Plasma histamine changes during provoked bronchospasm in asthmatic patients

Bhat, Khurshid; Arroyave, Carlos M.; Marney, Samuel R.; Stevenson, Donald D.; Tan, Eng M.

doi:10.1016/0091-6749(76)90176-7

Cited by 104 publications

(21 citation statements)

References 21 publications

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“…During an acute episode of asthma, activation of mast cells might cause abnormal release of chemical mediators, resulting in excessive stimulation of smooth muscle and mucous glands. This hypothesis is supported by the findings of elevated amounts of mast-cell derived mediators in BAL fluid from cases of asthma following allergen challenge [26] and lower numbers of mast cells in biopsies obtained from patients during an episode of asthma than during symptom-free periods [27].…”

Section: Discussionsupporting

confidence: 69%

Distribution and degranulation of airway mast cells in normal and asthmatic subjects

Carroll

Mutavdzic²,

James³

2002

Eur Respir J

232

186

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It was hypothesized that the distribution and activation of mast cells across the airway wall may reflect their function in asthma.The density of mast cells (intact and degranulated) within airway compartments in cartilaginous and membranous airways, obtained from autopsies on patients with fatal asthma, nonfatal asthma, and nonasthmatic control cases have been examined.In cartilaginous airways, the mean¡SE density of mast cells in control cases was 27¡9 cells?mm -2 . It was similar in nonfatal asthma (24¡2 cells?mm -2 ) but reduced (pv0.05) in fatal asthma cases (16 ¡ 2 cells?mm -2 ). In membranous airways, the density of mast cells in control cases was 155 ¡ 21 cells?mm -2 and was higher (pv0.05) in cases of nonfatal (270 ¡ 51 cells?mm -2 ) and fatal asthma (219 ¡ 26 cells?mm -2 ). Mast-cell density was greatest on the smooth muscle and mucous glands in cartilaginous airways and on the smooth muscle and outer airway wall in membranous airways. The percentage of degranulated mast cells was higher (pv0.05) in cases of asthma, related to disease severity, and was higher in cartilaginous than membranous airways. Degranulation was greatest on the smooth muscle in fatal asthma cases.Mast-cell distribution and degranulation varies between cartilaginous and membranous airways and across the airway wall. Degranulation of mast cells is related to asthma severity. The increased degranulation in proximal airways may reflect stimulation via the inhaled route.

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Section: Discussionsupporting

confidence: 69%

Distribution and degranulation of airway mast cells in normal and asthmatic subjects

Carroll

Mutavdzic²,

James³

2002

Eur Respir J

232

186

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“…The se verity of bronchoconstriction with a relative low arterial plasma histamine concentration during antigen or histamine inhalation sug gest that a higher local histamine concentra tion at the site of the receptors is responsi ble for the bronchoconstriction [Zimmer mann et al, 1980d]. This is consistent with the report that greater changes in pulmonary function have been induced by histamine inhalation than by its systemic administration [Brown et al, 1977;Douglas et al, 1976;StaszewskaBarczak and Vane, 1965;Zimmermann et al, 1980d], Studies reported by Bhat et al [1977] suggest that the degree of responsiveness of an individual's bronchial tree to mediators, such as histamine, might be more important than the total amount of histamine availa ble. Although toxic doses of histamine pro duce no appreciable constriction of the bronchial tree in the normal man, small amounts evoke a definite bronchial con strictor effect in patients with bronchitis [Weiss et al, 1929;Curry, 1946;Krell, 1976].…”

Section: Discussionsupporting

confidence: 81%

Effect of Intravenous Histamine, Allergen <i>(Ascaris suum</i> Extract) and Compound 48/80 and Inhaled Allergen-Aerosol on Bronchoconstriction and Histamine Release

Zimmermann¹,

Ulmer²

1981

Respiration

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The effect of a histamine releaser (48/80), an antigen (Ascaris suum extract) and of exogenous histamine infusion on antigen aerosol-induced bronchoconstriction was investigated in 24 mongrel dogs. During these substance infusions, the high values of arterial plasma histamine did not correlate with the degree of bronchoconstriction. Further, a severe bronchoconstriction with a relatively low arterial plasma histamine concentration was observed during antigen inhalation. During substance inhalation, a high local concentration of histamine is assumed to explain the increased bronchial ‘sensitivity’ to actual plasma levels of histamine. Also, the responsiveness of the bronchial tree to antigen aerosol was observed to be reduced 90 min after induction of a strong histamine release. The importance of histamine in the first phase of immediate hypersensitivity is discussed.

