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Inhaled procaterol inhibits histamine‐induced airflow obstruction and microvascular leakage in guinea‐pig airways with allergic inflammation
Author(s) -
Mirza,
Tokuyama,
Arakawa,
Ryu Kato,
Mochizuki,
Masahiro Morikawa
Publication year - 1998
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.1998.00263.x
Subject(s) - evans blue , extravasation , histamine , sensitization , medicine , airway resistance , ovalbumin , inhalation , guinea pig , saline , eosinophil , bronchoconstriction , anesthesia , lung , allergy , allergic inflammation , pharmacology , immunology , asthma , airway , antigen
Background β 2 ‐adrenoceptor agonists (β 2 ‐agonists) are shown to inhibit airway microvascular leakage in experimental animals. This effect may change in animals with chronic airway inflammation. Objective We examined whether inhaled β 2 ‐agonists inhibit microvascular leakage in guinea‐pig airways with chronic allergic inflammation. Methods Three weeks after the sensitization with ovalbumin (OA; 6 mg/mL), each guinea‐pig was challenged with inhaled OA once a day for 1 or 3 weeks. Control animals without sensitization with OA also inhaled vehicle for OA (saline) for 3 weeks. One day after the last challenge, different doses of inhaled procaterol (1, 3 or 10 μg/mL) or vehicle was given to animals for 10 min after an anaesthesia. Fifteen minutes after the end of inhalation, the animals were given i.v. Evans blue dye (EB dye; 20 mg/kg), a marker of microvascular leakage, and then i.v. histamine (3 or 30 μg/kg) or vehicle. Lung resistance, a parameter of airflow obstruction, was measured for 6 min and the lungs were removed to calculate the amount of extravasated EB dye into the airways. Results A significant increase in eosinophil infiltration into the airways was seen in sensitized and challenged animals compared with control animals without sensitization. Among animals receiving antigenic exposure for either 0 (control), 1 or 3 weeks, 10 μg/mL procaterol significantly inhibited 30 μg/kg histamine‐induced increase in EB dye extravasation to a similar degree (ranged from 28.7 to 69.8% inhibition) as well as that in lung resistance (more than 90% inhibition in all groups). The minimal dose of procaterol to inhibit 3 μg/kg histamine‐induced microvascular leakage was not different between non‐sensitized control animals and those sensitized and challenged for 3 weeks at all airway levels. Conclusion Inhaled β 2 ‐adrenoceptor agonists may be also potent in attenuating microvascular leakage even in the airways with chronic allergic inflammation.