Exercise-induced release of histamine and neutrophil chemotactic factor in atopic asthmatics

Lee, T.H.; Brown, M. J.; Nagy, L; Causon, R. C.; Walport, Mark J.; Kay, A. B.

doi:10.1016/0091-6749(82)90232-9

Cited by 186 publications

(48 citation statements)

References 21 publications

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“…However, NAGAKURA et al [40] demonstrated a rise in histamine that was restricted to those who had experienced EIB, despite the fact that both EIB-positive and EIB-negative asthmatics had similar postexercise basophilia. Measurements of increased mast cell-associated neutrophil chemotactic factor (NCF) following exercise [15,41] lend further support to the hypothesis that mast cells are activated during EIB.…”

Section: Discussionmentioning

confidence: 75%

“…Previously, several groups have utilized histamine as a marker for mast cell activation in EIB, without producing conclusive results [14][15][16][17]. This confusion is probably due to the technical difficulties with measuring small changes in circulating concentrations of histamine following exercise.…”

Section: Discussionmentioning

confidence: 99%

“…Some studies have reported an elevation in plasma and whole blood histamine concentrations following EIB [14,15], while other studies have failed to verify those findings [16,17]. Apart from the methodological problems encountered when sampling plasma histamine [18] and its short half-life in the circulation, approximately 1 min [19], it has been suggested that elevations in plasma histamine mainly reflect the basophilia which normally accompanies exercise [20].…”

Section: Aamentioning

confidence: 99%

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Evidence for mast cell activation during exercise-induced bronchoconstriction

O’Sullivan¹,

Roquet²,

Dahlén³

et al. 1998

Eur Respir J

125

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Exercise-induced bronchoconstriction (EIB) is thought to occur in 70-80% of asthmatics, most commonly amongst those with moderate-to-severe airway hyperresponsiveness [1]. It is characterized by transient airflow obstruction resulting in a Š15% decrease in forced expiratory volume in one second (FEV1) following 5-8 min of exercise. The fall in FEV1 reaches a maximum approximately 10 min after exercise and gradually normalizes over the next hour [2]. The precise pathophysiology of EIB remains unclear, although it is widely accepted that during exercise the upper airways are unable to adequately warm and humidify the increased volumes of inspired air. This results in airway cooling and increased airway fluid osmolality in the lower airways [3,4]. One hypothesis suggests that hyperosmolar triggering of mast cells and possibly other inflammatory cells results in the release of bronchoconstricting mediators, e.g. cysteinyl-leukotrienes (cys-LTs), histamine and prostaglandin (PG)D 2 [5].Previous indications for the participation of mast cell mediators in the pathogenesis of EIB are based on pharmacological data. For example, disodium cromoglycate (DSCG), a drug which stabilizes mast cell membranes, is effective in blunting exercise-induced asthma [6,7]. Pretreatment with a number of H 1 receptor antagonists has been shown to attenuate EIB [8][9][10]; however, the degree of protection afforded by this class of drugs has been modest. More recently, studies employing leukotriene receptor antagonists [11,12] and biosynthesis inhibitors [13] have implicated leukotrienes in the airway bronchoconstrictor response to exercise.The direct approach of measuring mast cell mediator release in response to exercise challenge has yielded ambiguous results. Some studies have reported an elevation in plasma and whole blood histamine concentrations following EIB [14,15], while other studies have failed to verify those findings [16,17]. Apart from the methodological problems encountered when sampling plasma histamine [18] and its short half-life in the circulation, approximately 1 min [19], it has been suggested that elevations in plasma histamine mainly reflect the basophilia which normally accompanies exercise [20]. Increases in the levels of tryptase and PGD 2 , both specific mast cell markers, have been detected in nasal lavage following nasal provocation with cold dry air [21], but not after exercise [22,23].The purpose of this study was to provide evidence to establish mast cell activation as a feature of EIB. To this end, a combination of mast cell markers, 9α,11β-PGF 2 Sullivan, A. Roquet, B. Dahlén, F. Larsen, A. Eklund, M. Kumlin, P.M. O'Byrne, S-E. Dahlén. ©ERS Journals 1998. ABSTRACT: Controversy remains about the causative mediators in the bronchoconstrictive response to exercise in asthma. This study examined whether mast cell activation is a feature of exercise-induced bronchoconstriction by measuring urinary metabolites of mast cell mediators. Evidence for mast cell activation during exercise-induced bronchoconstriction....

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Section: Aamentioning

confidence: 99%

See 1 more Smart Citation

Evidence for mast cell activation during exercise-induced bronchoconstriction

O’Sullivan¹,

Roquet²,

Dahlén³

et al. 1998

Eur Respir J

125

View full text Add to dashboard Cite

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“…It has been postulated that cooling and/or drying of the airways by hyperventilation acts as a stimulus for mast cell degranulation since elevation of histamine (Harries et al, 1979) and neutrophil chemotactic factor (NCF) (Lee et al, 1982a) have been reported in association with EIA and the mast cell stabilising agent sodium cromoglycate is known to inhibit both the EIA and the accompanying rise in histamine (Lee et al, 1982b). Baseline Exercise Time post-exercise (min) Figure 2 The effect of placebo (0) and three oral doses of nifedipine (10 mg *, 20 mg, A, 30 mg *) on heart rate, systolic and diastolic blood pressure.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of exercise‐induced asthma by nifedipine: a dose‐response study.

