Pulmonary function was investigated in 31 consecutive patients with relatively severe Parkinson's disease. Clinical disability was assessed by Hoehn and Yahr scale, Northwestern University Disability Scale and Websterscore. All patients were on levodopa substitution therapy and used anticholinergics. Pulmonary function was investigated by spirography, determination of a maximal inspiratory and expiratory flow-volume curve and, when possible, maximal static mouth pressures were determined. Peak inspiratory and expiratory flow, maximal expiratory flow at 50% and maximal static mouth pressures were significantly below normal values. Vital capacity, forced inspiratory volume in 1 s and the ratio of forced expiratory volume in 1 s and vital capacity were relatively normal. Nine patients had upper airway obstruction (UAO) as judged by abnormal values for peak inspiratory flow, the ratio of forced expiratory volume in 1 s and peak expiratory flow and the ratio of maximal expiratory and inspiratory flow at 50%. Flow-volume curves were normal in eight patients; four patients demonstrated flow decelerations and accelerations (type A) and 16 had a rounded off flow-volume curve (type B). Type A can be explained by UAO and type B by a combination ofdecreased effective muscle strength and possible UAO. Overall results ofpulmonary function tests in patients without any clinical signs or symptoms of pulmonary disease point to subclinical upper airway obstruction and decreased effective muscle strength in a significant proportion of patients.

A mathematical model was developed describing the entire expiratory flow pattern during spontaneous, tidal breathing in the absence of expiratory muscle activity. It provides estimates for the time constants of the respiratory system (tau RS(model)) and of the decay of continuing inspiratory muscle activity in early expiration (tau mus(model)). In ten anesthetized, tracheostomized cats flow, tracheal pressure and diaphragmatic EMG were measured during normal expirations and expirations with four different added resistances. No significant differences were found between tau RS(model) (0.21-0.49 sec) obtained by fitting the model to the flow data and tau RS obtained from the straight part of the expiratory flow-volume curve. tau mus(model) (0.050-0.052 sec) was comparable to similar time constants obtained from the integrated diaphragmatic EMG or from end-inspiratory, tracheal occlusion pressure. Fitted peak flow and time to peak tidal expiratory flow were not significantly different from those measured. In conclusion, for spontaneously breathing, anesthetized cats our model provides a close fit of the expiratory flow and parameter estimates were comparable with independently measured values.

OBJECTIVE:To assess the effects of different oxygen concentrations and flow rates on the measurement errors of neonatal pneumotachometers in heated and unheated situations and to develop correction factors to correct for these effects.DESIGN:Prospective laboratory study.SETTING:Outpatient clinic with equipment in a standardized setting.SUBJECTS:Neonatal pneumotachometers.INTERVENTIONS:In standardized conditions, the tested pneumotachometer was calibrated at a flow rate of 3 L/min with 60% oxygen and was set in series with a closed spirometer system being used as a reference. Different air-flow levels (1-9 L/min) and oxygen concentrations (21-100%) were infused into the closed system with the pneumotachometer and spirometer.MEASUREMENTS AND MAIN RESULTS:The pneumotachometers were significantly affected by changing oxygen concentrations (p < .01) and increasing flow rates (p < .01), increasing the actually measured flow rate. Correction factors, developed by multiple regression analysis, significantly reduced the overall maximum errors of the pneumotachometers from -1.1 to 0.6 L/min to -0.5 to 0.4 L/min.CONCLUSIONS:The effects of changes in oxygen concentrations and flow rates on neonatal pneumotachometers could be considerably decreased by the use of correction factors such as were calculated in this study. This will preclude frequent calibration procedures with actual flow and oxygen levels during changes in experimental settings.

