title: Platelet role in pathogenesis of atopic and nonimmunologic asthma.
abstract: Platelet activating factor (PAF) holds the leading role among allergy mediators in pathogenesis of bronchial asthma. PAF ability to induce bronchospasms is manifested in the presence of intact platelets. Platelet function in patients with atopic and nonimmunologic aspirin-induced asthma was investigated. Aggregation increase (platelet activation) correlating with IgE level and mediator release from target cells of I order was stated to be the most important component of pathologic process in atopy. Under the influence of aggregation inducers (ADP and adrenaline) in platelets of patients with atopic asthma the level of cAMP is reduced, greater amounts of TxB2 and PGF2 alpha are produced. In cyclo-oxygenase blockade their production is not stopped. The decrease of platelet ability to aggregate is observed in patients with nonimmunologic aspirin-induced asthma. In non-stimulated platelets high levels of PGF2 alpha and TxB2 are noted. Their production is somewhat reduced and cAMP level is elevated during action of aggregation inducers on platelets preincubated with non-steroidal anti-inflammatory drugs. Metabolism disorder of membrane phospholipids affects platelet activity to fix Ig and to decrease receptor accessibility for action of aggregation inducers. Efficacy of therapy by different anti-allergic drugs depends greatly on the drug ability to normalize platelet function. Analysis of platelet functions is of great importance for diagnosis of atopic and nonimmunologic forms of bronchial asthma and for choice of adequate therapy.
authors.affiliation: Medical Institute, Saratov, USSR.
authors.forename: N G
authors.initials: NG
authors.lastname: Astafieva
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001241:Aspirin / Q000009:adverse effects; D001249:Asthma / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*; D001792:Blood Platelets / Q000502:physiology*; D000242:Cyclic AMP / Q000096:biosynthesis; D003937:Diagnosis, Differential; D015237:Dinoprost / Q000096:biosynthesis; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008563:Membrane Lipids / Q000378:metabolism; D008875:Middle Aged; D010743:Phospholipids / Q000378:metabolism; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors / Q000502:physiology*; D010974:Platelet Aggregation / Q000187:drug effects; D013929:Thromboxane B2 / Q000096:biosynthesis
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D008563:Membrane Lipids; D010743:Phospholipids; D010972:Platelet Activating Factor; D013929:Thromboxane B2; D000244:Adenosine Diphosphate; D015237:Dinoprost; D000242:Cyclic AMP; D001241:Aspirin; D004837:Epinephrine