Early asthmatic response mechanism

The bronchospasm that occurs immediately after aeroallergen inhalation in allergic asthmatic subjects is at least partly an IgE-mediated immediate hypersensitivity reaction (1). At least two lines of evidence support this mechanism for the early asthmatic response. Eirst, pretreatment with an anti-IgE monoclonal antibody attenuates the early phase response in asthmatic subjects (Fig. 1) (2,3). Second, analysis of bronchoalveolar lavage fluid collected immediately after air-... 

In summary, current information suggests that the mechanism of airway narrowing during the early asthmatic response is an acute bronchoconstrictor response caused mainly by an IgE-dependent immediate hypersensitivity reaction. Of the preformed and newly synthesized mediators released from mast cells during these reactions, the cysteinyl leukotrienes appear to be the most important in the pathogenesis of the EAR. 

Mechanism of Action A mast cell stabilizer that prevents the activation and release of inflammatory mediators, such as histamine, leukotrienes, mast cells, eosinophils, andmonocytes.T herapeuticEffect Prevents both early and late asthmatic responses. Pharmacokinetics The extent of absorption is 7% to 9% of a single inhaled dose of 3.5 to 4 mg and 17% of multiple inhaled doses, with absorption largely from the respiratory tract. Although most of the inhaled dose is subsequently swallowed, only 2% to 3% is absorbed from the G1 tract. Less than 4% of the total dose is systemically absorbed following multiple doses of ophthalmic solution. Protein binding 89%. Not metabolized. Excreted in urine. Half-life 1.5-3.3 hr. 

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