Venous Plasma Histamine in Exercise- and Hyperventilation Induced Asthma in Man

1981 ◽  
Vol 61 (2) ◽  
pp. 159-162 ◽  
Author(s):  
P. J. Barnes ◽  
M. J. Brown

1. Venous plasma histamine was measured by a specific and sensitive radioenzymatic assay in seven male extrinsic asthmatic and six age-matched non-atopic non-asthmatic male subjects during exercise and voluntary isocapnic hyperventilation. 2. There was no change in peak expiratory flow in normal subjects with exercise or hyperventilation, but asthmatic subjects showed a 29.4 ± sem 5.8% fall after exercise and a 29.0 ± 5.4% fall after matched hyperventilation. 3. Plasma histamine was significantly higher (P < 0.05) in asthmatic (6.2 ± 0.95 nmol/l) than that in normal subjects (3.4 ± 0.61 mmol/l) and showed a significant (P < 0.01) rise (to 14.4 ± 1.83 nmol/l) during exercise in asthmatic, but not in normal subjects. This suggests that discharge of mast-cell mediators may occur during exercise in asthmatic subjects who develop exercise-induced asthma. 4. With hyperventilation there was no change in plasma histamine in either asthmatic or normal subjects, but this does not exclude the possibility that mediators may be released locally in the airways.

1981 ◽  
Vol 61 (2) ◽  
pp. 151-157 ◽  
Author(s):  
J. P. R. Hartley ◽  
T. J. Charles ◽  
R. D. H. Monie ◽  
A. Seaton ◽  
W. H. Taylor ◽  
...  

1. Arterial plasma histamine concentrations, forced expiratory volume in 1.0 s (FEV1.0) and peak expiratory flow rate were determined in nine patients with exercise-induced asthma and in five control subjects before and after 8 min of cycle-ergometer exercise. 2. In the controls neither FEV1.0 nor peak expiratory flow rate fell by more than 5% in any individual during the 30 min postexercise period. The asthmatic patients all experienced a fall in FEV1.0 or peak expiratory flow rate, or both, of 15% or more in the period 5–20 min after completion of the exercise. 3. There was no difference between the control subjects and the asthmatic patients in the plasma histamine response to exercise. In both groups there was an insignificant rise of about 40% during exercise, although the initial levels were higher in the asthmatic patients. 4. The mean plasma histamine peak of the asthmatic patients preceded the mean maximal fall of FEV1.0 and peak expiratory flow rate by approximately 15 min. However, no positive correlation was found between rise in, or peak, plasma histamine levels and decrease in lung function. 5. Three non-atopic asthmatic patients had a significantly higher mean plasma histamine concentration during exercise than had the atopic subjects. 6. A strong positive correlation in asthmatic patients, and asthmatic and control subjects together was found between age and mean postexercise plasma histamine concentrations. 7. The results do not support a direct role for histamine in the production of exercise-induced asthma.


BMJ ◽  
1973 ◽  
Vol 3 (5874) ◽  
pp. 282-284 ◽  
Author(s):  
I. Gregg ◽  
A. J. Nunn

1973 ◽  
Vol 45 (4) ◽  
pp. 533-541
Author(s):  
P. Jaffe ◽  
P. König ◽  
O. Ijaduola ◽  
S. Walker ◽  
S. Godfrey

1. The changes in peak expiratory flow rate (PEF) and plasma cortisol were studied in relation to a 6 min period of treadmill running in six normal and eighteen asthmatic subjects. Of the asthmatics patients, five were not receiving treatment with steroids, six were receiving low doses of steroids (under 7·5 mg of prednisone daily) and seven were receiving high doses of steroids (over 7·5 mg of prednisone daily) at the time of study. 2. All subjects were studied twice within 1 week at similar times of day, once after premedication with sodium cromoglycate (SCG) and once after a placebo. 3. Resting PEF and plasma cortisol did not differ between placebo and SCG tests. 4. No change in PEF occurred as a result of exercise in the control subjects. The asthmatic patients developed post-exercise bronchoconstriction which was partly prevented by SCG but was not affected by steroids. 5. Plasma cortisol rose after exercise in the asthmatic subjects but not in the control subjects. The rise may have been related to the stress of exercise-induced asthma. SCG had no significant effect on plasma cortisol after exercise.


