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Biomedical subjects

N B Pride

Publications and source records attributed to N B Pride.

At least 19 recordsLinked to original sources
PubMed1992

Asthma. Definition and clinical spectrum.

When variability and periodicity of symptoms and of airway function are accompanied by evidence of an allergic pathogenesis (identified inhalant precipitants, atopy, raised IgE, eosinophilia) the diagnosis of asthma is obvious to patient and physician. But many patients with asthma do not conform to this classic stereotype, so that considerable problems of distinction from other types of airway obstruction exist. These difficulties have practical significance because conferring the label of asthma is associated with physicians prescribing more intensive and effective treatment.

Asthma↗
PubMed1992

Failure of inhaled corticosteroids to modify bronchoconstrictor or bronchodilator responsiveness in middle-aged smokers with mild airflow obstruction.

We have compared the effects of three-month periods of treatment with an inhaled corticosteroid, budesonide 600 micrograms twice daily and with placebo on bronchial responses to inhaled histamine and to bronchodilators in a double-blind crossover trial in 14 middle-aged male smokers (mean age, 59.6 years) with mild airways obstruction (mean FEV1 2.42 L, 80 percent predicted [range, 48 to 110 percent]). Responsiveness to inhaled histamine was assessed monthly by the provocative concentration (mg/ml) reducing FEV1 by 20 percent (PC20). Bronchodilator response to a combination of inhaled salbutamol (5 mg) and ipratropium (0.5 mg) was assessed before and after three months' treatment. Compliance with treatment was checked by weighing aerosol canisters, and by measuring plasma budesonide and metabolites. There was no significant change in FEV1 (budesonide mean 2.38 L [SEM 0.17] vs placebo 2.40 L [0.17]), vital capacity (budesonide mean 3.69 L [0.17] vs placebo 3.81 L [0.17]) or in bronchodilator responsiveness (mean increase over baseline FEV1, budesonide 11.6 [2.7] percent vs placebo 10.5 [3.2] percent). There was a small overall reduction in bronchoconstrictor responsiveness over the period of the trial, but there was no effect of 12 weeks of budesonide treatment compared with 12 weeks of placebo treatment (mean log PC20 during budesonide 0.595 [SEM 0.063], placebo 0.591 [SEM 0.055]). Following the three-month crossover trial, six men continued for nine more months to receive budesonide in a single-blind trial and the results were compared with those in six men who took no active treatment for the subsequent nine months. No improvements in baseline spirometry, home peak flow measurements, bronchoconstrictor or bronchodilator responsiveness were observed after 12 months of budesonide treatment. Thus, a regimen of budesonide treatment that consistently attenuates bronchial responsiveness in asthmatic subjects had no effect in these men; larger and longer trials will be required to establish whether a subgroup of smokers shows a favorable response.

Administration, Inhalation↗
PubMed1992

European Respiratory Society study on chronic obstructive pulmonary disease (EUROSCOP): hypothesis and design.

Chronic obstructive pulmonary disease (COPD) is a common disease in industrialised countries and responsible for a considerable morbidity and mortality. Cigarette smoking is the most important aetiological factor. The EUROSCOP trial aims at investigating the hypothesis that airway inflammation plays an important pathogenic role in the development of chronic obstructive airway disease in smokers. In cigarette smokers with poorly reversible airflow obstruction, the effect over 3 yrs of an inhaled glucocorticosteroid, budesonide 400 micrograms b.i.d., on the decline of lung function, measured as postbronchodilator forced expiratory volume in one second (FEV1), will be compared with that of placebo. The trial has been designed to detect a difference in yearly decline of at least 30 ml.year-1. The study is a parallel group, randomised, double-blind, multicentre study. Patients will be recruited from 47 centres in 12 countries in Europe. It will start with a run-in consisting of two 3 month periods. During the first 3 months, the patients will be offered a smoking cessation programme. All patients who have not stopped smoking during this period will enter the second half of the run-in where compliance with the dosage regimen will be tested. After these two periods, patients will be randomised to receive either inhaled budesonide, 400 micrograms b.i.d., or placebo for a period of 3 yrs.

