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Biomedical subjects

N B Pride

Publications and source records attributed to N B Pride.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1989

Sensitivity of the human cough reflex: effect of inflammatory mediators prostaglandin E2, bradykinin, and histamine.

Prostaglandins may cause hyperresponsiveness to bronchoconstrictor agents in the lung and hyperalgesia in the skin. Increased airway concentration of both prostaglandins and bradykinin has been suggested as the possible cause of the increased cough sensitivity sometimes found in patients with cough associated with taking drugs that inhibit angiotensin-converting enzyme. We have therefore investigated the effect of prostaglandin E2 (PGE2), bradykinin (BK), histamine (H), and citric acid (C) on capsaicin-induced cough and increase in respiratory resistance (Rrs). Capsaicin-induced changes in Rrs and dose-cough response were measured before and after inhaling 0.76 mumol of PGE2, BK, H, and C. All the test substances caused cough, which was subject to tachyphylaxis, but no significant change in Rrs. Neither BK, H, nor C altered the capsaicin cough or Rrs response. However, PGE2 significantly increased both responses to capsaicin, the geometric mean (95% Cl) for the dose of capsaicin causing 5 or more coughs being 16.2 (14.3 to 18.3) nmol before and 4.4 (2.4 to 7.9) nmol after PGE2 (p less than 0.05). The percent increase (95% Cl) in Rrs after capsaicin was 20 (16.5 to 23.5)% before and 37.2 (32.2 to 43.2)% after PGE2 (p less than 0.05). The results suggest that the cough reflex will be increased in the presence of PGE2 in the airway.

Adult↗
PubMed1989

Diagnostic labels applied to model case histories of chronic airflow obstruction. Responses to a questionnaire in 11 North American and Western European countries.

In Canada, USA and 9 Western European Countries, 121 respiratory physicians responded to an English language questionnaire asking them to state how they would investigate, treat and label four model patients, chosen to represent well-recognized patterns of clinical features of chronic airflow obstruction. Selection of further investigations appeared to be determined more by the probable diagnostic label than by the need to define selected characteristics in the whole range of such patients. Differences in recommended treatment between countries were less than others have reported for the treatment of asthma. Analysis of the diagnostic labels showed: the classic terms asthma, chronic bronchitis, emphysema still predominated in clinical practice and were considered to be better defined entities than any of the many terms introduced to describe chronic airflow obstruction in the last 30 yrs; the term chronic bronchitis was a source of confusion unless qualified to indicate presence or absence of obstruction; the use of combination terms such as chronic asthmatic bronchitis and chronic obstructive bronchitis showed large differences between countries; there were few differences related to national language. The implications of these findings are discussed.

Aged↗
PubMed1988

Changes in bronchial responsiveness to inhaled histamine over four years in middle aged male smokers and ex-smokers.

Bronchial hyperresponsiveness to inhaled histamine in smokers is associated with an accelerated annual decline in FEV1 and low baseline FEV1 values. The evolution of bronchial hyperresponsiveness and whether it precedes or follows the accelerated decline in FEV1 and reduction in FEV1 is unknown. Measurements of the provocative concentration of inhaled histamine required to reduce FEV1 by 20% (PC20) were repeated after a four year interval in 27 male smokers (mean age 59 years, smoking on average 27 cigarettes a day in 1986) and 16 men who were ex-smokers in 1982 and who remained non-smokers until 1986 (mean age 53 years in 1986). These men were originally recruited to a prospective study in 1974 and had their first PC20 measurement in 1982. PC20 was positively related to baseline FEV1 in both smokers and ex-smokers in both 1982 and 1986 (r ranging from 0.56 to 0.76, p less than 0.01). In smokers mean FEV1 fell from 83% to 77% predicted (p less than 0.001) and geometric mean PC20 from 7.11 to 3.27 mg/ml (p less than 0.001) between 1982 and 1986. The change in PC20 in individual smokers over the four years was related to change in FEV1 (p = 0.012). In ex-smokers mean FEV1 was 93% predicted both in 1982 and in 1986 and there was no significant difference in geometric mean PC20 between 1982 (6.68 mg/ml) and 1986 (5.98 mg/ml). Thus in smokers there was an accelerated annual decline in FEV1 and an increase in bronchial hyperresponsiveness as FEV1 fell. The ex-smokers had comparable levels of bronchial hyperresponsiveness in 1982. Mean PC20 values were unchanged in 1986 in these men, who showed a normal age related decline in FEV1. These longitudinal results emphasise the importance of baseline airway geometry in influencing bronchial hyperresponsiveness to histamine in middle aged smokers and ex-smokers.

