Mechanisms of Forssman‐induced Bronchospasm and Their Inhibition

Butler, K.D.; Smith, J. F.

doi:10.1111/j.1476-5381.1981.tb16767.x

Cited by 18 publications

(4 citation statements)

References 10 publications

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“…Removal of circulating platelets (Pinckard et al, 1977;Butler & Smith, 1981;Lellouch-Tubiana et al, 1988) or neutrophils (Wedmore & Williams, 1981;O'Byrne et al, 1984) has been shown to diminish inflammatory reactions. In the present study, neither platelets nor neutrophils contribute to either antigen-induced airway eosinophilia or hyperreactivity.…”

Section: Discussionmentioning

confidence: 99%

Antigen challenge induces pulmonary airway eosinophil accumulation and airway hyperreactivity in sensitized guinea‐pigs: the effect of anti‐asthma drugs

Sanjar

Kristersson

et al. 1990

British J Pharmacology

188

114

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Guinea‐pigs were sensitized with 3 injections of ovalbumin (OA) (1 or 10 μg per animal) using Al(OH)3 and pertussis vaccine as adjuvants at two week intervals. Sensitized guinea‐pigs were challenged with an aerosol of OA (0.1%) over a one hour period and both airway reactivity and cellular content of bronchoalveolar lavage (BAL) fluid were assessed at intervals for up to 7 days. Guinea‐pigs sensitized with 1 μg of ovalbumin responded to an aerosol of OA with increased pulmonary airway eosinophilia, which was evident 1 day after challenge and was present for up to 7 days. Airway hyperreactivity was not detectable in these animals. Guinea‐pigs sensitized with 10 μg of ovalbumin responded to an aerosol of OA with increased pulmonary airway neutrophilia and eosinophilia and with increased airway reactivity which was maximal between 8 and 24 h after exposure to OA. Depletion of circulating platelets or neutrophils, by use of selective antisera, did not alter either the magnitude of eosinophilia or the intensity of airway reactivity in sensitized guinea‐pigs (10 μg) exposed to an aerosol of OA. Pretreatment of sensitized guinea‐pigs (10 μg) for 6 days with AH 21–132, aminophylline, dexamethasone or ketotifen inhibited pulmonary airway eosinophilia, but did not diminish airway hyperreactivity. Neither eosinophil accumulation nor development of airway hyperreactivity was influenced by treatment with mepyramine or salbutamol over a 6 day period before OA inhalation. Although eosinophilia may occur in association with increased airway reactivity in this animal model, there is no evidence of a causal relationship.

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Section: Discussionmentioning

confidence: 99%

Antigen challenge induces pulmonary airway eosinophil accumulation and airway hyperreactivity in sensitized guinea‐pigs: the effect of anti‐asthma drugs

Sanjar

Kristersson

et al. 1990

British J Pharmacology

188

114

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“…Guinea-pig anti-rabbit platelet serum (APS) was a kind gift of Dr K.D. Butler (Ciba-Geigy Pharmaceuticals, Horsham, U.K.), prepared according to the protocol described by Butler & Smith (1982).…”

Section: Preparation Of Anti-platelet Serummentioning

confidence: 99%

PAF‐induced bronchial hyperresponsiveness in the rabbit: contribution of platelets and airway smooth muscle

Coyle

Spina

Page

1990

British J Pharmacology

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Aerosol administration of platelet activating factor (PAF) to normal rabbits induced an enhanced airway responsiveness to inhaled histamine, 6 and 24 h after exposure. Following exposure to bovine serum albumin (BSA) as the carrier molecule for PAF, there was an increase in airway responsiveness to histamine 6h after challenge, although by 24 h this was not significantly different from the responsiveness of airways to histamine before BSA. PAF‐induced bronchial hyperresponsiveness at 24 h was associated with a substantial increase in the number of neutrophils and mononuclear cells and a small, but significant increase in the number of eosinophils in the lungs as assessed by bronchoalveolar lavage. BSA exposure failed to alter the total number of cells in the lungs, although there was a significant increase in the number of neutrophils in the bronchoalveolar lavage fluid. Selective platelet depletion with a guinea‐pig anti‐rabbit platelet serum inhibited PAF‐induced bronchial hyperresponsiveness. In addition, there was an attenuation of PAF‐induced airway inflammation in animals rendered thrombocytopenic. The contractile potency to histamine, methacholine and carbachol was similar in intrapulmonary bronchi taken from rabbits exposed to an aerosol of BSA or PAF. Furthermore, the relaxant potency to the non‐selective β‐adrenoceptor agonist isoprenaline, was unaltered in PAF‐treated rabbits. In contrast, there was a 2.58 fold reduction in the relaxant potency to theophylline in rabbits exposed to PAF compared with rabbits exposed to BSA. These results suggest that in the rabbit, PAF‐induced bronchial hyperresponsiveness at 24 h is associated with airways inflammation and is dependent upon platelet activation, but is not related to changes in airway smooth muscle function.

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“…Histological examination of lungs excised from experimental animals undergoing bronchoconstrictor responses confirms that platelet aggregates are pres ent within the pulmonary vasculature [9,11], How ever, use of histological procedures for routine assess ment of platelet accumulation in experimental ani mals is both laborious and relatively insensitive, since large numbers of animals are needed to define the kinetics of platelet accumulation in any detail. In the present study, a non-invasive technique for continu ous monitoring of platelet accumulation in vivo [12] has been used to investigate the temporal relationship between platelet accumulation and increased airway resistance during responses to PAF-acether or anti gen.…”

Section: Introductionmentioning

confidence: 99%

“…These clin ical observations have an experimental counterpart, since bronchospasm may accompany intravascular aggregation of platelets, or embolization of inert par ticles [3][4][5][6][7], Platelet activation might be considered important in the bronchoconstrictor responses pro duced by collagen [8], Forssman antiserum [9], platelet-activating factor (PAF-acether) [10] or antigen [11], since such responses can be inhibited by pretreat ment with either anti-platelet antiserum or with drugs which inhibit the release reaction of platelets.…”

Section: Introductionmentioning

confidence: 99%

Platelets and Bronchospasm

Page¹,

Paul²,

Morley³

1984

Int Arch Allergy Immunol

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The intrathoracic accumulation of radiolabelled platelets and concomitant changes in airway resistance have been recorded continuously in anaesthetised guinea pigs. Platelet-activating factor (PAF-acether) and antigen (in sensitised animals) elicited dose-related intrathoracic accumulation of platelets that could be associated with an increase in airway resistance. Maximal increases in airway resistance preceded maximal increases in platelet accumulation. Low doses of antigen could elicit substantial platelet accumulation, without detectable changes in lung function. It is concluded that physical obstruction of the pulmonary vasculature is not the sole determinant of platelet-dependent bronchoconstriction.

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Mechanisms of Forssman‐induced Bronchospasm and Their Inhibition

Cited by 18 publications

References 10 publications

Antigen challenge induces pulmonary airway eosinophil accumulation and airway hyperreactivity in sensitized guinea‐pigs: the effect of anti‐asthma drugs

Antigen challenge induces pulmonary airway eosinophil accumulation and airway hyperreactivity in sensitized guinea‐pigs: the effect of anti‐asthma drugs

PAF‐induced bronchial hyperresponsiveness in the rabbit: contribution of platelets and airway smooth muscle

Platelets and Bronchospasm

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