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Special attention has emerged towards biomass smoke-induced chronic obstructive pulmonary disease (COPD), providing new knowledge for prevention and therapeutic approach of non-smoker COPD patients. However, the understanding of biomass smoke COPD is still limited and somewhat controversial. The aim of the present study was to compare COPD exclusively caused by tobacco smoking with COPD exclusively caused by environmental or occupational exposures. For this cross-sectional study, COPD patients were recruited from outpatient clinics and formed two groups: non-smoker COPD group (n=16) with exposure to biomass smoke who did not smoke cigarette and tobacco smoker COPD group (n=15) with people who did not report biomass smoke exposure. Subjects underwent pulmonary function tests, thoracic high-resolution computed tomography, 6-min walk test, and sputum induction. The non-smoker COPD group had biomass smoke exposure of 133.3±86 hour-years. The tobacco COPD group smoked 48.5±27.4 pack-years. Women were 62.5 and 66.7%, respectively, of non-smokers and smokers. The non-smoker COPD group showed higher prevalence of dyspnea, lower arterial oxygen tension (PaO2), and lower arterial oxygen saturation (SaO2%) with similar spirometry results, lung volumes, and diffusion capacity. Regarding inflammatory biomarkers, differences were detected in sputum number of lymphomononuclear cells and in sputum concentrations of interleukin (IL)-6 and IL-8 with higher values in the smoker group. Emphysema was more prevalent in the tobacco smoker group, which also showed higher relative bronchial wall thickness and lower lung density by quantitative analysis. Biomass smoke induced more hypoxemia compared to tobacco in COPD patients with similar severity.

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Special attention has emerged towards biomass smoke-induced chronic obstructive pulmonary disease (COPD), providing new knowledge for prevention and therapeutic approach of non-smoker COPD patients. However, the understanding of biomass smoke COPD is still limited and somewhat controversial. The aim of the present study was to compare COPD exclusively caused by tobacco smoking with COPD exclusively caused by environmental or occupational exposures. For this cross-sectional study, COPD patients were recruited from outpatient clinics and formed two groups: non-smoker COPD group (n=16) with exposure to biomass smoke who did not smoke cigarette and tobacco smoker COPD group (n=15) with people who did not report biomass smoke exposure. Subjects underwent pulmonary function tests, thoracic high-resolution computed tomography, 6-min walk test, and sputum induction. The non-smoker COPD group had biomass smoke exposure of 133.3±86 hour-years. The tobacco COPD group smoked 48.5±27.4 pack-years. Women were 62.5 and 66.7%, respectively, of non-smokers and smokers. The non-smoker COPD group showed higher prevalence of dyspnea, lower arterial oxygen tension (PaO2), and lower arterial oxygen saturation (SaO2%) with similar spirometry results, lung volumes, and diffusion capacity. Regarding inflammatory biomarkers, differences were detected in sputum number of lymphomononuclear cells and in sputum concentrations of interleukin (IL)-6 and IL-8 with higher values in the smoker group. Emphysema was more prevalent in the tobacco smoker group, which also showed higher relative bronchial wall thickness and lower lung density by quantitative analysis. Biomass smoke induced more hypoxemia compared to tobacco in COPD patients with similar severity.