Airway Resistance↗
PubMed1988

Effect of inhaled and systemic opiates on responses to inhaled capsaicin in humans.

To determine the site of action of opiates in humans, we have studied the effect of systemic and inhaled opiates on cough and increase in respiratory resistance (Rrs) caused by inhaled capsaicin. In 13 subjects, a range of doses of capsaicin inhaled in single breaths given in random order produced a reproducible dose-cough response. Inhalation of a dose of capsaicin that caused fewer than two coughs increased Rrs by 28% (21-35, mean 95% confidence interval). Inhaled codeine (50 mg) and morphine (10 mg) did not alter the cough response. In contrast, both drugs increased base-line Rrs by 24% (16-44) and 13% (3-23), respectively, and significantly reduced the increase in Rrs after inhaled capsaicin (P less than 0.05). Oral codeine (60 mg) significantly (P less than 0.05) reduced the number of coughs at 1 and 2 h but did not alter base-line Rrs or its increase after capsaicin. Intravenous morphine (0.15 mg/kg) significantly reduced the sensitivity of the cough response (P less than 0.05), which was reversed by naloxone. However, there was no significant drug effect on either the base-line Rrs or its increase after capsaicin. Systemic dosing of opiates is therefore required to reduce the cough reflex, whereas inhaled opiates may reduce the increase in Rrs after inhaled capsaicin.

Administration, Inhalation↗
PubMed1987

Airway caliber and the work of breathing in humans.

Mechanical work rate of breathing was measured in five normal subjects during voluntary eucapnic hyperventilation at rates of approximately 10, 20, 40, 60, and 80 l/min before and after inhalation of 1 mg of ipratropium bromide, an anticholinergic agent. Chest wall recoil pressure was measured over a range of lung volumes in each subject and was used as the reference pressure in the calculation of work rate. There was little change in elastic or resistive work rate at rest when vagal tone was reduced by ipratropium. The mean work at 40, 60, and 80 l/min was 8.9, 17.2, and 34.0 cmH2O.l-1.s before and 5.6, 12.4 and 25.8 cmH2O.l-1.s after ipratropium. This suggests that vagal tone significantly influences the work of breathing at high ventilatory rates, such as occur during strenuous exercise.

Adult↗
PubMed1987

Effects of volume history during spontaneous and acutely induced air-flow obstruction in asthma.

We examined the volume history effect on maximal expiratory flow (Vmax) in patients with asthma by comparing Vmax at 60% of VC from forced exhalation maneuvers begun just above FRC (partial, P) with those begun from TLC (maximal, M) and expressed the results as M-P ratios. In a clinic population with varying degrees of obstruction, we found that M-P ratios varied inversely with the severity of the obstructive process, i.e., the more severely obstructed patients had a fall in Vmax after a deep inhalation (DI). By contrast, equally severe obstruction acutely induced in subjects with mild asthma was associated with an increase in Vmax after a DI. There was no difference between the spontaneous versus the induced groups in degree of nonhomogeneity as assessed by single-breath nitrogen tests. Changes in specific airway conductance after a DI during spontaneous obstruction were in the same direction as the changes in Vmax, and the time course for restitution of airway caliber in subjects who showed bronchoconstriction after a DI was significantly longer than for those subjects who showed bronchodilatation. We conclude that in severe bronchial asthma with spontaneous obstruction, a DI produces an increase in severity that is opposite to the results found in acutely induced obstruction, and the time course for reestablishing baseline airway caliber is more prolonged. We suggest that mechanisms for and sites of obstruction vary between the 2 groups.

