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Little is known about the fundamental causes of bronchial asthma and the alterations in pulmonary physiology leading to an attack. The abnormal reaction of the tracheobronchial tree to histamine and to cholinergic substances such as methacholine and pilocarpine has been studied in detail (1-3). The parenteral administration of these drugs brings about a sharp reduction in maximum minute ventilation and vital capacity associated with an evanescent asthma-like attack. The intensity of the pulmonary reaction appears to be associated with the degree of asthma (4), and may be modified by various anti-asthmatic agents such as epinephrine, Orthoxine, aminophylline, Benadryl, Pyrrolazote and hyoscyamine (5). A relationship also exists between the clinical effectiveness of anti-asthmatic agents and the degree of protection they afford against the pulmonary response to injected methacholine and histamine (6). It is not clear why the tracheobronchial tree in asthmatic subjects reacts in an abnormal manner. It is not likely that infection of the mucous membranes in the lungs is the sole cause since some of our reactive subjects had not had an attack of asthma in over 20 years, and some had no history of bronchitis or other pulmonary infection. Moreover, in a few subjects with hay fever who had never suffered with asthma, the injection of methacholine produced a notable reduction in vital capacity (2). The clinical improvement reported in some patients after surgical interruption of the para-sympathetic and sympathetic pathways of. the lungs (7, 8) suggests that a reflex mechanism may be involved. Further support of this idea is furnished by studies carried out in conjunction with Dr. George Whitelaw in which bilateral procaine block of stellate ganglia modified the pulmonary response to methacholine and histamine (9). It was felt worthwhile, therefore, to observe the effect of a sympatholytic drug in similar studies.

THE EFFECT OF DIHYDROERGOCORNINE ON THE PULMONARY RESPONSE TO METHACHOLINE AND HISTAMINE IN SUBJECTS WITH BRONCHIAL ASTHMA