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Inhalation of hypertonic saline (HS) causes bronchoconstriction in asthmatic subjects. Repeated inhalation of HS leads to substantially reduced bronchoconstriction, known as the refractory period. Refractoriness due to different stimuli has also been described (cross-refractoriness). Nocturnal asthma is defined as an increase in symptoms, need for medication, airway responsiveness, and/or worsening of lung function that usually occurs from 4 to 6 am. Our objective was to determine the effect of refractoriness on nocturnal asthma. The challenge test consisted of inhalations of 4.5% saline with increasing durations until a reduction of 20% in forced expiratory volume in 1 s (FEV1) (PD20HS) or total time of 15.5 min. Twelve subjects with nocturnal asthma were challenged with HS at 16:00 and 18:00 h and FEV1 was measured at 4:00 h. One to 2 weeks later, FEV1 was determined at 16:00 and 4:00 h. LogPD20HS at 18:00 h was significantly greater than logPD20HS at 16:00 h, 0.51 +/- 0.50 and 0.69 +/- 0.60 mg, respectively (P = 0.0033). When subjects underwent two HS challenges in the afternoon, mean (+/- SD) FEV1 reduction was 206 +/- 414 mL or 9.81 +/- 17.42%. On the control day (without challenge in the afternoon) FEV1 reduction was 523 +/- 308 mL or 22.75 +/- 15.40% (P = 0.021). Baseline FEV1 values did not differ significantly between the control and study days, 2.48 +/- 0.62 and 2.36 +/- 0.46 L, respectively. The refractory period following HS challenges reduces the nocturnal worsening of asthma. This new concept may provide beneficial applications to asthmatic patients.

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Inhalation of hypertonic saline (HS) causes bronchoconstriction in asthmatic subjects. Repeated inhalation of HS leads to substantially reduced bronchoconstriction, known as the refractory period. Refractoriness due to different stimuli has also been described (cross-refractoriness). Nocturnal asthma is defined as an increase in symptoms, need for medication, airway responsiveness, and/or worsening of lung function that usually occurs from 4 to 6 am. Our objective was to determine the effect of refractoriness on nocturnal asthma. The challenge test consisted of inhalations of 4.5 percent saline with increasing durations until a reduction of 20 percent in forced expiratory volume in 1 s (FEV1) (PD20HS) or total time of 15.5 min. Twelve subjects with nocturnal asthma were challenged with HS at 16:00 and 18:00 h and FEV1 was measured at 4:00 h. One to 2 weeks later, FEV1 was determined at 16:00 and 4:00 h. LogPD20HS at 18:00 h was significantly greater than logPD20HS at 16:00 h, 0.51 ± 0.50 and 0.69 ± 0.60 mg, respectively (P = 0.0033). When subjects underwent two HS challenges in the afternoon, mean (± SD) FEV1 reduction was 206 ± 414 mL or 9.81 ± 17.42 percent. On the control day (without challenge in the afternoon) FEV1 reduction was 523 ± 308 mL or 22.75 ± 15.40 percent (P = 0.021). Baseline FEV1 values did not differ significantly between the control and study days, 2.48 ± 0.62 and 2.36 ± 0.46 L, respectively. The refractory period following HS challenges reduces the nocturnal worsening of asthma. This new concept may provide beneficial applications to asthmatic patients.

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Bronchial responsiveness to methacholine or histamine increases at night and may contribute to the mechanisms of nocturnal asthma. Hypertonic saline (HS) is a more clinically relevant stimulus for the diagnosis and assessment of the severity of asthma, but the circadian variation in bronchial responsiveness to hypertonic challenges has not been addressed. The aim of this study was to compare the responsiveness to hypertonic saline at 4:00 AM and at 4:00 PM. Eighteen diurnally active patients (11 women) with asthma, 31 +/- 9 years of age (mean +/- SD) and with a forced expiratory volume in 1 s (FEV(1)) of 79.11% +/- 12.85%, underwent two challenge tests (4:00 AM and 4:00 PM) in random sequence separated by an interval of 7 days. The challenge test consisted of inhalations of 4.5% saline with increasing doses by doubling the duration of nebulization (0.5, 1, 2, 4, and 8 min). The inhalation continued until a drop of 20% in FEV(1) was achieved or total time of 15.5 min. The provocative dose that caused the 20% drop in FEV(1) (PD(20)) was calculated. Differences were found between 4:00 PM and 4:00 AM values for inhalation times [3.80 +/- 3.57 min and 2.19 +/- 2.42 min (p = 0.001), respectively] and for PD(20) [4.94 +/- 6.77 ml and 2.93 +/- 4.74 ml (p = 0.002), respectively]. Eight patients with a home-assessed nocturnal peak expiratory flow (PEF) drop of more than 15% formed the nocturnal asthma group. The behavior of these patients was similar to that of the non-nocturnal asthma group. We conclude that the bronchial responsiveness to HS increases at night.