Acute Disease↗
PubMed1987

Epidemiology of bronchial hypersecretion: recent studies.

The predominant cause of mucus hypersecretion in Westernized countries is smoking. Mucus hypersecretion in smokers is correlated with the subsequent development of bronchial carcinoma but there is no definite causal relation to progressive airflow obstruction. The distinction between hypersecretion and the development of airflow obstruction may also be relevant in childhood and occupational respiratory disease. Endogenous factors may also be important, as suggested by the increased prevalence of hypersecretion in asthma, but are difficult to detect by epidemiological techniques.

Airway Obstruction↗
PubMed1985

Smoking, allergy, and the differential white blood cell count.

Dutch workers have proposed that people with asthma and those smokers who develop chronic airflow obstruction share a common allergic constitution. To study whether smoking itself is associated with indicators of allergy, we have examined 237 men aged 51-61 years (120 smokers, 73 ex-smokers, and 44 non-smokers) who were recruited to a long term study of lung function in 1974, at which time men with a clinical diagnosis of asthma were excluded. Smokers, ex-smokers, and non-smokers did not differ in personal or family history of allergic disease, but the prevalence of positive responses to skinprick tests was greater in ex-smokers (59%) than in the other two groups (33% and 34%). In men with negative responses to skinprick tests total serum IgE was greater in smokers (log10 mean 1.41 IU/ml) and in ex-smokers (log10 mean 1.53 IU/ml) than in non-smokers (log10 mean 1.12 IU/ml). In men with positive skin test responses serum IgE was similar in the three groups (log10 mean ranging from 1.68 to 1.78 IU/ml). Geometric mean total white cell counts in the peripheral blood were higher in smokers (7.34 X 10(9)/l) than in non-smokers (5.82 X 10(9)/l); the value in ex-smokers (6.16 X 10(9)/l) was intermediate. Absolute blood eosinophil counts were increased in smokers disproportionately to the increase in total white cell count. Thus smoking is associated with small increases in some markers of allergy. These changes are probably acquired after the onset of smoking but sequential studies are required to amplify these cross sectional observations. Smokers whose skin test responses are positive appear more likely to give up smoking.

Adult↗
PubMed1985

Bronchial reactivity to inhaled histamine and annual rate of decline in FEV1 in male smokers and ex-smokers.

We examined the relations between bronchial reactivity, baseline FEV1, and annual decline of height corrected FEV1 (delta FEV1/ht3) over 7.5 years in 227 men (117 smokers, 71 ex-smokers, and 39 non-smokers). Men with a clinical diagnosis of asthma or receiving bronchodilator treatment were excluded. Bronchial reactivity was determined as the provocation concentration (PC20) of inhaled histamine sufficient to reduce FEV1 by 20%; subjects were divided into reactors (PC20 less than or equal to 16 mg/ml) and non-reactors (PC20 greater than 16 mg/ml). Thirty per cent of smokers, 24% of ex-smokers, and 5% of non-smokers were reactors. When smokers who were reactors were compared with non-reactors, the reactors showed a lower baseline FEV1 as percentage predicted in 1981-2 (85% v 108%), and a faster delta FEV1/ht3 (14.1 v 9.2 ml/y/m3). Baseline FEV1 correlated with PC20 in both smokers (rs = 0.51) and ex-smokers (rs = 0.61), and all 15 subjects with an FEV1 under 80% of the predicted value were reactors. In ex-smokers delta FEV1/ht3 was similar in reactors and non-reactors (m 9.0 v 7.4 ml/y/m3), despite significant differences in baseline FEV1. When analysis was confined to men with a baseline FEV1 over 80% predicted, the prevalence of reactors was significantly increased among smokers and slightly increased among ex-smokers compared with non-smokers, though the mean FEV1 was higher in the non-smokers. Bronchial reactivity was not increased in smokers aged 35 years or less. In smokers delta FEV1/ht3 was faster in those with a personal history of allergy (usually allergic rhinitis), but was not related to a family history of allergic disease, total serum immunoglobulin E level, absolute blood eosinophil count, or skinprick test score. delta FEV1/ht3 was also faster in all subjects taking beta blocker drugs. Thus increased bronchial reactivity was associated with accelerated decline of FEV1 in smokers. Although the association could be a consequence of a lower lower baseline FEV1, a trend towards increased reactivity was found in smokers with normal baseline FEV1 and delta FEV1/ht3 was dissociated from increased reactivity in ex-smokers. These findings are compatible with the "Dutch hypothesis," but the association between allergic features and accelerated delta FEV1/ht3 was relatively weak, and increased reactivity may follow rather than precede the onset of smoking.