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“…Two markers have attracted most at tention, histamine and high-molecular-weight neutro phil chemotactic factor (NCF). Early studies, which reported increases in circulating histamine following antigen provocation [36,37], are now thought to be largely invalid since the methods used to measure his tamine were insensitive, and the levels reported were higher than the physiological range [38], With the in troduction of single and double isotope methyltransferase assays for histamine, a number of independent laboratories have reported resting plasma levels in the region of 0.1-0.5 ng/ml in normal subjects and pa tients with mild asthma [39,40].…”

mentioning

confidence: 99%

Relationship between Mediator Release from Human Lung Mast Cells in vitro and in vivo

Holgate

Benyon

Howarth

et al. 1985

Int Arch Allergy Immunol

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There is now compelling evidence to incriminate bronchial mast cells in the pathogenesis of bronchoconstriction of allergic asthma. Human mast cells isolated from lung tissue or bronchoalveolar lavage release histamine and generate eicosanoids upon IgE-dependent activation. In this paper we present data that raise doubts about the significance of phospholipid methylation in IgE-dependent activation-secretion coupling and provide evidence that drugs such as 3-deazaadenosine inhibit mediator secretion by inhibiting phosphodiesterase, in addition to inhibiting putative methylation pathways. Activation of human mast cells and basophils also stimulates adenylate cyclase to increase levels of cyclic AMP, which, on the basis of pharmacological manipulation with purine nucleosides, we believe is involved in the progression of the secretory response. Human lung cells also generate both cyclo- and lipoxygenase products of arachidonate upon Ca⁺⁺-dependent stimulation with complex interactions occurring between these pathways in the presence of the leukotriene inhibitor, Piriprost. The role of mast cells in the immediate airway response to inhaled allergens in asthma was demonstrated by showing an interaction between nonspecific bronchial reactivity and mast cell reactivity in predicting the airway response upon antigen inhalation. Further confirmation of this concept was obtained by showing an inverse relationship between the release of histamine and neutrophil chemotactic factor (NCF) into the circulation induced by antigen challenge, and nonspecific airway reactivity. The identification of significant increases in circulating mediators following antigen provocation of patients with seasonal asthma enabled the effects of drugs used in the treatment of asthma to be compared on airway calibre and mast cell mediator release. Sodium cromoglycate partially inhibited the airway and plasma histamine responses with antigen, but totally inhibited the increases in NCF. Salbutamol completely inhibited all responses, while ipratropium bromide, which produced the same bronchoconstriction as achieved with salbutamol, had no effect. The potent H₁-antagonist astemizole partially inhibited bronchoconstriction without affecting histamine release. Antigen provocation produced a significant increase in circulating levels of the 13,14-dihydro-15-keto metabolite of PGF_2α which could originate from mast cell-derived PGD₂. In both retrospective and prospective studies, a close relationship was shown between nonspecific bronchial reactivity and resting airway calibre in asthma. These data suggest that release of inflammatory mediators are involved in the pathogenesis of the immediate airway response with antigen challenge, and that drugs used to treat asthma may have useful effects, both on the airways and on mediator-secreting cells. Since acquired bronchial hyperreactivity is related to airway inflammation and airway calibre, we propose that pharmacological control of mediator release in vivo represent...

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Plasma histamine changes during provoked bronchospasm in asthmatic patients

Cited by 104 publications

References 21 publications

Distribution and degranulation of airway mast cells in normal and asthmatic subjects

Distribution and degranulation of airway mast cells in normal and asthmatic subjects

Effect of Intravenous Histamine, Allergen <i>(Ascaris suum</i> Extract) and Compound 48/80 and Inhaled Allergen-Aerosol on Bronchoconstriction and Histamine Release

Relationship between Mediator Release from Human Lung Mast Cells in vitro and in vivo

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