Background: Treatment of chronic obstructive pulmonary disease (COPD) with inhaled corticosteroids does not appear to be as effective as similar treatment of asthma. It seems that only certain subgroups of patients with COPD benefit from steroid treatment. A study was undertaken to examine whether inhaled fluticasone propionate (FP) had an effect on lung function and on indices of inflammation in a subgroup of COPD patients with bronchial hyperresponsiveness (BHR). Methods: Twenty three patients with COPD were studied. Patients had to be persistent current smokers between 40 and 70 years of age. Non-specific BHR was defined as a PC20 for histamine of ≤8 mg/ml. Patients received either 2 × 500 μg FP or placebo for 6 months. Expiratory volumes were measured at monthly visits, BHR was determined at the start of the study and after 3 and 6 months, and bronchial biopsy specimens were taken at the start and after 6 months of treatment. Biopsy specimens from asymptomatic smokers served as controls. Results: In contrast to asthma, indices of BHR were not significantly influenced by treatment with FP. Forced expiratory volume in 1 second (FEV1) showed a steep decline in the placebo group but remained stable in patients treated with FP. FEV1/FVC, and maximal expiratory flows at 50% and 25% FVC (MEF50, MEF25) were significantly increased in the FP treated patients compared with the placebo group. Biopsy specimens were analysed for the presence of CD3+, CD4+, CD8+, MBP+, CD15+, CD68+, CD1a, and tryptase cells. FP treatment resulted in marginal reductions in these indices of inflammation. Conclusion: In patients with COPD and BHR, FP has a positive effect on indices of lung function compared with placebo. Bronchial inflammation analysed in bronchial biopsy specimens is only marginally reduced.

Objective.In mechanically ventilated patients the expiratorytime constant provides information about respiratory mechanics. In thepresent study a new method, fuzzy clustering, is proposed to determineexpiratory time constants. Fuzzy clustering differs from other methodssince it neither interferes with expiration nor presumes any functionalrelationship between the variables analysed. Furthermore, time constantbehaviour during expiration can be assessed, instead of an average timeconstant. The time constants obtained with fuzzy clustering are comparedto time constants conventionally calculated from the same expirations.Methods.20 mechanically ventilated patients, including 10patients with COPD, were studied. The data of flow, volume and pressurewere sampled. From these data, four local linear models were detected byfuzzy clustering. The time constants (τ) of the local linear models(clusters) were calculated by a least-squares technique. Time constantbehaviour was analysed. Time constants obtained with fuzzy clusteringwere compared to time constants calculated from flow-volume curves usinga conventional method. Results.Fuzzy clustering revealed twopatterns of expiratory time constant behaviour. In the patients withCOPD an initial low time constant was found (mean τ 1: 0.33 s, SD0.21) followed by higher time constants; mean τ 2: 2.00 s (SD0.91s), mean τ 3: 3.45 s (SD 1.44) and mean τ 4: 5.47 s (SD2.93). In the other patients only minor changes in time constants werefound; mean τ 1: 0.74 s (SD 0.30), mean τ 2: 0.90 s (SD 0.23),mean τ 3: 1.04 s (SD 0.42) and mean τ 4: 1.74 s (SD 0.78). Boththe pattern of expiratory time constants, as well as the time constantscalculated from the separate clusters, were significantly differentbetween the patients with and without COPD. Time constants obtained withfuzzy clustering for cluster 2, 3 and 4 correlated well with timeconstants obtained from the flow-volume curves. Conclusions.Inmechanically ventilated patients, expiratory time constant behaviour canbe accurately assessed by fuzzy clustering. A good correlation was foundbetween time constants obtained with fuzzy clustering and time constantsobtained by conventional analysis. On the basis of the time constantsobtained with fuzzy clustering, a clear distinction was made betweenpatients with and without COPD.