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OBJECTIVES: To investigate the prevalence and predictors of work related asthma in young adults from the general population. METHODS: A total of 1922 subjects randomly selected from a birth cohort 1978/79 in Brazil, aged 23-25 years, completed a respiratory symptoms questionnaire based on the European Community Respiratory Health Survey, and underwent spirometry, bronchial challenge test with methacholine, and skin prick test. For subjects presenting with bronchial hyperresponsiveness, workplace exposure and its relationship with symptoms were assessed by a specific questionnaire and individualised job description to define cases of work related asthma. RESULTS: The prevalence of work related asthma was 4.2% (81 cases): 1.5% (29 cases) were classified as aggravated asthma and 2.7% (52 cases) as occupational asthma. Work related asthma was associated with atopy and education. Lower educational level (1-8 years of schooling) was associated with work related asthma (odds ratio 7.06, 95% CI 3.25 to 15.33). There was no association between work related asthma and smoking, gender, or symptoms of rhinitis. CONCLUSION: The prevalence of work related asthma was high (4.2%), and was associated with low schooling, probably because of low socioeconomic level. The disease may therefore be a consequence of poverty.

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Fitness improvement was used to compare morning with afternoon exercise periods for asthmatic children. Children with persistent moderate asthma (according to GINA criteria), 8 to 11 years old, were divided into 3 groups: morning training group (N = 23), afternoon training group (N = 23), and non-training group (N = 23). The program was based on twice a week 90-min sessions for 4 months. We measured the 9-min running distance, resting heart rate and abdominal muscle strength (sit-up number) before and after the training. All children took budesonide, 400 microg/day, and an on demand inhaled ss-agonist. The distance covered in 9 min increased (mean +/- SEM) from 1344 +/- 30 m by 248 +/- 30 m for the morning group, from 1327 +/- 30 m by 162 +/- 20 m for the afternoon group, and from 1310 +/- 20 m by 2 +/- 20 m for the control group (P < 0.05 for the comparison of morning and afternoon groups with the control group by ANOVA and P > 0.05 for morning with afternoon comparison). The reduction of resting heart rate from 83 +/- 1, 85 +/- 2 and 86 +/- 1 bpm was 5.1 +/- 0.8 bpm in the morning group, 4.4 +/- 0.8 bpm in the afternoon group, and -0.2 +/- 0.7 bpm in the control group (P > 0.05 for morning with afternoon comparison and P < 0.05 versus control). The number of sit-ups in the morning, afternoon and control groups increased from 22.0 +/- 1.7, 24.3 +/- 1.4 and 23 +/- 1.1 sit-ups by 9.8 +/- 0.9, 7.7 +/- 1.4, and 1.9 +/- 0.7 sit-ups, respectively (P > 0.05 for morning with afternoon comparison and P < 0.05 versus control). No statistically significant differences were detected between the morning and afternoon groups in terms of physical training of asthmatic children.

