Experiments on the role of virus infections in the pathogenesis of bronchial asthma. The role of innate or acquired insufficiency or ergotropic adaptation in the mechanism of genesis of bronchial asthma.
The wide mosaic of congruent clinical and experimental observations led to the postulation that the cause of the pharmacological abnormality of the asthmatic patient, i.e. the immensely increased reactivity of the bronchial smooth muscles, is to be sought in an insufficiency of the beta-adrenergic receptor system. It is to be assumed that the so-called asthma diatheses is based inter alia on a genetically determined defect of the adenyl cyclase system. The role of previous infections of the respiratory tract in asthmagenesis should lie--following this working theory--not in a sensitization in the sense of an allergic reaction of the immediate type, but in the formation of a defective beta-adrenergic substance or in a blockade of the beta-receptor. A genetically determined innate defect of the beta-adrenergic receptors, or a defect acquired through infections of the respiratory tract, is hence likely to be the cause of the pathologically potentiated reactivity of the bronchia. It is likely that the infective stimuli--quite apart from this preparatory role--are later capable of triggering asthmatic paroxysms when the vegetative homeostasis is impaired. We know from the experiments of many authors that a blockade of the beta-receptors produced by chemical blocker substances, or by pertussis vaccine or various bacterial substances, results in a significant increase in bronchial reactivity towards histamine, serotonin, acetylcholine and other stimuli. We have shown in our experiments that heat-inactivated adeno viruses and influenza viruses also increase the anaphylactic shock reactivity and the histamine reactivity of the organism. On the basis of this working hypothesis, the pathomechanism of the asthmatic process is as follows in individual asthma forms: 1) In the 'purely" allergic asthma form, the antigen-antibody reaction that occurs after sensitization (i.e. formation of skin-sensitizing allergic antibodies of the class IgE) results in re-formation and release of slow-reacting-substances.


RESULTS
spasm of the bronchial muscles, asthmatic paroxysm. The expulsion of catecholamines that follows the release of slow-reacting-substances makes a decisive contribution to the reestablishment of the impaired homeostatic balance. It is to be assumed that this form of asthma both symptomatically and causally--using specific desensitization--can be influenced more easily than other forms of asthma with a more complicated pathogenic background. 2) In the second allergically determined form of asthma, we are confronted by the genetically fixed or acquired insufficiency of the beta-receptors in addition to the immunological mechanism. As a result of the innate or acquired blockade of the beta-receptive substance, or the relative dominance of the alpha-receptors, the catecholamines (that physiologically serve to maintain homeostasis) contribute to a protraction, intensification and perpetuation of the bronchial obstruction. In this way the asthmatic circulus vitiosus is complete...
D000256:Adenoviridae / Q000276:immunology; D000262:Adenylyl Cyclases / Q000378:metabolism; D000319:Adrenergic beta-Antagonists; D000707:Anaphylaxis / Q000209:etiology; D000818:Animals; D001249:Asthma / Q000209:etiology* / Q000276:immunology; D002395:Catecholamines / Q000378:metabolism*; D006168:Guinea Pigs; D006632:Histamine / Q000276:immunology; D006969:Hypersensitivity, Immediate / Q000276:immunology; D051379:Mice; D009975:Orthomyxoviridae / Q000276:immunology; D010567:Pertussis Vaccine / Q000276:immunology; D011433:Propranolol / Q000494:pharmacology; D011941:Receptors, Adrenergic; D013189:SRS-A / Q000096:biosynthesis; D014777:Virus Diseases
D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D010567:Pertussis Vaccine; D011941:Receptors, Adrenergic; D013189:SRS-A; D006632:Histamine; D011433:Propranolol; D000262:Adenylyl Cyclases