Effects of Inhibitors of Anaphylactic Mediators in Two Models of Bronchial Anaphylaxis in Anaesthetized Guinea‐pigs

Andersson, Paul

doi:10.1111/j.1476-5381.1982.tb09299.x

Cited by 50 publications

(25 citation statements)

References 36 publications

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“…It was found that guinea-pigs undergoing the full sensitization procedure had heat-labile reaginic antibodies in significant amounts. Using adjuvants, Perini & Mota (1973) and more recently Andersson (1981Andersson ( , 1982 have obtained similar results and have characterized the antibody as IgE. In the present study the identity of the heat labile antibodies was not determined.…”

Section: Discussionsupporting

confidence: 58%

A new in vivo method for the measurement of repetitive anaphylactic responses in the guinea‐pig

Bottomley¹,

Lewis²,

Rising³

et al. 1984

British J Pharmacology

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Section: Discussionsupporting

confidence: 58%

A new in vivo method for the measurement of repetitive anaphylactic responses in the guinea‐pig

Bottomley¹,

Lewis²,

Rising³

et al. 1984

British J Pharmacology

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“…To give one example of such a possibility, leukotriene C4 was recently reported to be produced by rat alveolar macrophages in an IgE-dependent process (Rankin et al, 1982). However, histamine is a mediator of main importance in guinea-pigs (Andersson, 1982 (Andersson 1981). Thus, the above mentioned data do not clarify the mechanism of action of the drugs at the physiological level.…”

Section: Discussionmentioning

confidence: 76%

Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H₂‐agents

Andersson¹,

Bergstrand²

1984

British J Pharmacology

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Guinea‐pigs were sensitized to ovalbumin (OA) by immunization regimens chosen to cause antigen‐induced bronchial anaphylactic responses mediated mainly either by IgE‐like antibodies or by IgG1‐like antibodies. Treatment of the IgE‐producing animals for three weeks with the histamine H2‐receptor antagonist cimetidine (1 mg kg−1 i.p. once a day) or with the H2‐agonist dimaprit (0.1, 1.0, or 10 mg kg−1 i.p. once a day) led to a significantly reduced bronchial response capacity compared with that of the saline‐treated controls challenged intravenously with antigen one week after the end of treatment. The changes were biphasic and not strictly dose‐dependent. In contrast, acute treatment of immunized animals with a single dose of cimetidine (10 or 30 mg kg−1 i.v.) or dimaprit (1 or 10 mg kg−1 i.v.) 2 min before challenge with OA did not significantly affect the bronchial anaphylactic response. However, long‐term treatment with cimetidine (10 mg kg−1) or the dimaprit analogue, S‐[4‐(N, N‐dimethylamino)‐butyl] isothiourea (SKF Compound 91488) (1 mg kg−1), which is reported not to activate H2‐receptors, had no effect on the response capacity. Treatment with cimetidine (1 mg kg−1) or dimaprit (1 mg kg−1) did not influence the response capacity to antigen challenge in IgG1‐ type animals. Dimaprit (1 mg kg−1) did not affect the responsiveness to intravenous provocation with histamine in ‘IgE‐type’ animals. Antigen‐induced release of histamine from chopped lung tissue in vitro was not significantly affected in ‘IgE‐type’ animals treated with cimetidine (1 mg kg−1) or dimaprit (1 mg kg−1). Treatment of immunized animals with cimetidine or dimaprit one week before and one week after a booster injection of antigen also led to reduced response capacity compared with that of saline‐treated controls. However, the serum levels of IgE‐like homocytotropic antibodies of these animals were not reduced; on the contrary, those of IgG1‐antibody were increased in dimaprit‐treated animals. These data show that intermittent treatment with histamine H2‐agents reduces reagin‐mediated anaphylactic response capacity in vivo in actively sensitized guinea‐pigs by an as yet undefined mode of action.

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“…and s.c. A booster dose of 50mg ovalbumin was injected i.p. 3 days later and they were studied after 21-28 days (Andersson, 1982). Sham-sensitized animals were similarly treated with saline alone.…”

Section: Sensitizationsmentioning

confidence: 99%

“…During anaphylaxis in animal and human lung in vitro, histamine and a number of metabolites of arachidonic acid such as prostaglandins, thromboxanes and leukotrienes are released (Piper & Vane, 1969;Schulman et al, 1981). Pharmacological studies have implicated histamine and the peptidoleukotrienes as the major mediators of antigen-induced contractions of bronchial smooth muscle in vivo and in vitro (Andersson, 1982;Burka, 1985a, b;Adams & Lichtenstein, 1985), however, there seems to be some uncertainty over the bio-1 Author for correspondence. logical significance of cyclo-oxygenase products.…”

Section: Introductionmentioning

confidence: 99%

Release of arachidonic acid metabolites and histamine from sensitized guinea‐pig lung following antigen challenge

Turner

Dollery

1988

British J Pharmacology

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1 The time course of mediator release and the hypothesis that the ratio of eicosanoids to histamine might alter with the intensity of stimulus or its route of administration has been explored in isolated perfused lung from sensitized guinea-pigs challenged with ovalbumin. 2 Histamine and prostaglandin release was rapid in onset and virtually complete within 10min. Thromboxane B2 (TXB2) and leukotriene D4 (LTD4) release, however, was more sustained. Release of the major prostanoid metabolites was relatively delayed compared to that of the parent compounds and was more sustained. 3 Mediator release was antigen-dose dependent and TXB2, prostaglandin D2 (PGD2) and LTD4 release linearly related to histamine concentrations (P < 0.05). However, the ratio of the percentage maximum release of eicosanoids relative to histamine was greatest with low doses of ovalbumin.4 At a low antigen dose (10yg ovalbumin), histamine and prostanoid release was greatest when the challenge was via the airway rather than into the pulmonary artery and the greatest differences were in PGF2,, levels. At near maximal challenge (1 mg ovalbumin) there was little difference in concentrations of PGD2, TXB2, 6-oxo-PGFI. and LTD4 by either route, but PGF2. levels remained greater. 5 The results indicate that biologically active amounts of prostanoids may be released from sensitized lung at low degrees of mast cell activation and that differences in mediator release following antigen administration to the airway or into the pulmonary vasculature simply reflects its accessibility to sensitized cells.

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Effects of Inhibitors of Anaphylactic Mediators in Two Models of Bronchial Anaphylaxis in Anaesthetized Guinea‐pigs

Cited by 50 publications

References 36 publications

A new in vivo method for the measurement of repetitive anaphylactic responses in the guinea‐pig

A new in vivo method for the measurement of repetitive anaphylactic responses in the guinea‐pig

Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H₂‐agents

Release of arachidonic acid metabolites and histamine from sensitized guinea‐pig lung following antigen challenge

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Effects of Inhibitors of Anaphylactic Mediators in Two Models of Bronchial Anaphylaxis in Anaesthetized Guinea‐pigs

Cited by 50 publications

References 36 publications

A new in vivo method for the measurement of repetitive anaphylactic responses in the guinea‐pig

A new in vivo method for the measurement of repetitive anaphylactic responses in the guinea‐pig

Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H2‐agents

Release of arachidonic acid metabolites and histamine from sensitized guinea‐pig lung following antigen challenge

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Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H₂‐agents