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Fitness improvement was used to compare morning with afternoon exercise periods for asthmatic children. Children with persistent moderate asthma (according to GINA criteria), 8 to 11 years old, were divided into 3 groups: morning training group (N = 23), afternoon training group (N = 23), and non-training group (N = 23). The program was based on twice a week 90-min sessions for 4 months. We measured the 9-min running distance, resting heart rate and abdominal muscle strength (sit-up number) before and after the training. All children took budesonide, 400 æg/day, and an on demand inhaled ß-agonist. The distance covered in 9 min increased (mean ± SEM) from 1344 ± 30 m by 248 ± 30 m for the morning group, from 1327 ± 30 m by 162 ± 20 m for the afternoon group, and from 1310 ± 20 m by 2 ± 20 m for the control group (P < 0.05 for the comparison of morning and afternoon groups with the control group by ANOVA and P > 0.05 for morning with afternoon comparison). The reduction of resting heart rate from 83 ± 1, 85 ± 2 and 86 ± 1 bpm was 5.1 ± 0.8 bpm in the morning group, 4.4 ± 0.8 bpm in the afternoon group, and -0.2 ± 0.7 bpm in the control group (P > 0.05 for morning with afternoon comparison and P < 0.05 versus control). The number of sit-ups in the morning, afternoon and control groups increased from 22.0 ± 1.7, 24.3 ± 1.4 and 23 ± 1.1 sit-ups by 9.8 ± 0.9, 7.7 ± 1.4, and 1.9 ± 0.7 sit-ups, respectively (P > 0.05 for morning with afternoon comparison and P < 0.05 versus control). No statistically significant differences were detected between the morning and afternoon groups in terms of physical training of asthmatic children.

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BACKGROUND: Inhaled steroids are the most commonly used anti-inflammatory agents for asthma and are increasingly recognised as having a more rapid onset of action than was previously thought. We have investigated the effect of a single dose of inhaled steroid on nocturnal worsening of asthma. METHODS: Ten patients with steroid naive moderate asthma and nocturnal asthma participated in a randomised, double blind, placebo controlled, crossover trial. Participants spent three nights in the laboratory, one week apart. On each night they underwent spirometric testing at 16.00 hours and received one of the three treatments (placebo, beclomethasone 1000 micro g, or fluticasone 1000 micro g) delivered by metered dose inhaler. Spirometric tests were repeated at 04.00 hours the following morning. RESULTS: Following placebo administration the mean (SE) overnight fall in FEV(1) was 0.65 (0.27) l compared with -0.02 (0.13) l following fluticasone (p=0.019) and 0.23 (0.12) l following beclomethasone (p=0.048 v placebo). CONCLUSION: A single dose of inhaled steroid (within the therapeutic range) reduced the fall in FEV(1) in patients with nocturnal asthma when administered at 16.00 hours. Nocturnal worsening of asthma is a useful model for testing inhaled steroid activity in a single night study.

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This prospective study analyzed the involvement of the autonomic nervous system in pulmonary and cardiac function by evaluating cardiovascular reflex and its correlation with pulmonary function abnormalities of type 2 diabetic patients. Diabetic patients (N = 17) and healthy subjects (N = 17) were evaluated by 1) pulmonary function tests including spirometry, He-dilution method, N2 washout test, and specific airway conductance (SGaw) determined by plethysmography before and after aerosol administration of atropine sulfate, and 2) autonomic cardiovascular activity by the passive tilting test and the magnitude of respiratory sinus arrhythmia (RSA). Basal heart rate was higher in the diabetic group (87.8 +/- 11.2 bpm; mean +/- SD) than in the control group (72.9 +/- 7.8 bpm, P<0.05). The increase of heart rate at 5 s of tilting was 11.8 +/- 6.5 bpm in diabetic patients and 17.6 +/- 6.2 bpm in the control group (P<0.05). Systemic arterial pressure and RSA analysis did not reveal significant differences between groups. Diabetes intragroup analysis revealed two behaviors: 10 patients with close to normal findings and 7 with significant abnormalities in terms of RSA, with the latter subgroup presenting one or more abnormalities in other tests and clear evidence of cardiovascular autonomic dysfunction. End-expiratory flows were significantly lower in diabetic patients than in the control group (P<0.05). Pulmonary function tests before and after atropine administration demonstrated comparable responses by both groups. Type 2 diabetic patients have cardiac autonomic dysfunction that is not associated with bronchomotor tone alterations, probably reflecting a less severe impairment than that of type 1 diabetes mellitus. Yet, a reduction of end-expiratory flow was detected.

