Mediators of Passive Lung Anaphylaxis in the Rat

Farmer, J. B.; Richards, Ivan M.; Sheard, Philip W.; Woods, Audrey M.

doi:10.1111/j.1476-5381.1975.tb07610.x

Cited by 57 publications

(44 citation statements)

References 28 publications

(22 reference statements)

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“…3). Antagonists of serotonin and SRS-A, such as methysergide or FPL 55712 partially inhibit bronchoconstriction induced in rats (2,5,16). In the present experi ment, a partial inhibition of the bronchoconstriction in rats occurred following treatment with cyproheptadine.…”

supporting

confidence: 51%

Anti-anaphylactic activities of a new benzopyranopyridine derivative Y-12,141 in rats and guinea pigs.

Goto¹,

Terasawa²,

Kadobe³

et al. 1980

Jpn.J.Pharmacol

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Abstract-The active anaphylactic bronchoconstriction of rats mediated by IgE-like antibody against DNP-Ascaris was inhibited by intravenous and intratracheal treat ment with Y-12,141 in a dose-dependent manner. In both routes, the inhibitory effect of Y-12,141 on this response was more potent than that of disodium cromoglycate (DSCG). The oral administration of Y-12,141 also produced a similar inhibition of the response. The passive anaphylactic bronchoconstriction of guinea pigs mediated by IgG-like antibody against egg albumin was also prevented dose-dependently by treatment with Y-12,141 given intravenously, but not with DSCG. The present results suggest that Y-12,141 may be effective for the treatment of allergic bronchial asthma.In a previous paper (1), we demonstrated that 9-chloro-5-oxo-7-(1H-tetrazol-5-yl) The active anaphylactic bronchoconstriction in rats sensitized with several antigens such as egg albumin provides a model which is similar to human bronchial asthma im munologically and in the response to DSCG (2-6). In addition, the anaphylactic broncho constriction in guinea pigs is usually chosen for the experimental simulation of human allergic bronchial asthma (7). However, the anaphylactic bronchoconstriction in guinea pigs differs from human allergic asthma both in the immunoglobulins involved (8, 9) and in the response to DSCG (10). The present studies were designed to elucidate the effectiveness of Y-12,141 for prophylaxis in the bronchial anaphylaxis in both rats and guinea pigs. MATERIALS AND METHODS Animals:Rats, guinea pigs and rabbits were used. The animals were housed under ordinary conditions and allowed free access to food and water.

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supporting

confidence: 51%

Anti-anaphylactic activities of a new benzopyranopyridine derivative Y-12,141 in rats and guinea pigs.

Goto¹,

Terasawa²,

Kadobe³

et al. 1980

Jpn.J.Pharmacol

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“…Rat anaphylactic bronchoconstriction, which is due to the release and action of 5-hydroxytryptamine and possibly slow reacting substance of anaphylaxis (SRS-A) (Church et al, 1972;Farmer, Richards, Sheard & Woods, 1975) is inhibited only by a high dose of dexamethasone and after a long lag period, possibly because the steroid depresses the release of mediators. Dexamethasone does not reduce the bronchoconstrictor effects of exogenous 5-hydroxytryptamine or SRS-A (Church, 1975).…”

Section: Discussionmentioning

confidence: 99%

Time Courses of the Anti‐anaphylactic and Anti‐inflammatory Effects of Dexamethasone in the Rat and Mouse

Miller

1978

British J Pharmacology

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1 The time course of the activity of dexamethasone has been studied in a variety of anaphylactic and inflammatory reactions in the rat and the mouse. 2 The times of peak activity of dexamethasone, expressed as time between oral dosage and induction of response, and the approximate ED50 values (mg/kg) found were: anaphylactic bronchoconstriction in rats, 12-24 h, ED50 1.8; passive cutaneous anaphylaxis in rats, 6 h, ED50 0.04; cutaneous reactions to histamine in rats, 4 h, ED50 0.01; carrageenin-induced paw oedema in rats, 4 h, ED50 0.03; pinnal anaphylaxis in mice, 6 h, ED50 0.82; histamine-induced pinnal reactions in mice, 6 h, ED50 0.05. 3 In rats, the characteristics of the inhibitory effects of dexamethasone indicate a differential activity against anaphylactic and inflammatory reactions and between different types of inflammatory reactions. Possible reasons for these differences are discussed. 4 In mice there was little difference between the inhibition by dexamethasone of cutaneous allergic and histamine-induced reactions. 5 Pinnal anaphylaxis in mice was potentiated by dexamethasone given 1-2 h before challenge.

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“…Anaphylaxis-producing homologous antibody (IgE) can be produced in the Sprague-Dawley rats but this strain maybe cannot elicit bronchial constriction because of the lack of histamine receptor in the trachea of this strain. When Wistar rats were passively immunized with Sprague-Dawley-produced antibody, bronchial constriction occurred (Farmer et al, 1975). The current result indicates that Sprague-Dawley rats can be a model to study cardiovascular anaphylaxis without the involvement of bronchial system.…”

Section: Discussionmentioning

confidence: 74%

Induction of Cardiovascular Anaphylaxis and Basic Pharmacological Analysis of Involved Mediators in Pithed Rats

Park¹

2008

Biomolecules and Therapeutics

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− Active cardiovascular anaphylactic response was induced in ovalbumin-sensitized, pithed SpragueDawley and Wistar rats. On intravenous administration of the antigen, ovalbumin, marked tachycardia and pressor responses were immediately elicited. Thereafter, a delayed long-lasting severe hypotensive response was observed. These anaphylactic cardiovascular responses were maximal 2-3 weeks after the sensitization, and the response was slightly diminished 6 weeks after sensitization. The immediate pressor response was blocked by a non-selective serotonin antagonist methysergide at a dose-dependent manner, but not by histamine receptor antagonists mepyramine (pyrilamine) or cimetidine. The delayed hypotension was reduced either by histamine H 1 receptor antagonist mepyramine or H 2 receptor antagonist cimetidine, both in a dose-dependent manner. The tachycardic response was not influenced by serotonin or histamine receptor antagonists examined in this study. Differently from the cardiovascular responses, there was no observable bronchial contraction in Sprague-Dawley rat trachea in contrast to Wistar rat where the trachea contracted to in vitro antigen challenge. The cardiovascular anaphylactic model seems to be useful for studying cardiovascular events that occur exclusively in peripheral heart-blood vessel systems. The involvement of two major anaphylactic mediators, serotonin and histamine, is partially demonstrated.

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Mediators of Passive Lung Anaphylaxis in the Rat

Cited by 57 publications

References 28 publications

Anti-anaphylactic activities of a new benzopyranopyridine derivative Y-12,141 in rats and guinea pigs.

Anti-anaphylactic activities of a new benzopyranopyridine derivative Y-12,141 in rats and guinea pigs.

Time Courses of the Anti‐anaphylactic and Anti‐inflammatory Effects of Dexamethasone in the Rat and Mouse

Induction of Cardiovascular Anaphylaxis and Basic Pharmacological Analysis of Involved Mediators in Pithed Rats

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