been established that an adaptation of the ventilatory response to CO2 occurs within seconds of a peak response (Dutton et al., 1967). Similarly, the carotid chemoreceptors appear to adapt (Black et al.,1971), at least in hypoxia or under specific stimulation (Lahiri et al. 1982, 1989). However, these results have only been observed in adult animals. In newborns, the weak chemosensory reactivity of carotid body is well documented (Blanco et al., 1984) but no information on the neonatal development either of the dynamic CO2- response of peripheral chemoreceptors or of the O2-CO2 interaction was available.

The respiratory effects of analgesia with nalbuphine were studied in 9 patients after thoracotomy. The pain score was measured by a visual analogue scale. Ventilatory pattern and occlusion pressure (P0.1) were studied during spontaneous breathing and during CO2 rebreathing, before and 0.5, 1, 2.5, 3.5 and 6 h after a 0.3-mg.kg-1 dose of intravenous nalbuphine. Compared to baseline values obtained before the injection, nalbuphine produced a decrease in the pain score (p0.001) during the 6-hour experiment period. In spontaneous breathing, P.01 was reduced by 15% in 1 h and remained decreased during 3.5 h (p0.05), whilst PaCO2 and ventilation (VE) remained unchanged. The P0.1 responsiveness to CO2 was decreased from 0.5 to 2.5 h after the nalbuphine injection (p0.05), but the VE responsiveness to CO2 was reduced only after 1 h (p0.01). This study shows that, while post-thoracotomy pain was reduced by analgesia, neuromuscular inspiratory drive and chemosensitivity to CO2 were weakened, without any change in spontaneous ventilation. A partial improvement in the thoracopulmonary mechanics induced by the reduction in chest pain could explain the maintenance of ventilatory level in spite of a decreased neuromuscular inspiratory drive.

Hypoxic ventilatory response (HVR) is known to be increased by female as well as male sex hormones, but whether there are differences in HVR between men and women remains unclear. To determine whether gender differences exist in HVR, we undertook systematic comparisons of resting ventilation and HVR in awake male and female cats. Furthermore to explore the potential contribution of sex hormones to gender differences observed, we compared neutered and intact cats of both sexes. Resting ventilation differed among the four groups, but differences disappeared with correction for body weight. Intact females had a lower end-tidal PCO2 than intact male cats (females: 31.6 +/- 0.4 Torr vs. males: 33.6 +/- 0.4 Torr, P less than 0.05), indicating an increased alveolar ventilation per unit CO2 production. HVR expressed as the shape parameter A was similar among the four groups of animals. However, baseline (hyperoxic; end-tidal PO2 greater than 200 Torr) minute ventilation [VI(PO2 greater than 200)] differed among the groups. Therefore we normalized HVR by dividing the shape parameter A by VI(PO2 greater than 200) to compare the relative hypoxic chemosensitivity among the various groups of animals. In addition, we further normalized HVR for body weight, because body size influences ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Six pulse oximeters with finger probes were studied in three groups of 17 hypoxemic patients with COPD aged 50 to 75 years. Transcutaneous arterial oxygen saturation (SpO 2 ) was measured with the Nellcor N101 (oximeter 1a), the Ohmeda Biox III (oximeter 1b), the Nellcor N200 (oximeter 2a), the Critikon Oxyshuttle (oximeter 2b), the Radiometer Oxi100 (oximeter 3a), and the Ohmeda Biox 3700 (oximeter 3b). The SpO 2 was compared with SaO 2 measured in simultaneously withdrawn samples of arterial blood (Radiometer OSM2) at three 20-minute steady-state levels of Flo 2 ranging from 0.21 to 0.40 (SaO 2 , 62 to 100 percent). The bias (mean SpO 2 -SaO 2 difference) and the error in precision (SD of the differences) were both below 4 percent for instruments 1a and 1b and remained below 1.2 and 3 percent, respectively, for the others. A good agreement between SpO 2 and SaO 2 , as reflected by the Bartko intraclass correlation coefficient, was observed in instruments 2a, 3a, and 3b. The individual relationships between SpO 2 -SaO 2 differences and SaO 2 appeared to be linear and parallel. With four instruments (1a, 1b, 2a, and 2b), the mean slope of this relationship was negative, showing a systematic instrumental error: the lower the SaO 2 , the larger the overestimation of SaO 2 . The scattering of the data (precision) principally reflects a subject source of error. In most instruments a technical adjustment could greatly improve instrumental errors and accuracy. The correction of the errors due to between-subject variation would require a system of calibration adjustable by the users to each individual.

