Release of Additional Factors in Anaphylaxis and its Antagonism by Anti-inflammatory Drugs

Piper, Priscilla J.; Vane, John R.

doi:10.1038/223029a0

Cited by 837 publications

(269 citation statements)

References 39 publications

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“…Many fundamental processes, mediators and regulators of airways disease pathogenesis were discovered or demonstrated first in guinea pigs, including the Schultz-Dale (immediate type hypersensitivity) reaction, the actions of histamine, the cysteinyl-leukotrienes and their two receptors, beta adrenoceptor subtypes, thromboxane, vascular endothelial growth factor (VEGF), eotaxin, alveolar macrophage derived neutrophil chemotactic factor(s) (leukotriene B 4 and/or IL-8) and the roles of cAMP and inositol triphosphate in signal transduction [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19]. Receptor pharmacology in guinea pigs more closely matches that of human receptor pharmacology than most other commonly used species [1,20,21] (Table 1, Figs.…”

Section: Introductionmentioning

confidence: 99%

Using guinea pigs in studies relevant to asthma and COPD

Canning

Chou

2008

Pulmonary Pharmacology & Therapeutics

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The guinea pig has been the most commonly used small animal species in preclinical studies related to asthma and COPD. The primary advantages of the guinea pig are the similar potencies and efficacies of agonists and antagonists in human and guinea pig airways and the many similarities in physiological processes, especially airway autonomic control and the response to allergen. The primary disadvantages to using guinea pigs are the lack of transgenic methods, limited numbers of guinea pig strains for comparative studies and a prominent axon reflex that is unlikely to be present in human airways. These attributes and various models developed in guinea pigs are discussed.

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Section: Introductionmentioning

confidence: 99%

Using guinea pigs in studies relevant to asthma and COPD

Canning

Chou

2008

Pulmonary Pharmacology & Therapeutics

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“…We also studied the interference of some inhibitors of the formation and/or of the effects of the leukotrienes with shock in vivo and with the effects of Paf-acether and of antigen on the lung parenchyma strip. Evidence is provided that a non-histamine component of active anaphylaxis is not accounted for by the formation of leukotrienes and of Paf-acether and that additional factors, apart from those described (Piper & Vane, 1969;Nijkamp et al, 1976) may be important in models for immediate hypersensitivity.…”

Section: Introductionmentioning

confidence: 99%

Histamine and leukotriene‐independent guinea‐pig anaphylactic shock unaccounted for by Paf‐acether

Detsouli

Lefort

Vargaftig

1985

British J Pharmacology

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1 Ovalbumin induced dose-dependent contractions of lung parenchyma strips from sensitized guinea-pigs, whereas Paf-acether (I -alkyl-2-acetyl-sn-glycero-3-phosphoryl choline), a potential mediator of immediate hypersensitivity, induced a single contraction, followed by specific desensitization to a second exposure. 2 Lung strips desensitized to Paf-acether contracted to ovalbumin as did non-desensitized controls, even in the presence of inhibitors of other mediators of anaphylaxis. 3 Contractions by Paf-acether and by ovalbumin were reduced by nordihydroguaiaretic acid (NDGA) and by the phospholipase A2 inhibitorp-bromophenacyl bromide (0.1 -0.3 mM). Three other anti-lipoxygenase agents (diethylcarbamazine, 5 mM; eicosatetraynoic acid and BW755c, 0.1 mM), reduced the contractions by ovalbumin but also those due to acetylcholine, indicating non-specific effects. Neither the anti-allergic compound sodium cromoglycate (3 mM) nor the anti-leukotriene agent, FPL 55712 (0.01 mM), inhibited the contractions by ovalbumin or by Paf-acether. 4 A sensitized strip stimulated with ovalbumin released substances which contracted a non-sensitized strip mounted in the same organ bath. The contractions of the non-sensitized strip were abolished by FPL 55712 (0.01 mM), by NDGA and BW755c, (0.1 mM), whereas those of the sensitized one were unaffected. Leukotrienes are formed by the lung strips during shock but alone, they do not explain the contractile activity.5 The intravenous administration of ovalbumin (1 mg kg-') led to bronchoconstriction and thrombocytopenia, which were not modified by the anti-leukotriene substance FPL 55712 nor by aspirin. Bronchoconstriction was suppressed if FPL 55712 was used in combination with aspirin (20 mg kg-'), mepyramine and methysergide (200 jg kg-of either). Pretreatment of the guinea-pigs with propranolol reduced this inhibition to approximately 60%. In no instance was thrombocytopenia prevented. 6 In vitro contractions of the actively sensitized lung strip are not fully accounted for by histamine, FPL 55712-inhibitable leukotrienes or Paf-acether, whereas in systemic anaphylaxis histamine and leukotrienes (inhibited respectively by mepyramine and by FPL 55712) have a significant role.

