ABSTRACT
Studies performed in both experimental animals and in man suggest that bronchial hyperresponsiveness is associated with airway inflammation and particularly with an eosinophilic infiltration. Selective platelet depletion with a cytotoxic antiplatelet antiserum will inhibit allergen-induced heightened airway responsiveness in IgE-immunized rabbits. Numerous studies have attempted to determine whether platelets from asthmatic patients have an abnormal aggregatory response to various platelet agonists in vitro. An increased platelet turnover and a shortened survival time have been reported inallergic asthmatics, changes indicative of increased platelet consumption in vivo. Platelets can release a number of mediators, such as cationic protein, which is a potent inducer of increased vascular permeability in experimental animals. Allergen exposure of experimental animals has been demonstrated to induce a pulmonary sequestration of platelets in experimental animals which is associated with an increase in the plasma concentration of the platelet-specific protein PF4.