A mechanical lung simulator is described (an extension of a previous mechanical simulator) which simulates normal breathing and artificial ventilation in patients. The extended integration of hardware and software offers many new possibilities and advantages over the former simulator. The properties of components which simulate elastance and airway resistance of the lung are defined in software rather than by the mechanical properties of the components alone. Therefore, a more flexible simulation of non-linear behaviour and the cross-over effects of lung properties is obtained. Furthermore, the range of lung compliance is extended to simulate patients with emphysema. The dependency of airway resistance on lung recoil pressure and transmural pressure of the airways can also be simulated. The new approach enables one to incorporate time-related mechanics such as the influence of lung viscosity or cardiac oscillation. The different relations defined in the software can be changed from breath to breath. Three simulations are presented: (1) computer-controlled expiration in the artificially ventilated lung; (2) simulation of normal breathing; and (3) simulation of viscoelastance and cardiac influences during artificial ventilation. The mechanical simulator provides a reproducible and flexible environment for testing new software and equipment in the lung function laboratory and in intensive care, and can be used for instruction and training.

BACKGROUND:The majority of patients with severe chronic obstructive pulmonary disease (COPD) have flow limitation, which has deleterious side effects. If these patients are mechanically ventilated, this often results in difficult weaning. Spontaneously breathing COPD patients experience a beneficial effect of pursed lip breathing. We investigated whether in intubated COPD patients application of an external resistance could produce the same beneficial effects on breathing pattern and gas-exchange as pursed lip breathing.METHODS:Ten COPD patients with flow limitation were studied during pressure support mechanical ventilation. Two types of expiratory resistances were applied: one fixed level of resistance and one with a resistive pressure decay. Each resistance was applied in 5 patients and the highest level was chosen that did not cause hyperinflation. Blood gas values and breathing pattern with and without resistance were compared.RESULTS:With resistance 1, gas-exchange and breathing pattern did not change significantly; average PCO2 changed from 8.0 to 8.1 kPa, PO2 from 10.2 to 10.3 kPa, tidal volume from 0.380 to 0.420 l, respiratory rate from 25 to 23 bpm and inspiratory:expiratory ratio from 1:1.9 to 1:2.0. With resistance 2, gas-exchange and breathing pattern did not change significantly; average PCO2 changed from 5.8 to 6.0 kPa, PO2 from 11.1 to 12.1 kPa, tidal volume from 0.733 to 0.695 l, respiratory rate from 16 to 18 bpm and inspiratory:expiratory ratio from 1:2.3 to 1:2.9.CONCLUSION:In intubated COPD patients being weaned from the ventilator, application of an external resistance did not have the same beneficial effects as pursed lip breathing.

Objectives: Assessment of the long-term effect of uvulopalatopharyngoplasty (UPPP) on snoring, excessive daytime sleepiness, and nocturnal oxygen desaturation index (ODI) in patients with obstructive sleep apnea syndrome. Study Design: Evaluation of snoring, excessive daytime sleepiness, and ODI in patients treated by UPPP earlier. Materials and Methods: Patients (n = 58) with a follow-up period of 11 to 74 months (median, 34 mo) were included in this study. Snoring and excessive daytime sleepiness were scored on specially designed semiquantitative scales. In all patients ODI was calculated from pulse-oximetry combined with polysomnography at base line and by polygraphy (MESAM 4) during follow-up in 38 patients. Long-term response was compared with g-month response in the same cohort. Results: There was a long-term improvement of snoring in 63% of patients, no change in 23%, and a deterioration in 14% (P <.00001). Overall snoring increased slightly between 6 months and long-term follow-up. There was an improvement of excessive daytime sleepiness in 38%, no change in 27%, and a deterioration in 35% (P =.80). Excessive daytime sleepiness showed a relapse to preoperative levels between 6 months and long-term follow-up. The median improvement of ODI was -1 (95% interpercentile range, 73-51) and was not significant (P =.35). In 5 of 13 patients in whom ODI at baseline exceeded 20, ODI was reduced to less than 20. In 4 of the 38 patients ODI was reduced to less than 5. The improvement of ODI decreased significantly between 6 months and long-term follow-up (P =.03). No relation was found between body mass index, Mueller maneuver, X-cephalometry, and long-term outcome. An additional finding was that the ODI decreased after UPPP in combination with tonsillectomy, compared with a slight increase after UPPP alone; the difference was significant (P =.008). Conclusion: The response to UPPP for obstructive sleep apnea syndrome decreases progressively over the years after surgery. UPPP in combination with tonsillectomy was more effective than UPPP alone.

