Exercise and isocapnic hyperventilation-induced bronchoconstriction in asthma: Relevance of circulating basophils to measurements of plasma histamine

Howarth, Peter H.; Pao, George J-K; Church, Martin K.; Holgate, Stephen T.

doi:10.1016/0091-6749(84)90414-7

Cited by 46 publications

(24 citation statements)

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“…Some investigators have reported increased levels of histamine and neutrophil chemotactic factors in the serum ofpatients postexercise, and suggest that exercise-induced asthma is due to mediator release from mast cells (9,10,16,17). Other investigators have failed to detect such mediators (11,12,15), while yet others report similar increases after exercise of nonasthmatic individuals (13,14). We feel that our finding of mediator release in the upper respiratory tract supports the hypothesis that mast cell mediator release is involved in exercise-induced asthma.…”

Section: Discussionsupporting

confidence: 79%

“…This condition is experienced by most asthmatic patients, and controversy exists among investigators regarding its pathogenesis. Attempts to establish the involvement of mast cell mediators have led to ambiguous results (9)(10)(11)(12)(13)(14)(15)(16)(17). Recently, low levels of histamine and another mediator, neutrophil chemotactic factor, have been found in the circulation of asthmatic patients when they exercise while breathing cold air (9,10,16,17), but not upon breathing warm and moist air (WMA) (18).…”

Section: Introductionmentioning

confidence: 99%

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Nasal challenge with cold, dry air results in release of inflammatory mediators. Possible mast cell involvement.

et al. 1985

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The purpose of our study was to assess the effect of cold, dry air (CDA) on the nasal mucosa of selected individuals in relation to the release of inflammatory mediators associated with mast cells. 12 subjects with a history of nasal symptoms of rhinorrhea and congestion upon cold or dry environmental exposure were challenged by nasal breathing of CDA and warm, moist air (WMA). Each subject was tested on two occasions with the order of the challenges reversed. Symptom scores were recorded, and the levels of histamine, prostaglandin (PG) D2, kinins, and 1H1-N-a-tosyl-L-arginine methyl ester (TAME)-esterase activity in nasal lavage fluids were measured.CDA caused a significant increase in mediator levels and in symptom scores as compared to baseline or to WMA. No significant increase in symptom scores or mediators was noted after WMA challenge, with the exception of a marginal increase in kinins. The response to CDA was similar, regardless of challenge order. Changes in mediators correlated with one another, and symptom scores correlated significantly with the levels of histamine, kinins, and PGD2. Five subjects without a history of nasal symptoms on cold air exposure had no change in mediators or symptom scores after CDA or WMA challenge. We conclude that CDA causes the release of inflammatory mediators possibly associated with mast cells and speculate that such a mechanism may be involved in the bronchospasm induced by CDA in asthmatics.

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Section: Discussionsupporting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Nasal challenge with cold, dry air results in release of inflammatory mediators. Possible mast cell involvement.

et al. 1985

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“…This confusion is probably due to the technical difficulties with measuring small changes in circulating concentrations of histamine following exercise. Since the basophil is another potential source of histamine, it has been suggested that the increases in plasma or whole-blood histamine can be attributed to the basophilia which ensues exercise [20,39]. 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.…”

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]. 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].…”

Section: Aamentioning

confidence: 99%

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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“…It has been shown that in asthmatic subjects bronchoconstriction can be induced after dry and/or cold air hyperventilation challenge (Howarth et al 1984;Farley et al 1988;Gilbert et al 1988). The mechanism of HIB has been studied mainly in humans (Howarth et al 1984;Farley et al 1988 ;Gilbert et al 1988) but it is still unclear. In the human, it has been proposed that water loss or heat loss from airways plays an important role in HIB and also in exercise induced bronchoconstriction (EIB) (Farley et al 1988; Gilbert et al 1988).…”

Section: Discussionmentioning

confidence: 99%

Eucapnic Hyperventilation-Induced Bronchoconstriction in Rabbits.

Koyama

Ohtsuka

Horie

1992

Tohoku J. Exp. Med.

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We examined whether eucapnic hyperventilation with dry air produces the bronchoconstriction in anesthetized, non-sensitized rabbits and in ovalbumin sensitized rabbits. Eucapnic hyperventilation challenge with dry air containing 5% COZ at room temperature was performed with 4 non-sensitized and 7 sensitized rabbits by mechanical ventilation for 15 min (120 breaths/min, 7 ml tidal volume/kg body weight). Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before and 0, 5, 15, and 30 min after hyperventilation. In non-sensitized rabbits, RL and Cdyn did not change significantly. However, in sensitized rabbits, RL increased maximally by 48.9%±9.0% at 5 min, and then decreased to the baseline level at 30 min after challenge. Cdyn decreased maximally by 12.5%± 3.5% at 15 min after challenge. These changes were significantly different from the baselines (p <0.05). Furthermore, to investigate the role of histamine on hyperventilation-induced bronchoconstriction (HIB) in sensitized rabbits, we performed the hyperventilation challenges in 5 sensitized rabbits with the pretreatment of Hl-receptor antagonist (chlorpheniramine, 1 mg/kg, iv.) and found that the maximum increment of RL was suppressed to 24.2%± 7.4% of the control, which was significantly lower than the maximal RL in nontreated sensitized rabbits (p <0.05). We concluded that HIB occurrs only in sensitized rabbits and that histamine may play an important role in the development of HIB in sensitized rabbits.hyperventilation-induced bronchoconstriction ; ovalbumin sensitized rabbits ; chlorpheniramine It has been reported that hyperventilation or exercise challenge can produce bronchoconstriction in some asthmatic subjects. However, the mechanisms of hyperventilation-induced (HIB) and exercise-induced bronchoconstriction (EIB) remain uncertain. Recently, several animal studies were reported clarifying the mechanisms of HIB. coworkers (1988, 1989) demonstrated that HIB in guinea pigs was diminished with humidification of inspired gas, which was reproduced on consecutive identical challenges, and that HIB was independent of

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Exercise and isocapnic hyperventilation-induced bronchoconstriction in asthma: Relevance of circulating basophils to measurements of plasma histamine

Cited by 46 publications

References 38 publications

Nasal challenge with cold, dry air results in release of inflammatory mediators. Possible mast cell involvement.

Nasal challenge with cold, dry air results in release of inflammatory mediators. Possible mast cell involvement.

Evidence for mast cell activation during exercise-induced bronchoconstriction

Eucapnic Hyperventilation-Induced Bronchoconstriction in Rabbits.

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