Rafferty

Varley

et al. 1987

Brit J Clinical Pharma

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1. The effect of three single doses of nifedipine on exercise‐induced asthma has been examined in 11 asthmatic subjects. 2. On four separate days patients undertook 6 min of exercise on a treadmill 30 min after taking placebo or nifedipine 10, 20 or 30 mg administered double‐blind and in random order. 3. Nifedipine had no significant effect on resting FEV1 measurements. 4. Nifedipine, in doses of 10, 20 and 30 mg, inhibited exercise induced bronchoconstriction, reducing the maximum fall in FEV1 from 30.8 +/‐ 3.5% after placebo to 21.9 +/‐ 3.4% (NS), 13 +/‐ 3.4% (P less than 0.01) and 15 +/‐ 3.9% (P less than 0.01) respectively. 5. This study has shown that the protective effect of nifedipine against exercise‐induced asthma is dose related with the maximum inhibitory effect being observed with a single dose of 20 mg.

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“…Although it is widely accepted that either heat or water loss from the airways during exercise is the stimulus for EIA, the mechanism by which these stimuli induce constriction of the bronchial smooth muscle remains unknown (I). One hypothesis is that EIA develops after the release of chemical mediators, such as histamine and neutrophil chemotactic factor, from cells located in the bronchial mucosa (2,3). However, the involvement of histamine release in EIA is controversial because several laboratories have failed to demonstrate histaminemia in this condition (4), suggesting that plasma histamine changes may be related to the associated basophilia and sample handling rather than to intrapulmonary mast cell activation (S).…”

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confidence: 99%

Exercise-Induced Urinary Excretion of Leukotriene E4 in Children with Atopic Asthma

et al. 1991

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MATERIALS AND METHODSbeen suggested to have an important role not only in asthma but also in other diseases, such as neonatal persistent pulmonary hypertension and acute viral respiratory infections in children (6)(7)(8). However, little is known about the role of the sulfidopeptide LT in EIA. Arterial blood sampling is considered necessary to preclude the artificial formation of these sulfidopeptide LT (9), inasmuch as the high concentrations reportedly detected in plasma derived from venous blood are probably due to cellular injury during sample collection (9, 10). This seems to be an especially big problem in blood collection from infants and young children. Furthermore, the initial product of sulfidopeptide LT, LTC, is reportedly unstable even when stored at low temperatures (II), whereas LTE 4 is relatively more stable than LTC or LTD 4 in urine, even at 37°C (12). Therefore, to examine the role of these sulfidopeptide LT in EIA, we measured urinary LTE 4 concentrations before and after exercise in children with asthma of varying severities and explored the relationship of the urinary LTE4 concentration to the severity of asthma in EIA.Thirty-six children with a history of EIA, positive skin test to common allergens, and elevated IgE levels were entered into this study after informed consent was obtained. A control study with healthy children was not performed, because we could obtain informed consent from only a small number of healthy children and their parents. The children were classified as having either mild, moderate, or severe asthma, according to the criteria of the Japanese Research Group for Pediatric Allergy (Table 1). The classification of the patients was performed independently by other doctors unrelated to the measurement of urinary LTE 4 , before the urinary LTE 4 assay. The children with mild asthma could not produce enough urine for the assay. Urinary LTE 4 levels were measured in 10 children with severe asthma (age range: 7-12 y, mean: 9 y) and in seven children with moderate asthma (age range: 7-10 y, mean: 9 y), all of whom produced the required amount of urine (more than 60 mL) both before and after exercise. None of our subjects had used steroids or disodium chromoglycate for at least several months before the start of this investigation, with the exception of three children in the moderate asthma group who were using disodium chromoglycate. Subjects were asked to abstain from the intake of any medications for 12 h before the study.Exercise testing. Exercise was performed on a treadmill for 6 min with the speed set at 6.0 km/h and the incline set at a 10°. PEFR was measured using a peak flow meter (AS-SOO, Minato Medical Science, Osaka, Japan) before exercise and after exercise for up to 30 min. The best of three consecutive PEFR readings at each time point was used for subsequent analysis. All procedures were undertaken at ambient room temperature.Collection of urine samples. Subjects were asked to pass urine 2 h after exercise. Urine was actually collected from I to 2 h after exerc...

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Exercise-induced release of histamine and neutrophil chemotactic factor in atopic asthmatics

Cited by 186 publications

References 21 publications

Evidence for mast cell activation during exercise-induced bronchoconstriction

Evidence for mast cell activation during exercise-induced bronchoconstriction

Inhibition of exercise‐induced asthma by nifedipine: a dose‐response study.

Exercise-Induced Urinary Excretion of Leukotriene E4 in Children with Atopic Asthma

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