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“…After three weeks the animals were anesthetized with pentobarbital and the lungs were removed, suspended in a chamber and perfused through the pulmonary artery with Krebs bicarbonate at 10 ml/min as previously described (Piper and Vane, 1969). For the bioassay of prostaglandins, prostaglandin endoperoxides and thromboxanes, the effluent from the lung was used to superfuse a strip of rabbit aorta, rat stomach and rat colon (Piper and Vane, 1969). The assay tissues were treated with a combination of antagonists (Gilmore et al, 1968) which prevented the actions of histamine, acetylcholine, catecholamines and 5-hydroxytryptamine.…”

Section: Lung Perfusion and Bioassaymentioning

confidence: 99%

“…Arachidonic acid injected in the pulmonary artery leads to the formation of prostaglandins, prostaglandin endoperoxides and thromboxanes (Hamberg and Samuelsson, 1974;Piper and Vane, 1969;Vargaftig and Dao, 1971). We constructed a dose-response curve for arachidonic acid injected through the pulmonary artery and the subsequent release of prostaglandins and thromboxanes.…”

Section: Measurement Of Anaphylactic Release Of Prostaglandins Thrommentioning

confidence: 99%

“…In the guinea pig, mediators of anaphylaxis are histamine, slow reacting substance of anaphylaxis (SRS-A), prostaglandins (PGs), prostaglandin endoperoxides and thromboxane A2 (Brocklehurst, 1960;Dawson et al, 1976;Piper and Vane, 1969;Svensson et al, 1975}. Besides immunological hypersensitivity, another fundamental characteristic of asthma is the bronchial hyperreactivity. Szentivanyi (1968) postulated, in this respect, that the pathogenesis of atopy was due to a mal, functioning of ~-adrenergic receptors resulting in an imbalance of ~-and fl-adrenoceptors.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The effects of Haemophilus influenzae vaccination on an aphylactic mediator release and isoprenaline-induced inhibition of mediator release

Schreurs¹,

Terpstra²,

Raaijmakers³

et al. 1980

European Journal of Pharmacology

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European J. Pharmacol. 62 (1980) 261--268.The influence of Haemophilus influenzae on anaphylactic mediator release from ovalbumin-sensitized isolated guinea pig lungs was investigated. Lungs from H. influenzae-vaccinated animals released prostaglandins and thromboxanes following a smaller dose of ovalbumin than was effective in non-vaccinated animals. Histamine release was significantly increased in 4 day-vaccinated animals but not 1 or 10 days after vaccination, while bronchoconstriction was potentiated in 1 and in 4 day-vaccinated animals. This increased histamine release was achieved following 2 pg ovalbumin. In contrast, doses of 10 pg and 1 mg ovalbumin respectively did not affect and decreased histamine release in the vaccinated group. The inhibition of anaphylactic mediator release by an infusion of 6 × 10 -9 M isoprenaline was significantly attenuated by H. influenzae vaccination. These results indicate an increased sensitivity to antigenic challenge and suggest that the functioning of ~-adrenoceptors was decreased as a result ob H. influenzae vaccination. Haemophilus influenzae HistamineAnaphylactic shock Prostaglandins Thromboxane A2

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Release of Additional Factors in Anaphylaxis and its Antagonism by Anti-inflammatory Drugs

Cited by 837 publications

References 39 publications

Using guinea pigs in studies relevant to asthma and COPD

Using guinea pigs in studies relevant to asthma and COPD

Histamine and leukotriene‐independent guinea‐pig anaphylactic shock unaccounted for by Paf‐acether

The effects of Haemophilus influenzae vaccination on an aphylactic mediator release and isoprenaline-induced inhibition of mediator release

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