Administration, Inhalation↗
PubMed1991

Plasma leucocyte elastase concentrations in smokers.

The associations between cigarette smoking, plasma leucocyte elastase concentration, peripheral leucocyte count and FEV1 were examined in 148 men, 72 of whom were current cigarette smokers, 40 of whom were ex-smokers, and 36 who had never smoked. All men were part of a long-term survey. Smokers had significantly higher plasma leucocyte elastase concentrations than ex-smokers or those who had never smoked. Mean current FEV1 was lower, and the annual decline in FEV1 in the preceding 10 years was faster in smokers than the other two groups. A few smokers had slight increases in serum C-reactive protein concentrations. Although peripheral blood leucocyte counts were higher in smokers than in non-smokers or ex-smokers, no association was found in any of the three groups of men between plasma elastase concentration and peripheral leucocyte count, nor between either of these two variables and annual decline in FEV1 or current level of FEV1. There was also no relation between plasma elastase concentration and reported daily cigarette consumption or mixed expired carbon monoxide in smokers. The results indicate that some male smokers have increased in vivo release of elastase from peripheral blood neutrophils at a time when there is no evidence of acute infection. Because leucocyte elastase is a strong candidate for pulmonary tissue damage, further studies of the mechanisms that increase plasma concentrations are indicated.

Adult↗
PubMed1991

Maximum airflow through the nose in humans.

Inspiratory and expiratory flow via the nose and via the mouth during maximum-effort vital capacity (VC) maneuvers have been compared in 10 healthy subjects. Under baseline conditions maximum flow via the nose was lower than that via the mouth in the upper 50-60% of the VC on expiration and throughout the VC on inspiration. The mean ratio of maximum inspiratory to maximum expiratory flow at mid-VC was 1.38 during mouth breathing and 0.62 during nasal breathing. Inspiratory flow limitation with no increase in flow through the nose as driving pressure was increased above a critical value (usually between 12 and 30 cmH2O) was found in all six subjects studied. Stenting the alae nasi in seven subjects increased peak flow via the nose from a mean of 3.49 to 4.32 l/s on inspiration and from 4.83 to 5.61 l/s on expiration. Topical application of an alpha-adrenergic agonist in seven subjects increased mean peak nasal flow on inspiration from 3.25 to 3.89 l/s and on expiration from 5.03 to 7.09 l/s. Further increases in peak flow occurred with subsequent alan stenting. With the combination of stenting and topical mucosal vasoconstriction, nasal peak flow on expiration reached 81% and, on inspiration, 79% of corresponding peak flows via the mouth. The results demonstrate that narrowing of the alar vestibule and the state of the mucosal vasculature both influence maximum flow through the nose; under optimal conditions, nasal flow capacity is close to that via the mouth.

Adult↗
PubMed1991

Interaction between parenchyma and airways in chronic obstructive pulmonary disease and in asthma.

The extent of air-space destruction caused by emphysema is very variable in severe chronic obstructive pulmonary disease (COPD), constituting one of the most obvious differences between COPD and asthma. Differences in the static deflation pressure-volume curve between COPD and asthma can easily be shown, but it has been surprisingly difficult to find distinctive mechanical features of impaired airway function caused by air-space destruction. This may be because in mild airway obstruction related to smoking--particularly in younger subjects--emphysema may be absent, and the predominant site of airway narrowing in the smallest bronchi and respiratory bronchioles may be the same as that found in asthma in remission. In more severe obstruction caused by COPD there is almost always very severe intrinsic disease of the airways and this may so dominate the functional abnormality that it is difficult to detect any additional change because of airspace destruction. Overall, few studies have set out to detect specific effects of parenchymal destruction on airway function.