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This prospective study analyzed the involvement of the autonomic nervous system in pulmonary and cardiac function by evaluating cardiovascular reflex and its correlation with pulmonary function abnormalities of type 2 diabetic patients. Diabetic patients (N = 17) and healthy subjects (N = 17) were evaluated by 1) pulmonary function tests including spirometry, He-dilution method, N2 washout test, and specific airway conductance (SGaw) determined by plethysmography before and after aerosol administration of atropine sulfate, and 2) autonomic cardiovascular activity by the passive tilting test and the magnitude of respiratory sinus arrhythmia (RSA). Basal heart rate was higher in the diabetic group (87.8 ± 11.2 bpm; mean ± SD) than in the control group (72.9 ± 7.8 bpm, P<0.05). The increase of heart rate at 5 s of tilting was 11.8 ± 6.5 bpm in diabetic patients and 17.6 ± 6.2 bpm in the control group (P<0.05). Systemic arterial pressure and RSA analysis did not reveal significant differences between groups. Diabetes intragroup analysis revealed two behaviors: 10 patients with close to normal findings and 7 with significant abnormalities in terms of RSA, with the latter subgroup presenting one or more abnormalities in other tests and clear evidence of cardiovascular autonomic dysfunction. End-expiratory flows were significantly lower in diabetic patients than in the control group (P<0.05). Pulmonary function tests before and after atropine administration demonstrated comparable responses by both groups. Type 2 diabetic patients have cardiac autonomic dysfunction that is not associated with bronchomotor tone alterations, probably reflecting a less severe impairment than that of type 1 diabetes mellitus. Yet, a reduction of end-expiratory flow was detected

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A 46-year-old woman with a previous diagnosis of sarcoidosis presented with morphologically typical large granular lymphocyte (LGL) leukemia/lymphoma with an aggressive clinical course. Epstein-Barr virus DNA was detected in peripheral blood mononuclear cells by PCR. The phenotype was typical of the T cell lineage (CD2+ CD3+ CD5+ CD7+ CD8+ TCRalphabeta+) but with the absence of the CD16, CD56, CD57 NK cell markers. In addition, the LGLs expressed CD122 (p75) in the absence of CD25 which is characteristic of LGLs. These leukemic LGLs did not exhibit NK activity. The clonal nature of this proliferation was demonstrated by the rearrangement of the TCRgamma gene. This phenotypically unusual but morphologically typical LGL leukemia/lymphoma may represent the clonal expansion of a minor normal subset of T-LGLs which do not express any NK cell markers, probably corresponding to in vivo activated T cells.

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Mediastinal and subcutaneous emphysema have been reported as a consequence of deliberate manipulations of the breathing pattern producing a Valsalva-like maneuver in healthy subjects. We present a case of pneumomediastinum, pneumothorax and subcutaneous emphysema occurring in a normal volunteer after repeated measurements of the PEmax.

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The autonomic nervous system of the heart was evaluated in two male groups composed of 11 patients with mitral valve prolapse and of 10 normal subjects, using the heart rate response in two types of tests: respiratory sinus arrhythmia at rest and dynamic exercise. Sinus arrhythmia was of higher magnitude in patients with mitral valve prolapse when compared to the control group; however, the differences reached statistical significance only at a respiratory frequency of 7 cycles/min. With respect to dynamic exercise (25, 50, 100, 150 W during 4 min), the heart rate response, either in terms of the early, vagus-dependent fast tachycardia (first 10 s), or the late, sympathetic-dependent tachycardia (1-4 min) was normal in both groups studied, the same occurring with aerobic exercise capacity evaluated by measurement of the anaerobic threshold. Thus, our results show that in the group of male patients with mitral valve prolapse studied here, the parasympathetic abnormalities, if present, are of questionable physiological significance and do not affect the sympathetic and parasympathetic control of heart rate during dynamic exercise.