Bronchi↗
PubMed1985

Abnormal ventilation scans in middle-aged smokers. Comparison with tests of overall lung function.

We have assessed the uniformity of regional ventilation during tidal breathing using continuous inhalation of krypton-81m in 43 male, lifelong nonsmokers and 46 male, current cigarette smokers (mean daily consumption 24.1 cigarettes/day) between 44 and 61 yr of age and with mild or no respiratory symptoms. All subjects had normal chest radiographs. The results of the ventilation scans were compared with tests of overall lung function (spirometry, maximal expiratory flow-volume curves, and single-breath N2 test). Diffuse abnormalities of the ventilation scan were found in 19 (41%) of the 46 smokers but in none of the nonsmokers. Focal abnormalities were found in 7 smokers and 3 nonsmokers. Smokers showed the expected abnormalities in overall lung function (reduced FEV1 and VC, increased single-breath N2 slope, and closing volume), but in individual smokers there was only a weak relation between the severity of abnormality of overall lung function and an abnormal ventilation scan. Abnormal scans could be found when overall lung function was normal and were not invariably found when significant abnormalities in FEV1/VC or N2 slope were present. There was no relation between the presence of chronic expectoration and an abnormal scan. The prognostic significance of an abnormal ventilation scan in such smokers remains to be established.

Adult↗
PubMed1985

Increase in tracheal size with age. Implications for maximal expiratory flow.

Because mechanical properties of central airways play an important role in determining maximal expiratory flow, we examined how tracheal size and maximal expiratory flow changed with age in 50 asymptomatic men, 19 to 61 yr of age, who were lifelong nonsmokers. Cross-sectional area (X-SA) of the intrathoracic trachea was estimated from posteroanterior and lateral chest radiographs taken at full inflation. Maximal expiratory flow-volume curves and spirometry were measured by standard techniques. Tracheal X-SA averaged 2.81 cm2 (SD, 0.38) at mean age 21.1 yr and 3.22 cm2 (SD,0.41) at mean age 52.5 yr, and correlated with peak expiratory flow (PEF) (r = 0.522, p less than 0.001) and FEV1 (r = 0.437, p = less than 0.01) (both expressed as percent predicted values based on age and height). These relationships were weaker than previously described in young men. The results suggest that with increasing age, large airways lose elastic recoil, as previously described for the air spaces. Aging changes in the airways may offset the unfavorable effects of loss of lung recoil and account for the relatively good preservation of PEF and the lack of rise in airways resistance with increasing age.

Adult↗
PubMed1985

Smoking and the development of progressive airflow obstruction.

An overall relation between cigarette smoking and the development of progressive airflow obstruction is established but only a minority of smokers ever develop severe airway narrowing; with the striking but rare exception of homozygous alpha 1-antitrypsin deficiency, the causes of this variation in susceptibility between smokers are uncertain. Possible associated risk factors may be classified under three broad headings--exogenous irritants, broncho-pulmonary infections and endogenous or 'host' factors--and will be briefly reviewed in this paper. But first the natural history of progressive airflow obstruction must be considered because this determines how potential risk factors can be assessed.

Age Factors↗