Two sets of seven pulse oximeters (Criticare CSI-502; Nellcor-N200; Datex-Satlite; Physio-Control-Lifestat 1600; Critikon-Oxyshuttle; Ohmeda-Biox 3700; Ohmeda-Biox 3740; Radiometer-Oxi; Spectramed-Pulsat; Kontron-7840; Biochem-Ox2000; Invivo-4500; Engström-EOS; Novametrix-505) were studied in two groups of eight healthy subjects, aged 26-50 yrs. The transcutaneous oxygen saturation (SpO2) was compared with arterial oxygen saturation (SaO2) measured in simultaneously with drawn blood samples (OSM2 Radiometer) at four 20 min steady-state levels of inspired oxygen fraction (FIO2) (0.21, 0.10, 0.08 and 0.07; SaO2 99-55%) in a conditioned chamber. Both the error in accuracy (mean SpO2-SaO2 difference), and the error in precision (SD of the differences) remained less than 3% for the two highest FIO2 levels (SaO2 greater than 83%) but, during deeper hypoxia, they were increased to 8% and 5%, respectively. An instrumental systematic bias affected accuracy in particular. We concluded that a good agreement between SpO2 and SaO2, as reflected by the Bartko's intraclass coefficient, was observed in nine instruments.

L'insuffisance respiratoire aigue (IRA) hypercapnique survient essentiellement enpresence de lesions pleuro-parenchymateuses pulmonaires ou d'atteinte fonctionnelle de la mecanique ventilatoire. Cependant, l'IRA peut survenir en l'absence de telles anomalies. Le but de cette etude, est de verifier l'hypothese selon laquelle une decompensation respiratoire aigue non accompagnee de trouble mecanique ventilatoire est favorisee par un deficit des systemes de regulation de la ventilation. Nous avons etudie 31 patients au decours d'une IRA hypercapnique. Nous avons analyse chez eux la fonction mecanique pulmonaire et lachemosensibilite des centres respiratoi res mesuree par la methode de re-inspirationhypercapnique et hypoxique ainsi que la reponse a l'imposition d'une charge resistiveinspiratoire. Des troubles de la mecanique ventilatoire de type obstructif sont presents dans 55% des cas. Treize patients restants, sans syndrome obstructif ni restrictif, presentent tous une reponse au CO2 inferieures aux limites normales obtenues chez 20 sujets temoins. Cette defaillance se retrouve aussi chez 16 des 18 autres patients. Ces resultats confirment l'hypothese formulee : la deficience de la regulation respiratoire constituerait un facteur essentiel a la survenue d'une IRA grave non expliquee par des troubles de la mecanique ventilatoire. Dans tous les cas, un deficit du control e respir atoire resterait un facteur favorisant la decompensation respiratoire.

Mechanical properties of the lung were studied in nine healthy lowlanders during a 6-day sojourn at an altitude of 3,457 m. In comparison to sea-level values, it was found at altitude that 1) lung volumes measured by plethysmography including total lung capacity, vital capacity, and functional residual capacity (FRC) presented small changes not exceeding 300 ml; 2) static and dynamic lung compliances were not modified but static pressure-volume curves of lungs were shifted progressively to the left (the decrease in lung elastic recoil averaged about 2 cmH2O on days 4–6); and 3) maximal midexpiratory flow, forced expiratory volume in 1 s, and maximal expiratory and inspiratory flows were increased and, conversely, airways and pulmonary flow resistances were decreased on most days at altitude. The unchanged FRC in the face of a decreased lung recoil may be explained by an increase in thoracic blood volume at altitude, but other possible mechanisms are discussed. The decrease in resistances and increase in maximal flows may be partly explained by the decreased air density at altitude, but another contributing factor such as a bronchodilatation is also suggested. It is proposed that changes in lung mechanics at altitude may account for some of the changes in the pattern of breathing and mouth occlusion pressure (P0.1) observed during acclimatization of lowlanders to altitude.

