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Inhibition of Leukotriene (SRS‐A)‐Mediated Acute Lung Anaphylaxis by Azelastine in Guinea Pigs
Author(s) -
Chand N.,
Nolan K.,
Diamantis W.,
Perhach J. L.,
Sofia R. D.
Publication year - 1986
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.1986.tb00331.x
Subject(s) - azelastine , ketotifen , bronchospasm , pharmacology , anaphylaxis , leukotriene d4 , medicine , leukotriene , guinea pig , histamine , leukotriene c4 , allergy , chemistry , asthma , immunology
Azelastine hydrochloride, chemically known as l(2H)‐phthalazinone, 4‐[(4‐chlorophenyl)methyl] ‐2‐(hexahydro‐l‐methyl‐lH‐azepine‐4‐yl)‐, monohydrochloride, is a novel, orally effective, long‐acting, antiallergic/antiasthmatic agent. The ability of azelastine and selected antiallergic drugs to inhibit SRS‐A (leukotriene)‐mediated acute lung anaphylaxis in guinea pigs (Konzett‐Rossler method) was investigated. Azelastine and ketotifen were administered p.o. 2 and 24 h before antigen challenge; disodium cromoglycate (DSCG) was administered i.v. immediately before antigen challenge. The oral dose of azelastine required to inhibit leukotriene‐mediated allergic bronchospasm by 50% (ID 50 : mg/kg) was 0.063 at 2 h and 0.120 at 24 h. Ketotifen at a dose of 0.05 to 10 mg/kg at 2 and 24 h, p.o., as well as DSCG at a dosage of 0.3 to 10 mg/kg at 0 min, i.v., produced weak, inconsistent and nondose‐related antianaphylactic effects. Azelastine is an orally effective and long‐acting inhibitor of in vivo synthesis and/or release of leukotrienes.