Chronic inflammation and extracellular remodeling of the airway wall characterize asthma. The purpose of this study was to examine whether these features cause a change in airway mechanical properties. We examined 14 healthy and 10 young adults with long-lasting asthma, the latter treated with inhaled bronchodilators and corticosteroids. To obtain area-versus-transmural pressure (A-Ptm) curves during forced expiration (Pedersen, O. F., et al. J. Appl. Physiol. 1982;52:357-369), we used an esophageal balloon and a Pitot static probe positioned at five locations between the right lower lobe and midtrachea. Cross-sectional area (A), airway compliance (Caw = dA/dPtm), and specific airway compliance (sCaw = Caw/A) were obtained from the A-Ptm curves. Results showed that: (1) A was larger in males than in females; (2) Caw and sCaw decreased with a more downstream position; and (3) Caw and sCaw were significantly lower in the patients with asthma, with the differences between the asthmatic patients and the healthy subjects becoming smaller toward the trachea. The lower Caw and sCaw in the patients with long-lasting asthma support the concept that chronic inflammation and remodeling of the airway wall may result in stiffer dynamic elastic properties of the asthmatic airway.

STUDY OBJECTIVES:The interpretation of nonspecific bronchial provocation dose-response curves in COPD is still a matter of debate. Bronchial hyperresponsiveness (BHR) in patients with COPD could be influenced by the destruction of the parenchyma and the augmented mechanical behavior of the lung. Therefore, we studied the interrelationships between indexes of BHR, on the one hand, and markers of lung parenchymal destruction, on the other.PATIENTS AND METHODS:COPD patients were selected by clinical symptoms, evidence of chronic, nonreversible airways obstruction, and BHR, which was defined as a provocative dose of a substance (histamine) causing a 20% fall in FEV(1) (PC(20)) of </= 8 mg/mL. BHR was subsequently studied by methacholine dose-response curves to which a sigmoid model was fitted for the estimation of plateau values and reactivity. Model fits of quasi-static lung pressure-volume (PV) curves yielded static lung compliance (Cstat), the exponential factor (KE) and elastic recoil at 90% of total lung capacity (P90TLC). Carbon monoxide (CO) transfer was measured with the standard single-breath method.RESULTS:Twenty-four patients were included in the study, and reliable PV data could be obtained from 19. The following mean values ( +/- SD) were taken: FEV(1), 65 +/- 12% of predicted; reversibility, 5.6 +/- 3.1% of predicted; the PC(20) for methacholine, 4.3 +/- 5.2 mg/mL; reactivity, 11.0 +/- 5.6% FEV(1)/doubling dose; plateau, 48.8 +/- 17.4% FEV(1); transfer factor, 76.7 +/- 17.9% of predicted; transfer coefficient for carbon monoxide (KCO), 85.9 +/- 22.6% of predicted; Cstat, 4.28 +/- 2.8 kPa; shape factor (KE), 1.9 +/- 1.5 kPa; and P90TLC, 1.1 +/- 0.8 kPa. We confirmed earlier reported relationships between Cstat, on the one hand, and KE (p < 0.0001), P90TLC (p = 0.0012), and KCO percent predicted (p = 0.006), on the other hand. The indexes of the methacholine provocation test were not related to any parameter of lung elasticity and CO transfer.CONCLUSION:BHR in COPD patients who smoke most probably is determined by airways pathology rather than by the augmented mechanical behavior caused by lung parenchymal destruction.