2004 ◽  
Vol 11 (3) ◽  
pp. 197-199 ◽  
Author(s):  
Dianna Louie ◽  
Peter D Paré

Exercised-induced asthma is not due to exercise itself per se, but rather is due to cooling and/or drying of the airway because of the increased ventilation that accompanies exercise. Travel to high altitudes is accompanied by increased ventilation of cool, often dry, air, irrespective of the level of exertion, and by itself, this could represent an 'exercise' challenge for asthmatic subjects. Exercise-induced bronchoconstriction was measured at sea level and at various altitudes during a two-week trek through the Himalayas in a group of nonasthmatic and asthmatic subjects. The results of this study showed that in mild asthmatics, there was a significant reduction in peak expiratory flow at very high altitudes. Contrary to the authors' hypothesis, there was not a significant additional decrease in peak expiratory flow after exercise in the asthmatic subjects at high altitude. However, there was a significant fall in arterial oxygen saturation postexercise in the asthmatic subjects, a change that was not seen in the nonasthmatic subjects. These data suggest that asthmatic subjects develop bronchoconstriction when they go to very high altitudes, possibly via the same mechanism that causes exercise-induced asthma.


2012 ◽  
Vol 20 (01) ◽  
pp. 099-102
Author(s):  
SALMAN AYYAZ ◽  
M. AZAM MUSHTAQ ◽  
SHAKEEL AHMED KHAN

Objective: To ascertain the effects of cotton dust on the peak expiratory flow of cotton mill workers in comparison with thehealthy controls who never exposure to the cotton dust. Setting: Outpatient Department of Pulmonology, Nishtar Hospital, Multan.Period: August 2011 to March 2012. Material and methods: A total of 200 male subjects (100 healthy controls and 100 cotton millworkers) who strictly met the inclusion criteria were selected from the OPD. Results: The peak expiratory flow rate (PEFR) (L/min) ofcotton mill workers was significantly lower as compared to the control subjects and this impairment was directly proportional to theduration of exposure to the cotton dust in the mail. Conclusions: It was concluded from the study that the peak expiratory flow rate wasdecreased in the cotton mill workers.


2000 ◽  
Vol 89 (1) ◽  
pp. 283-290 ◽  
Author(s):  
Martin R. Miller ◽  
Ole F. Pedersen

Previous studies have shown that the added resistance of a mini-Wright peak expiratory flow (PEF) meter reduced PEF by ∼8% in normal subjects because of gas compression reducing thoracic gas volume at PEF and thus driving elastic recoil pressure. We undertook a body plethysmographic study in 15 patients with chronic obstructive pulmonary disease (COPD), age 65.9 ± 6.3 yr (mean ± SD, range 53–75 yr), to examine whether their recorded PEF was also limited by the added resistance of a PEF meter. The PEF meter increased alveolar pressure at PEF (Ppeak) from 3.7 ± 1.4 to 4.7 ± 1.5 kPa ( P = 0.01), and PEF was reduced from 3.6 ± 1.3 l/s to 3.2 ± 0.9 l/s ( P = 0.01). The influence of flow limitation on PEF and Ppeak was evaluated by a simple four-parameter model based on the wave-speed concept. We conclude that added external resistance in patients with COPD reduced PEF by the same mechanisms as in healthy subjects. Furthermore, the much lower Ppeak in COPD patients is a consequence of more severe flow limitation than in healthy subjects and not of deficient muscle strength.


