Prediction formulas f o r s t a t i c and dynamic spirometry, gas distribution, s t a t i c lung mechanics and the transfer t e s t were derived from measurements in healthy men. The measurements included total lung capacity, residual volume, airways resistance, s t a t i c elastic recoil pressure of the lung, s t a t i c compliance, closing volume, slope of the alveolar plateau (phase 1111, flow-volume variables (including mean t r a n s i t time) during breathing of a i r or a helium/oxygen mixture, and conventional spirometric indices. The results from 146 smokers and 124 never-smokers were evaluated separately and combined. For a l l lung function t e s t s a single regression equation was obtained. The prediction formulas included time-re1 ated smoking variables and were Val id for both smokers and never-smokers. For many lung function t e s t s , a nonlinear age coefficient resulted in a significant reduction in variance compared with.. simple linear models. Heavy tobacco smoking influenced most lung function t e s t s less than ageing from 20 t o 70 years, b u t for airways resistance, transfer factor and phase 111 the opposite was found.

The recommended method to measure exhaled nitric oxide (NO) cannot reveal the source of NO production. We applied a model based on the classical Fick's first law of diffusion to partition NO in the lungs. The aim was to develop a simple and robust solution algorithm with a data quality control feature, and apply it to patients with known alterations in exhaled NO. Subjects with allergic rhinitis, allergic asthma, chronic obstructive pulmonary disease (COPD) smokers and controls were investigated. NO was measured at three expiratory flow rates. An iteration method was developed to partition NO. The airway tissue content of NO was increased in asthma, 144 +/- 80 ppb (P = 0.04) and decreased in smokers, 56 +/- 36 ppb (P = 0.02). There was no difference between subjects with rhinitis, 98 +/- 40 ppb and controls, 98 +/- 44 ppb. The airway transfer rate was increased in allergic asthma and allergic rhinitis, 12 +/- 4 vs. 12 +/- 5 ml sec(-1), compared to controls, 8 +/- 2 ml sec(-1) (P < 0.001). The alveolar levels were no different from controls, 2 +/- 1 ppb. In COPD the alveolar levels were increased, 4 +/- 2 ppb (P < 0.001). Extended NO analysis reveals from where in the respiratory system NO is generated. Hence, this new test can be added to the tools the physician has for the diagnosis and treatment of patients with respiratory disorders.

Only a third of Swedish patients with COPD had their diagnosis confirmed with spirometry. Our data indicate that female gender, current smoking, higher BMI and short exhalation time increase the risk of being diagnosed with COPD without fulfilling the spirometric criteria for the disease.

We studied whether nitric oxide (NO), added at 80 ppm to inspired gas, can exert a bronchodilatory effect in humans. Four groups were studied: (1) healthy adult volunteers (n = 6), (2) adult subjects with hyperreactive airways (n = 6) during provocation with inhaled methacholine (MCh), (3) patients with bronchial asthma (n = 13), and (4) patients with chronic obstructive pulmonary disease (COPD, n = 6). All subjects were studied in a body plethysmograph, measuring volume-corrected specific airway conductance (SGaw). No patient or volunteer reacted with bronchoconstriction during NO inhalation. Nitric oxide did not affect SGaw in healthy volunteers or in patients with COPD. Inhaled NO modulated the MCh-induced bronchoconstriction toward dilatation. In patients with bronchial asthma, SGaw increased (p < 0.05) from 0.4 +/- 0.1 to 0.6 +/- 0.2 (kPa.s)-1. In a succeeding test with inhalation of a beta 2-agonist immediately after NO inhalation, a more marked increase in SGaw was seen, to 1.2 +/- 0.3 (kPa.s)-1 (p < 0.001). We conclude that NO inhaled at 80 ppm has no effect on airway tone in healthy volunteers, but modulates the response to MCh provocation toward bronchodilation. It exerts a weak bronchodilatory effect in bronchial asthma, but not in COPD.

The aim of this study was to compare the effects of interval training (3-min intervals) with continuous training on peak exercise capacity (W peak), physiological response, functional capacity, dyspnoea, mental health and health-related quality of life (HRQoL) in patients with moderate or severe COPD. Sixty patients exercised twice weekly for 16 weeks after randomisation to interval- or continuous training. Target intensity was 80% of baseline W peak in the interval group (I-group) and 65% in the continuous group (C-group). Patients were tested by spirometry, ergometer cycle test, cardiopulmonary test and a 12 min walk test. Dyspnoea was measured by the dyspnoea scale from Chronic Obstructive Disease Questionnaire (CRDQ), mental health by Hospital Anxiety and Depression scale (HAD) and HRQoL by the Medical Outcomes Survey Short Form 36 (SF-36). After training, W peak, peak oxygen uptake (VO(2) peak) and exhaled carbon dioxide (VCO(2) peak) increased significantly in both groups, no significant differences between the groups. Minute ventilation (V(E) peak) increased only in the C-group. At identical work rates (isotime) VO(2), VCO(2) and V(E) were significantly more decreased in the I-group than in the C-group (p<0.05). Functional capacity, dyspnoea, mental health, and HRQoL improved significantly in both groups, no difference between the groups. Interval training and continuous training were equally potent in improving peak exercise capacity, functional exercise capacity, dyspnoea, mental health and HRQoL in patients with moderate or severe COPD. At isotime, the physiological response to training differed between the groups, in favour of the interval training.