A computer-controlled flow resistance (CCR), to be used in a computer-controlled lung model, is presented. Flow is forced through a slit between a cylinder and a sleeve around the cylinder. The resulting flow resistance depends on the width, circumferences and the variable length of the slit. The variation in the length is computer-controlled by the position of the sleeve with respect to the cylinder. The total flow resistance also depends on inlet and outlet resistance at both sides of the slit and on flow. The dependence on flow is primarily due to the shape of the inlet of the slit. The resistance of the slit itself is almost independent of flow. The resistance is calculated during a calibration phase at different positions of the sleeve, for flow values from 0.05 to 1.0 litre.s-1 (inflow) and from -0.05 to -1.0 litre.s-1 (outflow). To simulate a required resistance pattern, as, for instance, will occur during breathing, at each moment the set position of the sleeve is calculated by means of an interpolation from the relationship between flow resistance and position of the sleeve. The internal diameter of the sleeve is fixed. To tune the resistance range for a specific simulation, the cylinder is changed for one with different diameter, changing the width of the slit.

BACKGROUND:Forced expiratory flow-volume curves are commonly used to assess the degree of airflow obstruction in patients with chronic obstructive pulmonary disease (COPD). In mechanically ventilated subjects, expiratory airways obstruction can only be estimated from relaxed expirations. The aim of this study was to quantify the degree of airways obstruction from relaxed expiratory flow-volume curves in mechanically ventilated patients with COPD.METHODS:As measure of airflow obstruction, the effective time constant during the last 50% of expired volume (tau) was calculated. For bedside monitoring, tau was recalculated as the slope of the flow during the last 50% of expired volume (SF50). In order to study reproducibility, the variables were calculated from consecutive breaths and at different levels of end-expiratory lung volume (EEV). The SF50 and the tau-were correlated with the forced expiratory volume in 1 s (FEV1) measured prior to the start of ventilatory support.RESULTS:Twenty-seven patients were studied with a FEV1 expressed as percentage predicted of 31 +/- 12% (mean +/- SD). The SF50 amounted to 19 +/- 10 degrees. A positive linear correlation was established between SF50 and the FEV1, (%pred), (r = 0.90, P < 0.0001). The tau showed an exponential relationship with FEV1 (%pred), (r2 = 0.78). From 5 consecutive breaths the mean variation coefficient of SF50 was 5 +/- 2%. Changes of delta EEV from 0.05 to 1.00 L did not affect the SF50-values. In 12 patients, mechanically ventilated for respiratory diseases other than COPD, mean tau and SF50 were significantly different from the COPD-patients (P < 0.0001).CONCLUSIONS:This study indicates that relaxed expiratory flow-volume curves can be used to assess airflow obstruction in mechanically ventilated patients with COPD. This information can be used to adapt ventilatory settings.

OBJECTIVE:To assess the feasibility of expiratory flow-volume curves as a measurement of respiratory mechanics during ventilatory support: to what extent is the shape of the curve affected by the exhalation valve of the ventilator?DESIGN:Prospective, comparative study.SETTING:Medical intensive care unit of a university hospital.PATIENTS:28 consecutive patients with various conditions, mechanically ventilated with both the Siemens Servo 900C and 300 ventilators, were studied under sedation and paralysis.INTERVENTIONS:The ventilator circuit was intermittently disconnected from the ventilator at end-inspiration in order to obtain flow-volume curves with and without the exhalation valve in place.MEASUREMENTS AND RESULTS:Peak flow (PEF) and the slope of the flow-volume curve during the last 50 % of expired volume (SF50) were obtained both with and without the exhalation valve in place. The exhalation valve caused a significant reduction in peak flow of 0.3 l/s (from 1.27 to 0.97 l/s) with the Siemens Servo 900 C ventilator and of 0.42 l/s (from 1.36 to 0.94 l/s) with the Siemens Servo 300 ventilator (p < 0.001). The SF50 was not affected.CONCLUSION:In mechanically ventilated patients, the exhalation valve causes a significant reduction in peak flow, but does not affect the SF50. This study further suggests that the second part of the expiratory flow-volume curve can be used to estimate patients' respiratory mechanics during ventilatory support.