The validity of a new method for measuring thoracic gas volume (Vtg) was studied in 18 bronchitic patients with mild to severe airway obstruction. The method entailed submitting the subject to very slow sinusoidal variations of ambient pressure (delta Pam) and studying the relationship between delta Pam and the resulting gas displacement at the mouth (delta Vaw): Vtgapc = PB.delta Vaw/delta Pam.cos phi, where PB is barometric minus alveolar water vapor pressure, and phi is the phase angle between Pam and Vaw. delta Pam of 40 cm H2O at 0.05 Hz were achieved by placing the subject in a 410-I body chamber connected to a large stroke volume reciprocating pump. Pam and Vaw were processed digitally by Fourier transform to obtain their amplitude ratio and phase angle at the frequency of interest. Vtg was also measured by body plethysmography (Vtgplet) during slow panting maneuvers (0.79 +/- 0.19 Hz) and also in order to detect any artifactual frequency dependence at a higher panting frequency (1.71 +/- 0.27 Hz); the agreement between the 2 estimates in all subjects (r = 0.975) suggested that Vtgplet could be taken as a valid reference. Functional residual capacities derived from Vtgapc and Vtgplet were not significantly different (5.113 +/- 1.198 versus 5.260 +/- 1.328 L) and were highly correlated (r = 0.915). Intermethod differences averaged 1.7 +/- 10.5% and were not significantly correlated to functional indices. We conclude that the new method provides accurate Vtg values in patients with chronic airway obstruction.

The effects of hypotension induced by trimetaphan on ventilatory control were assessed in sixteen normal subjects under halothane anaesthesia. The breathing pattern, mouth occlusion pressures, lung mechanics, acid-base balance, and arterial blood gases were analysed before and during trimetaphan infusion. During induced hypotension, the only significant change in the ventilatory variables was an increase in the ratio of inspiratory duration to total cycle duration from 0.39 +/- 0.05 (SD) to 0.42 +/- 0.03; P less than 0.01. The average minute ventilation remained unchanged. No modification in lung mechanics was observed, but all subjects developed a slight but significant hypocapnic alkalosis: PaCO2 was reduced from 5.5 +/- 0.4 to 5.2 +/- 0.4 kPa (P less than 0.001) and pH increased from 7.34 to 7.36 (P less than 0.05), without change in standard bicarbonate concentration. Our data indicate that the reduction in sympathetic nervous system activity induced by trimetaphan infusion in spontaneously breathing man causes only a minor alveolar hyperventilation. The weak respiratory response to hypotension suggests that changing peripheral afferent activity has little influence on the typically rapid breathing pattern induced by halothane.

We studied the correlation between density-dependence parameters (delta He, volume of isoflow) and age, body build, spirography and forced expiratory fows in 69 healthy non-smokers (16 females) aged 18 to 51 years. Density dependence variables showed no significant differences between young (less than 35 years) males and females. Volume of isoflow per cent of forced vital capacity (Viso V % FVC) was poorly significantly related to age (r = +0.25 P less than 0.05) and weight (r = +0.27 P less than 0.05). Significant correlations were found between density dependence at low lung volume and the FEV1/VC ratio (r = 0.31, P = 0.01 for delta He 25%; r = -0.40, P less than 0.001 for Viso V% FVC) or the forced expiratory flows with air (Viso V% FVC vs. FEF 25% r = -0.42, P less than 0.001). These correlations were closer in females as compared to males. Volume of isoflow was well related to delta He 25% (r = -0.64, P less than 0.001), but the relationship with delta He 50% was weaker (r = -0.38; P less than 0.01).

