The role of atropine as a mediator blocker of induced bronchial obstruction

Itkin, Irving H.; Anand, S.C.

doi:10.1016/0021-8707(70)90126-7

Cited by 46 publications

(19 citation statements)

References 9 publications

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“…Itkin and Anand reported that inhalation of diphenhydramine could block the airway obstruction by allergen inhalation challenge in most cases of bronchial asthmatic patients (29). From the present findings, it is considered that administration of antihistamines to asthmatics may well be reinvestigated; 1-11-receptor antagonist for attenuation of broncho constriction and H, and Ht-receptor antagonists for that of hypersecretion in asthma.…”

Section: Discussionmentioning

confidence: 67%

Cardiotonic Action of Ring a-Modified Cardenolides, With Special Reference to Cleavage of the Ring

Yamatake

Sasagawa

Yanaura

et al. 1977

Japanese Journal of Pharmacology

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Abstract-Participationof histamine H1 and H2-receptors in both asthmas, i.e. experimentally induced bronchoconstriction and bronchosecretion, with ascaris suum and histamine in anesthetized dogs was investigated.Dogs given 0.2% histamine solution or ascaris antigen (3 mg protein) by inhalation showed increases in respiratory resistance (Rrs) and respiratory rate to 2.5-5.0 fold. Airway secretion volume was also significantly increased 3-4 fold. The increase in Rrs by histamine inhalation was effectively inhibited or abolished by a histamine HI-receptor antagonist, chlorphenira mine (0.3-1 mg/kg i.v.), but not by a H2-receptor antagonist, cimetidine (1-3 mg/kg i.v.). The increase in Rrs by antigen inhalation was reduced by relatively high doses of chlorpheniramine (1-3 mg/kg i.v.), and not by cimetidine.In contrast, hyperse cretion of tracheobronchial fluid in both asthmas was significantly prevented by either chlorpheniramine or cimetidine. Combinations of both antagonists abolished the hypersecretion.Atropine (2 mg/kg i.v.) significantly inhibited the occurrence of responses in both asthmas. The results suggest that histamine is involved in the allergic asthma produced by ascaris suum and that histamine directly evokes airway constriction through Hl-receptors and hypersecretion of tracheobronchial fluid through H1 and H2-receptors, and, in a part, indirectly activates the cholinergic pathway.There has been much evidence that histamine is the chief chemical mediator released from mast cells during anaphylaxis (1-9).Experimental bronchial asthma in guinea pigs is prominently inhibited by classical antihistamines (10-12). Schild et al. (3) showed un equivocally that histamine release occurs in bronchial tissue of an asthmatic patient.Ash and Schild (13) demonstrated two types of histamine receptors and Black et al.(14) introduced specific antagonists of these receptors which made it possible to characterize and locate these receptors in the body. Data of the presence of H1 and H2-receptors in airway smooth muscle in different species have been documented, and are cited in the review of Chand and Eyre (15). There are, however, specifically no reports on the distribution of these receptors in the dog airway smooth muscle or on the role of these receptors in bron chosecretion. We attempted to characterize histamine receptors responsible for airway constriction and hypersecretion which occurs in ascaris and histamine-induced asthmas, using histamine H1 and H2-receptor antagonists. MATERIALS AND METHODSMale mongrel dogs weighing between 6 and 17 kg were anesthetized with sodium

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Section: Discussionmentioning

confidence: 67%

Cardiotonic Action of Ring a-Modified Cardenolides, With Special Reference to Cleavage of the Ring

Yamatake

Sasagawa

Yanaura

et al. 1977

Japanese Journal of Pharmacology

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“…This is not likely, however, because Tozzie, Roth & Tabachnick (1974) have shown that the anticholinergic activity of chlorpheniramine is only about 1/30th that of atropine and, therefore, 1O mg chlorpheniramine would exert little anticholinergic activity in man: certainly, no anticholinergic side-effects were detected in the volunteers. In other experiments Itkin & Anand (1970) gave 5 mg atropine i.v. to twenty subjects and found that only thirteen of the twenty were partially protected from the effects of inhaled methacholine.…”

Section: Discussionmentioning

confidence: 99%

Effects of H1‐ and H2‐receptor blocking agents on histamine‐induced bronchoconstriction in non‐asthmatic subjects.