We tested the hypothesis that airway wall dimensions are important determinants for the mechanical properties of airways. Lung tissue was obtained from 31 smokers with different degrees of chronic obstructive pulmonary disease (COPD) who were operated on for a solitary lung lesion. Segments of small airways (n = 35) were mounted on cannulas in an organ bath and inflated and deflated cyclically between +15 and -15 cm H(2)O. For each airway this was done at baseline, after methacholine, and after isoprenaline. Specific compliance (sCdyn), specific hysteresis (seta), and pressure at which the airways collapsed (Pcol) were calculated from each recording. Airway wall dimensions were measured morphometrically. Lung function parameters of airflow obstruction were correlated to sCdyn, seta, and Pcol. At baseline, after methacholine, and after isoprenaline sCdyn was 0.059, 0.052, and 0. 085 cm H(2)O(-)(1), seta was 13.5, 12.9, and 7.1%, and Pcol was -3.4, -3.5, and -1.9 cm H(2)O, respectively. Differences between sCdyn, seta, and Pcol after methacholine and after isoprenaline were highly significant (p < 0.001). Of all dimensions studied, smooth muscle area, but not total wall area, was the most important determinant for sCdyn and for seta after methacholine. Specific hysteresis at baseline correlated to residual volume as a fraction of total lung capacity (RV/TLC) (r = 0.5, p = 0.05) and, in the presence of methacholine, to FEV(1)/FVC (r = -0.68, p = 0.02) and RV/TLC (r = 0. 5, p = 0.05). We conclude that, in this study, smooth muscle area and smooth muscle tone, but not total wall area, are determinants for compliance, hysteresis, and collapsibility of isolated airways obtained from smokers.

During spontaneous breathing inspiratory muscle activity does not stop immediately at the start of expiration, but decays at a rate which can be influenced importantly by pulmonary receptors. 1 When the contribution of this decaying activity to the expiratory flow pattern is suppressed by a short end-inspiratory occlusion, the time constant of the respiratory system (τRS = RRS/ERS) can be estimated from the expiratory flow pattern using equation 1 and P(t) = 0.4

The ratio of the time needed to reach peak tidal expiratory flow (tPTEF) and the duration of expiration (tE) is used to detect airflow obstruction in young children. tPTEF is decreased in patients with asthma, but knowledge about the physiological determinants of this parameter is scarce. This study examined the relationship between tPTEF and postinspiratory activities of inspiratory muscles and evaluated the effects of changing sensory information from the lung. Airflow patterns and electromyographic (EMG) activity of inspiratory muscles were recorded in seven spontaneously breathing, anaesthetized cats. The trachea was cannulated and, as a result, the larynx and upper airways were bypassed. Changes in postinspiratory muscle activity were induced by changing afferent sensory nerve information (by cooling the vagus nerves, by administration of histamine and by additional application of continuous positive airway pressure (CPAP)). Durations of postinspiratory activities of the diaphragm and intercostal muscles (characterized by their time constants tau diaphr and tau interc) correlated strongly with tPTEF (r=0.85 and 0.77, respectively). Tau diaphr, tau interc and tPTEF were significantly increased during cooling of the vagus nerves (4-8 degrees C) compared with values at 22 and 37 degrees C (p<0.05). Conversely, administration of histamine and CPAP caused significant decreases in tau diaphr, tau interc and tPTEF, which were absent during cooling of the vagus nerves. In conclusion, the time needed to reach peak tidal expiratory flow is highly influenced by the activities of inspiratory muscles during the early phase of expiration which, in turn, depend on the activities of vagal receptors in the lung.