When the whole body is exposed to sinusoidal variations of ambient pressure (delta Pam) at very low frequencies (f), the resulting compression and expansion of alveolar gas is almost entirely achieved by gas flow through the airways (Vaw). As a consequence thoracic gas volume (TGV) may be computed from the imaginary part (Im) of the delta Pam/Vaw relationship: TGV = PB/[2 pi f X Im(delta Pam/Vaw)], where PB is barometric minus alveolar water vapor pressure. The method was tested in 35 normal subjects and compared with body plethysmography. The subjects sat in a chamber connected to a large-stroke-volume reciprocating pump that brought about pressure swings of 40 cmH2O at 0.05 Hz. delta Pam and Vaw were digitally processed by fast Fourier transform to extract the low-frequency component from the much larger respiratory flow. Total lung capacities (TLC) obtained by ambient pressure changes and by plethylsmography were highly correlated (r = 0.959, p less than 0.001) and not significantly different (6.96 +/- 1.38 l vs. 6.99 +/- 1.38). TLC obtained by ambient pressure changes were not influenced by lowering the frequency to 0.03 Hz, adding an external resistance at the mouth, or increasing abdominal gas volume. We conclude that the method is practical and in agreement with body plethysmography in normal subjects.

Pregnancy increases ventilation and ventilatory sensitivity to hypoxia and hypercapnia. To determine the role of the carotid body in the increased hypoxic ventilatory response, we measured ventilation and carotid body neural output (CBNO) during progressive isocapnic hypoxia in 15 anesthetized near-term pregnant cats and 15 nonpregnant females. The pregnant compared with nonpregnant cats had greater room-air ventilation [1.48 +/- 0.24 vs. 0.45 +/- 0.05 (SE) l/min BTPS, P less than 0.01], O2 consumption (29 +/- 2 vs. 19 +/- 1 ml/min STPD, P less than 0.01), and lower end-tidal PCO2 (30 +/- 1 vs. 35 +/- 1 Torr, P less than 0.01). Lower end-tidal CO2 tensions were also observed in seven awake pregnant compared with seven awake nonpregnant cats (28 +/- 1 vs. 31 +/- 1 Torr, P less than 0.05). The ventilatory response to hypoxia as measured by the shape of parameter A was twofold greater (38 +/- 5 vs. 17 +/- 3, P less than 0.01) in the anesthetized pregnant compared with nonpregnant cats, and the CBNO response to hypoxia was also increased twofold (58 +/- 11 vs. 29 +/- 5, P less than 0.05). The increased CBNO response to hypoxia in the pregnant compared with the nonpregnant cats persisted after cutting the carotid sinus nerve while recording from the distal end, indicating that the increased hypoxic sensitivity was not due to descending central neural influences. We concluded that greater carotid body sensitivity to hypoxia contributed to the increased hypoxic ventilatory responsiveness observed in pregnant cats.

"Sensitive" and "conventional" lung function tests were compared in a group of 114 males, aged 35-55 years, including healthy non-smokers, asymptomatic smokers with normal spirometry, and smokers with chronic bronchitis with or without mild airflow limitation. In non-smokers, with the exception of a MEF vs. FEV1 correlation, "sensitive" and "conventional" tests were independent of each other. In asymptomatic smokers the phase III slope and the closing volume were significantly related to FEV1, RV/TLC and CO transfer factor. In smokers with chronic bronchitis all the "sensitive" tests were related to the "conventional" tests (with the exception of the total lung capacity). Hyperinflation and CO transfer impairment suggest that early emphysema may accompany mucus hypersecretion in smokers.

'Conventional' (lung volumes, airway conductance, CO transfer factor) and 'small-airway dysfunction' (single-breath N2 washout, maximal expiratory flows with air and a helium-oxygen mixture) tests were performed in a group of asymptomatic male ex-smokers (n = 20) with normal spirometry and compared to those of a similar group of middle-aged nonsmokers (n = 41). The study group had a mean life-long consumption of 13.2 +/- (SD) 8.8 pack-years and had stopped smoking 1-21 years ago, mean 7.3 +/- (SD) 5.8 years. Among the conventional tests, a minimal increase in residual volume and residual volume/total lung capacity ratio was found. Ex-smokers had a steeper phase III slope, a higher closing volume/vital capacity ratio, lower forced flows with air and a higher volume of isoflow, but neither difference between the group means was significant. There was a trend to more abnormal small-airway tests as a function of increased smoking, but only the correlation between percent of predicted closing volume and pack-years reached significance (r = +0.51, p less than 0.05). We conclude that small-airway function normalizes in the long term in most ex-smokers if they become asymptomatic, with less than 10% still having abnormal results years after they stopped smoking.