Airway Resistance↗
PubMed1991

A "splitting" look at chronic nonspecific lung disease (CNSLD): common features but diverse pathogenesis.

The term chronic nonspecific lung disease (CNSLD) was proposed by the Ciba Symposium in 1959 as an umbrella term grouping chronic bronchitis, asthma, emphysema and irreversible or persistent obstructive lung disease. However, it has only been widely used by proponents of the Dutch Hypothesis, which states that these diseases all result from a common genetic root and should be considered as one disease. A major reason for proposing this hypothesis in 1961 was that these different entities share some common features, especially airway hyperresponsiveness. Although not formally disproven, evidence is accumulating--and reviewed here--against this "one disease concept"; hence, common features should not necessarily imply a common pathogenesis. Overlap features are sufficiently frequent in clinical practice to cause problems for labelling patients within the scope of CNSLD. The term could still be used as a starting point for a "splitting approach", identifying a small number of important basic features in order to allow a more systematic use of established labels for diseases within CNSLD. Our proposal for labelling emphasizes a consistent use of asthma, emphysema and chronic obstructive pulmonary disease (COPD), but restricts the use of chronic bronchitis to those patients with chronic bronchial hypersecretion without chronic airways obstruction.

Asthma↗
PubMed1990

Assessment of long-term changes in airway function.

There is some evidence supporting long-term 'tracking' of decline in FEV1 at least in middle-aged male smokers, so that a moderately reduced FEV1 predicts subsequent disability and death. Distribution of individual rates of decline in FEV1 stabilizes after follow-up for 4 to 5 years, but large and unexplained differences in decline in FEV1 are found between individuals with similar smoking history. There are theoretical advantages to following post-bronchodilator FEV1 but few studies of its usefulness are available. Changes in other tests derived from the single breath N2 test or the maximum expiratory flow-volume curve have been less informative than originally postulated and their long-term prognostic value remains unknown.

Forced Expiratory Volume↗
PubMed1990

Epidemiology of obstruction, exacerbations and hyperreactivity. Effects of glucocorticosteroids and other anti-inflammatory treatment.

Validated and standardized questions are available for self-reporting of exacerbations of symptoms due to bronchopulmonary infections but not for non-infective exacerbations. The presence of non-specific bronchial hyperresponsiveness may help to identify smokers with a high risk of rapid decline in lung function, but change in bronchial responsiveness with treatment probably cannot be used to predict subsequent long-term progression in FEV1. In non-asthmatic individuals three months' treatment with glucocorticosteroids has not improved FEV1 nor reduced bronchial responsiveness; the effects of glucocorticosteroids on bronchial secretions and infections and long-term decline in FEV1 are largely unknown.

Airway Obstruction↗
PubMed1990

Abnormal regional distribution of ventilation in middle-aged smokers: comparison of changes in 81Krm ventilation scans and computed tomography of the lung.

In 1980 we found that abnormalities in regional distribution of ventilation, as assessed by 81Krm lung scans, were common in middle-aged smokers with normal chest radiographs and mild impairment of overall lung function. In 1984 we repeated 81Krm scans in 16 continuing smokers then aged 50-64 years and with mean forced expiratory volume in one second 93% (20 SD) of predicted values who had previous 81Krm scans performed in 1980. To assess the role of disease of the peripheral airspaces in causing abnormal regional ventilation, we also obtained computed tomograms (CT) of the lungs and measured carbon monoxide transfer of the lungs in these men. Krypton scans in seven men who had normal or minor focal defects of ventilation in 1980 were unchanged in 1984. Scans in seven of the nine men who had abnormal scans in 1980 remained abnormal in 1984 but there was no overall deterioration in the abnormality of ventilation in these men; in men with similar grading in 1980 and 1984 some of the peripheral defects present in 1980 had resolved and some new abnormal areas had appeared. Minor localised abnormalities of CT scans, as assessed visually, were present in eight of the 16 men and were associated with lower values of carbon monoxide transfer coefficient (mean 78% vs 98% predicted in men with normal scans, P less than 0.01) and lung density (mean -894 vs -869 HU in men with normal scans, P less than 0.054) suggesting the CT changes were due to alveolar destruction. Abnormality of the krypton scan was not significantly associated with abnormality of the CT scan or with a reduction in carbon monoxide transfer. The results of the krypton lung scans confirm that non-uniformity of regional ventilation is often present in asymptomatic middle-aged smokers and suggest that this non-uniformity is in part due to temporary occlusion of airways. Abnormality in regional ventilation was not associated with the anatomical changes shown by the CT scan, suggesting that airway narrowing was more important than alveolar destruction in causing regional abnormalities of ventilation in these men.