A nasal dilatator contains two elastic strips, which provide the dilatator with a spring action. The aimed function of the nasal dilatator is to slightly open the nares and hereby facilitate nasal breathing. The aim of this study was to evaluate the effect of a nasal dilatator by measuring nasal airway resistance during normal breathing and nasal forced expiratory and inspiratory flows and Volumes with and without use of the nasal dilatator. Nasal resistance was measured with a whole body plethysmograph; maximal expiratory and inspiratory flow-volume curves were obtained with a pneumotachometer. These measurements were performed in ten healthy volunteers. No significant difference was found between nasal resistance with and without the nasal dilatator. However, values for forced inspiratory volume in 1 s (FIV 1) with the nasal dilatator, proved to be significantly higher (p = 0.045,paired t-test) than values obtained without the nasal dilatator; mean improvement was 0.26 L (sd = 0.36). No significant improvement in peak inspiratory flow (PIF) was found, as was the case for the other flows and volumes. It is concluded that the nasal dilatator causes no appreciable improvement of nasal patency during normal breathing. In view of the fact that FIV 1 values increased significantly, we believe that the nasal dilatator prevents collapse of the external nares during forced inspiration. A beneficial effect during exercise when Ventilation is increased is however doubtful because in that situation most volunteers switch to oronasal breathing already at submaximal exercise.

Studies in adults revealed that addition of salmeterol to a moderate dose of inhaled corticosteroid resulted in better symptom control and higher PEF compared with doubling the dose of inhaled corticosteroid. The aim of this three group study was to compare the effects of a moderate dose of beclomethasone, the same dose of beclomethasone with salmeterol, and a doubling dose of beclomethasone on lung function and symptoms in children with moderate asthma. A total of 177 children already treated with inhaled corticosteroids, were randomized in a double-blind parallel study either to salmeterol 50 mu g twice daily (BDP400+salm), beclomethasone 200 mu g twice daily (BDP800), or placebo (BDP400) in addition to beclomethasone 200 mu g twice daily. No significant differences between groups were found in FEV1, PD20 methacholine, symptom scores, and exacerbation rates after 1 yr. Salmeterol resulted in slightly better PEF in the first months of treatment. FEV1, and PD,, methacholine significantly improved in all groups. After 1 yr mean changes in FEV,, percent predicted were 4.3% (95% CI 1.3; 7.2), 5.8% (95% CI 2.9; 8.7), and 4.3% (95% CI 2.1; 6.5) for BDP400+salm, BDP800, and BDP400, respectively. Changes in airway responsiveness were 0.60 (95% CI 0.05; 1.14), 1.30 (95% CI 0.73; 1.87), and 0.80 (95% CI 0.33; 1.27) doubling doses. Growth was significantly slower in the BDP800 group. We conclude that no additional benefit was found of adding either salmeterol or more beclomethasone to a daily dose of 400 mu g beclomethasone in this group of children with excellent compliance of medication.

Although home recording of peak expiratory flow (PEF) is considered useful in managing asthma, little is known about the relationship of PEF variation to other indicators of disease activity. We examined the relationship of PEF variation, expressed in various ways, to symptoms, atopy, level of lung function, and airways hyperresponsiveness in schoolchildren with asthma. One hundred and two asthmatic children (aged 7-14 yrs) recorded symptoms and PEF (twice daily) in a diary for 2 weeks after withdrawal of all anti-inflammatory maintenance medication. PEF variation was expressed as amplitude % mean, as standard deviation and coefficient of variation of all recordings, and as low % best (lowest PEF as percentage of the highest of all values). Atopy and level of forced expiratory volume in one second (FEV1) % predicted were not significantly related to PEF variation. The provocative dose of histamine causing a 20% fall in FEV1 (PD20) and symptom scores were significantly, but weakly, related to PEF variation. The index, low % best, proved easy to calculate and effective in identifying a short-term episode of reduced PEF. We conclude that peak expiratory flow variation in children with stable, moderately severe asthma is significantly, but weakly, related to symptoms and airways hyperresponsiveness. These three phenomena, therefore, all provide different information on the actual disease state. Expressing peak expiratory flow variation as low % best is easy to perform and appears to be clinically relevant.