Maconochie¹,

Woodings²,

Richards³

1979

Brit J Clinical Pharma

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I Two studies have been carried out to investigate the effect of H1-and H2-receptor blocking agents on histamine-induced bronchoconstriction in non-asthmatic subjects. 2 The H2-receptor blocker cimetidine administered orally had no effect on histamine-induced bronchoconstriction on any of the subjects tested. In three of four subjects, the Hl-receptor blocker, chlorpheniramine given orally, inhibited the effect of the histamine in the lung. 3 The effects of intravenous chlorpheniramine and cimetidine, both alone and in combination, upon histamine-induced bronchoconstriction, were also studied. Chlorpheniramine inhibited the effect of the histamine and this was significantly dose related. This was not so with cimetidine and there was no evidence that the dose response curve to chlorpheniramine was affected by the additional administration of cimetidine. 4 The results show that histamine-induced bronchoconstriction in non-asthmatic subjects is not mediated by H2-receptors, but it is likely that H1-receptors are involved.

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“…However, the involvement of vagal reflexes in human bronchial asthma has not been clearly established. Some workers have shown atropine to be an effective inhibitor of antigen-induced bronchoconstriction in asthmatic patients (Yu, Galant & Gold, 1972) while others report little (Itkin & Anand, 1970), or no effect (Orie, Van Lookeren Campagne, Knol, Booij-Noord & De Vries, 1973;Rosenthal, Summer, Permutt & Norman, 1974). The relevance of anaphylactic bronchoconstriction in rats (or other animals) to asthma in man, with respect to vagal reflex involvement, cannot be resolved at present.…”

Section: Discussionmentioning

confidence: 99%

Mediators of Passive Lung Anaphylaxis in the Rat

Farmer¹,

Richards²,

Sheard³

et al. 1975

British J Pharmacology

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1 Passive lung anaphylaxis (PLA) was investigated in rats sensitized by the intravenous injection of high titre reaginic antiserum prepared in rats. 2 The effect of various pharmacological antagonists on anaphylactic bronchoconstriction in vivo were examined. An antihistamine (mepyramine), a kallikrein inactivator (aprotinin) or a prostaglandin synthesis inhibitor (aspirin) did not inhibit PLA, whereas an anti-5-hydroxytryptamine agent (methysergide) and an anti-slow reacting substance-A agent (FPL, 55712) significantly reduced the response. 3 Isolated perfused lungs taken from sensitized rats released, on challenge with the sensitizing antigen, histamine, 5-hydroxytryptamine, slow reacting substance of anaphylaxis (SRS-A) and prostaglandins, but no rabbit aorta contracting substance (RCS). 4 Disodium cromoglycate inhibited both anaphylactic bronchoconstriction in vivo and the anaphylactic release of mediators in vitro. Inhibition in vivo was dose-related. 5 Mediators from the intestine, the primary shock organ of anaphylaxis in the rat, did not contribute to the lung response. 6 Vagal reflex pathways were found not to be important in PLA in vivo. 7 The relationship between the mediators released following antigen challenge of passively sensitized rat lung in vitro and passive lung anaphylaxis in vivo is discussed.

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The role of atropine as a mediator blocker of induced bronchial obstruction

Cited by 46 publications

References 9 publications

Cardiotonic Action of Ring a-Modified Cardenolides, With Special Reference to Cleavage of the Ring

Cardiotonic Action of Ring a-Modified Cardenolides, With Special Reference to Cleavage of the Ring

Effects of H1‐ and H2‐receptor blocking agents on histamine‐induced bronchoconstriction in non‐asthmatic subjects.

Mediators of Passive Lung Anaphylaxis in the Rat

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