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Representative tidal, regionial and maximal flow–volume curves at baseline in a subject with low forced expiratory volume in step step step step one s (FEV1)/vital capacity ratio and normal FEV1. ——: 40% forced vital capacity indicating the point where instantaneous maximal and partial expiratory flows were measured.
An SBN2). After at least four regular breaths, the subjects were asked to fully expire to RV and then to take an IVC of 100% oxygen. This was followed, without breath-hold, by a full expiration to RV at a rate of 0.30–0.50 L·s ?1 . Expiratory nitrogen concentration was plotted against VC and the slope of nitrogen alveolar plateau (phase III) calculated by drawing the best-fit line. The first departure from this straight line exceeding cardiogenic oscillations was taken as the onset of phase IV. The open capacity (OC) was calculated as the difference between TLC and the volume at which phase IV (closing capacity) began 26. The slope of phase III and OC were measured at least in triplicate, and the mean value retained for analysis. The results were expressed as % predicted (% pred) 25.
Aerosols of MCh chloride solutions (0.2%, 1% and 6%) were delivered via a DeVilbiss 646 nebuliser attached to a KoKo (Rosenthal–French) breath-activated dosimeter (Ferraris, Louisville, CO, USA). Aerosols were inhaled during quiet tidal breathing in the sitting position 27. Increasing doses of MCh from 40 to 4,800 ?g were inhaled until a decrease of FEV1 ?20% from control was achieved. FVC, FEV1, V?max and V?part were measured only once at each step to avoid the effects of full lung inflation on airway calibre. The provocative dose of MCh causing an FEV1 decrease of 20% (PD20) was determined by interpolating between two adjacent points of the log dose–response curve. If the FEV1 decrease was sd . A generalised linear model was used for comparisons of the data between the 40 subjects with a low FEV1/VC ratio and normal FEV1 and controls.
A mixed between-within-groups ANOVA with Duncan’s post hoc comparisons was used to assess the significance of differences between categories of subjects with abnormally low FEV1/VC and controls. Chi-squared and Fisher’s exact test were used in the analysis of categorical data. Values of p ? ). Of the remaining 33 subjects, eight were assigned to the rhinitis group, 12 to the bronchial asthma group and 13 to the COPD group. Of the 13 subjects assigned to the COPD group, 12 had also a score of 3 for asthma, but the COPD score was prevalent. Four subjects from the asthma group and five subjects of the COPD group also had positive rhinitis scores.
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Slope of a good) stage III and you will b) unlock capability (OC) just like the % forecast (% pred) of the solitary-breathing nitrogen clean-away. Asymp: asymptomatic; COPD: persistent obstructive pulmonary situation. # : p = 0.011 versus rhinitis; ¶ : p = 0.011 versus manage, asymptomatic and rhinitis; ***: p = 0.001 rather than all other teams.
On average, the FEV1, IVC, FVC and lung volumes remained unchanged after inhaling salbutamol in all groups. Exceptions were observed in one subject of the control and asymptomatic groups, two of the asthma group, and romance tale visitors three of the COPD group, in whom the FEV1 increased by >12% and 200 mL of baseline. Interestingly, the FEV1/VC ratio was normalised after salbutamol in four subjects from each of rhinitis, asthma and COPD groups, and in two of the asymptomatic group. Post-bronchodilator changes in V?max were not significantly different among groups (p = 0.91), whereas V?part % showed a tendency (p = 0.070) to increase more after salbutamol in rhinitis (56±29%) and asthma (64±52%) groups of subjects as compared with those in the COPD group (30±41%).