1979 ◽  
Vol 57 (1) ◽  
pp. 39-45 ◽  
Author(s):  
T. J. Charles ◽  
S. J. Williams ◽  
A. Seaton ◽  
Christine Bruce ◽  
W. H. Taylor

1. Arterial and venous whole blood and plasma histamine concentrations and eosinophil and basophil counts were determined in five patients with acute severe asthma who had not previously received steroid therapy, in five who had been maintained on steroid therapy and in a control group of nine patients with acute non-respiratory illnesses. 2. No significant arteriovenous differences were observed for any of these measurements in any of the groups of patients. Significant net loss of arterial histamine does not therefore occur peripherally in acute asthma. 3. When compared with the values for the controls, statistically significant increases were observed, in the group not receiving steroids, for arterial and venous whole blood histamine concentrations, eosinophil counts and basophil counts, and, in those receiving steroids, for the venous basophil counts. 4. When compared with the venous plasma histamine concentration of normal subjects, that of the asthmatic subjects not receiving steroids was significantly raised. 5. The venous plasma histamine concentration of the control group was also significantly higher than that of normal subjects, but less so than in the asthmatic subjects, suggesting that acute illness per se produces an increased plasma histamine concentration. 6. Both groups of asthmatic patients were treated similarly with hydrocortisone and bronchodilators. There was a striking fall in whole blood histamine concentration and in eosinophil and basophil counts, but plasma histamine fell more slowly, especially in those who had not previously received steroids. 7. The mean histamine content of the basophil cell is 0·01 pmol and significant differences in this value did not occur within the various groups or as a result of treatment. The approximate number of molecules of histamine per basophil cell is 6·0 × 109.


1992 ◽  
Vol 83 (2) ◽  
pp. 227-232 ◽  
Author(s):  
Michael F. Fitzpatrick ◽  
Thomas MacKay ◽  
Carol Walters ◽  
Po-Chun Tai ◽  
Martin K. Church ◽  
...  

1. To investigate the role of mast cells and eosinophils in the pathogenesis of nocturnal asthma, the plasma methylhistamine concentration, serum eosinophil cationic protein level and peak expiratory flow rate were measured 2-hourly for 24 h in 10 patients with nocturnal asthma and in 10 healthy control subjects. Nocturnal asthma was defined as at least one nocturnal awakening per week due to cough, wheeze or breathlessness with an average overnight fall in peak expiratory flow rate of at least 15% during a 2-week run-in period. 2. The lowest peak expiratory flow rate occurred at 02.00–04.00 hours in the group with nocturnal asthma, whose overnight fall in peak expiratory flow rate was 29 ± 5% in comparison with 5 ± 1% (means ± sem) in the normal subjects. 3. Plasma methylhistamine levels at night (0.200–04.00 hours) were lower than during the day (10.00–20.00 hours) in both asthmatic patients and normal subjects (asthmatic patients: day, median 0.22 ng/ml, 95% confidence intervals 0.18–0.34 ng/ml; night, 0.17 ng/ml, 0.13–0.24 ng/ml; P<0.01; normal subjects: day, 0.31 ng/ml, 0.24–0.41 ng/ml; night, 0.24 ng/ml, 0.21–0.33 ng/ml; P<0.01). 4. The serum eosinophil cationic protein level was higher by day (30 ng/ml, 8–47 ng/ml) than by night (21 ng/ml, 5–34 ng/ml; P<0.04) in the group with nocturnal asthma, but did not change significantly with the time of day in the normal subjects (day: 8 ng/ml, 4–14 ng/ml; night: 8 ng/ml, 5–21 ng/ml). 5. Peripheral blood eosinophil counts fell in the early morning in the patients with nocturnal asthma (day: 0.52 × 109/l, 0.14–0.76 × 109/l; night: 0.29 × 109/l, 0.13–0.57 × 109/l; P= 0.03), but did not change significantly in the normal subjects. 6. This study indicates that a rise in plasma histamine concentration is not a prerequisite for nocturnal asthma.


2002 ◽  
Vol 165 (9) ◽  
pp. 1304-1308 ◽  
Author(s):  
Claudio Tantucci ◽  
Alexandre Duguet ◽  
Pietro Giampiccolo ◽  
Thomas Similowski ◽  
Marc Zelter ◽  
...  

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