[Physiopathological mechanisms in asthma. I. Bronchial hyperreactivity]

Asthma, a disease characterized by bronchial hyperreactivity to various physical, chemical, nd pharmacological stimuli, has been extensively studied, and many pathogenic hypotheses have been evoked. Theories attempting to explain the development of the asthmatic syndrome are still fragmentary: the parasympathetic system appears to be the predominant factor involved in changes in nervous system regulatory alterations, this hypothesis being suggested to explain the bronchial hyperreactivity occurring after viral infections or exposure to certain oxidizing agents. The results of morphological and ultrastructural studies of human bronchial muscle suggest the involvement of modifications in a non-adrenergic relaxant system, analogous to the purinergic system in the digestive tract, but supply marked evidence of changes in sympathetic innervation. An alteration in the smooth muscle itself may be implicated: muscle hyperplasia, increase in contractility, and especially modification in pharmacological receptors situated on the membrane of smooth muscle fibres : acquired or spontaneous blocking of beta receptors, activation of alpha receptors, and alteration of cholinergic receptors. The chemical theory suggests that bronchoconstriction is due to local excess of mediators from cells taking part in the allergic and inflammatory reactions, and which are found in the tracheobronchial tree. The possible relationships between repeated secretion of mediators in allergic subjects and the bronchial hyperreactivity to numerous non-specific stimuli appear to be a complex subject. The possibility that a single biochemical anomaly is involved in asthma has been raised, but further basic research is necessary to explain the alterations in biochemical processes involved in such different phenomena as muscle contraction, secretion of anaphylactic mediators, and nerve impulse transmission.