Forced Expiratory Volume↗
PubMed1990

Comparison of oscillation with three other methods for measuring nasal airways resistance.

In this study we have compared the sensitivity and reproducibility of nasal airways resistance measurements made using an oscillometer, with those made by passive anterior, active anterior and active posterior rhinomanometry. Nasal airways resistance values were compared in 12 patients with rhinitis and 15 normal subjects, of whom ten had additional measurements after a vasoconstrictor spray, oxymetazoline. The coefficients of variation of 6-8 technically satisfactory measurements were 9-19%. The decongestant effect of oxymetazoline was detected by all methods, with no decrease in reproducibility. Post vasoconstrictor nasal airways resistance fell by 28% (passive anterior), 35% (active anterior), 36% (active posterior) and 58% (oscillometry). In conclusion, the oscillation method for deriving nasal airways resistance is a useful, new, simple and noninvasive way of assessing nasal airways patency. Results compare favourably with other, more established techniques.

Adult↗
PubMed1990

Effect on histamine responsiveness of reducing airway dimensions by altering posture.

Baseline airway geometry is thought to be an important determinant of the airway response to challenge; this geometry is altered by changing posture. The effect of changes in posture on airway calibre, midtidal lung volume, and the airway response to inhaled histamine was studied in eight healthy subjects (four female; mean (SD) age 29.8 (5.1) years, FEV1 3.54 (0.65) 1). Each subject was studied in both sitting and supine postures on two days; airway calibre was assessed by measuring total respiratory resistance (Rrs) at 6 Hz with a forced oscillation technique applied over 16 seconds of tidal breathing. Appropriate doses of histamine were selected by preliminary experiments and were always inhaled with the subject in the supine posture. Midtidal lung volume was larger in the sitting (2.9 (0.8) 1) than in the supine posture (2.4 (0.5) 1). Baseline Rrs was lower in the sitting than in the supine posture (2.03 (0.44) and 3.12 (0.76) cm H2O.1(-1).s*). The mean absolute increase in Rrs after the same dose of histamine was 1.22 cm H2O.1(-1).s in the sitting position (65.8% increase over baseline) and 1.39 cm H2O.1(-1).s (48.8% increase over baseline) in the supine position. The geometric mean provocation concentration of histamine causing a given percentage increase in Rrs was similar in the sitting (8.26 mg/ml) and supine (8.65 mg/ml) positions. Thus there was no significant increase in responsiveness after the reduction of airway dimensions and extra-airway distending forces that occurs in the supine posture.

Adult↗
PubMed1990

Effects of nonsteroidal anti-inflammatory drugs on the bronchial hyperresponsiveness of middle-aged male smokers.

