ABSTRACT
The pathogenesis of atopic bronchial asthma (ABA) is examined from a membranologic viewpoint, with a methodological approach, postulating membrane-receptor pathology as the key pathogenetic element of the disease, taken as the basis. Major results of the study of the adrenoreactive system are analysed, and pathogenetic significance of the demonstrated paradoxal cell reaction to beta-adreno-antagonist is pointed out. Prospects related to the development of studies of morphofunctional erythrone properties as a new line of research in BA pathogenesis are demonstrated, and erythrocyte qualities applicable as marker of atopia, such as microcytosis and membrane glycoprotein distribution, are identified. Specific pattern of cell membrane response to aldehyde compounds seen in ABA is described. The data obtained are a development of the earlier-postulated hypothesis of ABA-associated dedifferentiation. A notion of ABA as a membrane-receptor disease is proposed.