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In eight normal subjects we studied the effects of intravenous (i.v.) injection of 2 mg atropine sulfate on the static lung recoil pressure-volume (PV) curves, plethysmographic airway resistance (Raw), and maximum expiratory flow rates (Vmax). In addition, we determined the influence of atropine injection in esophageal elastance (Ees) by measuring the esophageal pressure with an esophageal balloon containing five different volumes (0.5 to 4 ml) of air and by calculating the change in esophageal pressure per unit change in balloon volume (delta Pes/delta Vb). This procedure allowed us to obtain static lung recoil pressure (Pst(1] at a balloon volume extrapolated to zero, thus avoiding the interference of changes in esophageal tone following atropine administration with the measurement of Pst(1). After vagal blockade with atropine, Pst(1) significantly decreased with a shift to the left of PV curves, Raw decreased, and Vmax increased mainly at lower lung volumes. Ees also decreased with parasympathetic blockade. We interpret these findings to indicate that inhibition of vagal tone results in dilatation of large and small airways, and also in the relaxation of smooth muscle in terminal lung units.

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The effect of parasympathetic blockade with intravenously administered atropine (0.04 mg/kg body weight) on the heart rate (HR) of 11 normal males was evaluated using a standardized isometric exercise (handgrip). This type of exercise, when maintained for 10 s at the maximum intensity tolerated by the volunteer, causes tachycardia mediated almost exclusively by parasympathetic withdrawal. The test was performed under baseline conditions and at 20 +/- 3, 33 +/- 3, 42 +/- 3, 52 +/- 3 and 61 +/- 3 min after atropine infusion. The heart rate of the subjects at rest in the supine position (mean +/- SEM) was 70 +/- 2 bpm, reaching values of 119 +/- 3 bpm after atropine. Under control conditions (sitting position), the increase in HR induced by isometric exercise was 22 +/- 1.8 bpm. After blockade, the increase was 4 +/- 0.8, 4 +/- 0.7, 5 +/- 0.6, 4 +/- 1.0 and 4 +/- 0.8 bpm, respectively, at each repetition of the test. These results suggest that the blockade induced by this dose of atropine is effective for at least 1 h. They also indicate the need for a more rigorous definition of the functional half-life of atropine in the heart, when considering physiological tests that either stimulate or withdraw parasympathetic activity upon the heart.

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Sao relativamente poucos os estudos relacionados com o comprometimento primario dos pulmoes na forma cronica da doenca de Chagas. Exames anatomo-patologicos realizados anteriormente mostraram dilatacao das vias aereas e degeneracao dos ganglios parassimpaticos bronquicos em pacientes chagasicos cronicos. Dilatacoes anormais das vias aereas foram tabem observadas atraves de estudos broncograficos de pacientes com doenca de Chagas.Resultados de investigacoes anteriores sugeriram aumento da reatividade bronquica a drogas colinergicas neste grupo de pacientes. Entretanto em estudo recentemente realizado em nosso laboratorio, nao se observou diferenca significante de reatividade bronquica a metacolina entre individuos normais e pacientes chagasicos. A avaliacao cuidadosa de pacientes com a fase cronica da doenca de Chagas em laboratorio de funcao pulmonar levou a conclusao de que na ausencia de insuficiencia cardiacas os resultados dos diferentes testes estao nos limites normais. Em estudos anteriores foram referidos pequenos decrescimos dos fluxos expiratorios maximos ou do volume expiratorio forcado em um segundo em alguns grupos de pacientes chagasicos

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Em 10 cardiopatas chagasicos em situacao clinica de descompensacao circulatoria, examinam os autores os efeitos hemodinamicos de drogas vasodilatadoras: hidralazina (administracao central) e nitroprussiato de sodio (administracao periferica). Em comparacao com a hidralazina, o nitroprussiato de sodio produziu reducao mais apreciavel das pressoes vasculares na circulacao pulmonar e efeitos menos notaveis sobre o fluxo sanguineo. Esses resultados indicam efeitos hemodinamicos beneficos nesta doenca, em termos de reducao de "pre-carga" e "pos-carga"

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