Bronchial hyperresponsiveness (BHR) in smokers is believed to be a consequence of airway wall inflammation. We have examined the effects of treatment with nonsteroidal anti-inflammatory drugs (NSAID) on BHR to inhaled histamine, measured as the provocative concentration reducing forced expiratory volume in one second (FEV1) by 20% (PC20), in middle-aged male cigarette smokers in two separate double-blind, placebo-controlled, cross-over trials. Baseline FEV1 in these smokers ranged from 41-117% predicted values. In the first study 15 men (mean age 58 yrs, FEV1 2.20 l) were examined before and one hour after a single dose of 1.2 g aspirin. There was no significant change in PC20 (geometric mean 1.88 mg.ml-1 pre-aspirin, 1.89 mg.ml-1 post-aspirin) or baseline FEV1 and we observed no tachyphylaxis to the effects of inhaled histamine at one hour after placebo. In the second study 10 men (mean age 60 yrs, FEV1 2.53 l) were examined before and after three days' treatment with the NSAID flurbiprofen 50 mg t.d.s. Baseline PC20 was higher in this group than in the first study. There was no relationship between the excretion of urinary thromboxane metabolites and the intensity of BHR under baseline conditions; flurbiprofen greatly reduced the urinary excretion of thromboxane metabolites, but baseline FEV1 was not altered. Analysis of change in PC20 was complicated by a difference in baseline PC20 before the two treatments, but treatment with flurbiprofen did not significantly attenuate BHR. The results suggest that thromboxane or other cyclo-oxygenase products of arachidonic acid metabolism do not play an important role in the short-term maintenance of BHR to histamine in middle-aged male cigarette smokers.

Aged↗
PubMed1989

Effects of smoking on changes in respiratory resistance with increasing age.

1. The oscillation method for measuring total respiratory resistance (Rrs) is a simple method of assessing airway dimensions which can be applied in epidemiological surveys and potentially might be useful for detecting mild airway disease in smokers. However, it is not known whether abnormalities in Rrs are only present when there are also abnormalities in simple spirometric tests. 2. We have compared values of Rrs and its frequency-dependence (fR) using the oscillation technique applied over the frequency range 6-26 Hz in 42 healthy, non-asthmatic men who were never-smokers (aged 26-61 years) and in 41 male cigarette smokers (aged 32-64 years). The results were compared with those for spirometry and the single-breath N2 test which are the most commonly used techniques in epidemiological surveys for detecting the effects of smoking on the lungs. 3. There was a strong trend for Rrs (especially at lower oscillation frequency) and fR to increase with increasing age in smokers. Increases in Rrs and fR were usually present when forced expiratory volume in 1 s was less than 80% of predicted and the forced expiratory volume in 1 s/vital capacity ratio was less than 65%, but abnormal fR was present in some smokers whose spirometry was within conventional normal limits. 4. Abnormalities in Rrs and fR were weakly associated with abnormality of the single-breath N2 manoeuvre.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

The effect of prolonged submaximal warm-up exercise on exercise-induced asthma.

The effect of a prolonged warm-up period of exercise on subjects with exercise-induced asthma (EIA) has been studied. Seven asthmatic subjects with known EIA were exercised according to two different protocols on two separate days, which were randomized. On Day A, subjects performed a standard 6-min treadmill run (S1A), which increased heart rate to 98% predicted maximum, followed 45 min later by an identical run (S2A). Refractoriness was demonstrated on the second exercise test, with a mean maximal fall in FEV1 of 29 +/- 3.1% and a PEFR of 32 +/- 2.8% after S2A, compared with a mean maximal fall in FEV1 of 46 +/- 2.6% and a PEFR of 51 +/- 4.0% after S1A. On Day B, subjects performed a 30-min treadmill run at a lower gradient (W1B), followed 21 min later by another standard 6-min treadmill test (S2B). W1B was followed by significantly less EIA (mean maximal fall in FEV1 of 17 +/- 5.4% and a PEFR of 21 +/- 6.3%) than followed S1A. Nevertheless, when subjects subsequently performed a standard 6-min run (S2B), significant refractoriness to bronchoconstriction, comparable to that observed after S2A, developed, with a mean maximal fall in FEV1 of 26 +/- 3.6% and a PEFR of 27 +/- 2.3% (p less than 0.05). We conclude that a warm-up period of exercise can induce refractoriness to EIA without itself inducing marked bronchoconstriction.

Adolescent↗