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Biomedical subjects

H Magnussen

Publications and source records attributed to H Magnussen.

330 records · Page 19Linked to original sources

Effect of one hour of passive cigarette smoking on lung function and airway responsiveness in adults and children with asthma.

We exposed 18 adults with bronchial asthma, 16 healthy controls and 11 children with asthma for 1 h either to ambient air (AA) or to environmental tobacco smoke (ETS). Exposure was performed at rest in an exposure chamber. Before and after exposure symptom scores and lung function were determined. After exposure bronchoprovocation tests with methacholine (adults) or histamine (children) were performed to determine the concentrations causing a 100% increase in SRaw (PC100SRaw), and a 20% fall in FEV1 (PC20FEV1). In adult asthmatics mean (SD) SRaw before and after Sham was 8.8 (3.6) and 8.4 (3.6) cmH2O.s, and mean FEV1 (SD) was 3.18 (0.97) and 3.14 (0.9) 1, respectively. Before and after passive smoking mean SRaw (SD) was 7.5 (3.0) and 7.2 (2.7) cmH2O.s, and mean FEV1 (SD) was 3.31 (1.0) and 3.21 (0.88) 1, respectively. Geometric mean (SD) PC100SRaw and PC20FEV1 after Sham were 0.38 (4.5) and 0.29 (4.1) mg/ml, after passive smoking 0.39 (5.1) and 0.36 (4.7) mg/ml, respectively. In healthy controls there was no consistent effect on the respective parameters during exposure. In children mean (SD) SRaw before and after Sham was 8.7 (3.6) and 9.0 (3.2) cmH2O.s, and mean FEV1 (SD) was 1.97 (0.32) and 1.98 (0.40) 1, respectively. Before and after passive smoking mean SRaw (SD) was 10.4 (5.3) and 9.4 (3.3) cmH2O.s, and mean FEV1 (SD) was 1.95 (0.37) and 1.94 (0.35) 1, respectively. Geometric mean (SD) PC100SRaw and PC20FEV1 after Sham were 1.39 (3.0) and 0.70 (2.7) mg/ml, and after passive smoking 1.65 (2.5) and 0.96 (2.3) mg/ml, respectively. There were no significant differences in lung function and airway responsiveness between exposure to ambient air or ETS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Clinical benefits of a combined hospital and home-based exercise programme over 18 months in patients with severe COPD.

BACKGROUND: Long-term exercise training is capable of improving exercise performance and quality of life in patients with severe COPD. In the present study we examined the effects of an 18-month home-based training on the rate of hospital admissions and bronchodilator use as primary end-points. Secondary end-points were exercise capacity and quality of life. METHODS: The study comprised 26 patients with severe COPD (20m/6f; mean +/- SD FEV1, 37 +/- 6% pred) who were recruited in a previous trial and randomised into a training (n = 14) and a control group (n = 12). After initial recovery from an exacerbation the training group had performed a 10-day walking training in the hospital. This was followed by 18 months of individually defined, supervised training at home that was integrated into the patients' daily activities. The control group had no exercise programme, neither in hospital nor at home. RESULTS: During the 18-month period patients of the training group showed a lower number of hospital admissions (total, n = 3 vs n = 14, p = 0.026; disease-related, n = 3 vs n = 12, p = 0.050) and used less short-acting beta 2-agonists (mean [95% CI], 2.4 [1.4-3.4] vs 5.7 [4.2-7.2] puffs per day; p < 0.001) than the control group. Furthermore, the improvements in 6-min treadmill distance and quality of life (CRQ) achieved in the hospital were fully maintained in the training group, whereas the control group did not show significant improvements at any time but a tendency toward deterioration. CONCLUSIONS: Our data indicate that an individually defined, home-based, long-term walking programme initiated by a short hospital-based training can reduce disease-related medical consumption, in addition to sustained benefits in exercise performance and quality of life.

Adrenergic beta-2 Receptor Agonists↗

[Chronic respiratory tract diseases--environmentally or occupationally-induced].

Chronic bronchitis, lung emphysema and bronchial asthma are the most frequently encountered pneumological diseases. Most patients with chronic bronchitis and emphysema are smokers, therefore the development of the disease is closely related to self responsible habits. In asthmatics bronchial hyperresponsiveness favours a pathologic airway response induced by polluted air. SO2 is believed to only induce airway obstruction in patients with preexisting airway diseases. NO2 and ozone, however, have been shown to induce airway hyperresponsiveness in healthy subjects.

Environmental Pollution↗