Distribution of bronchodilatation in normal subjects: beta agonist versus atropine

Abstract

Bronchodilatation was produced in normal subjects by the inhalation of a parasympatholytic agent (atropine) and the response was compared to that occurring after the inhalation of a beta-adrenergic agent (isoetharine). Doses were chosen that resulted in equivalent increases in specific airway conductance (78 +/- 9% for atropine; 88 +/- 21% for isoetharine). Anatomic dead space and volume at the onset of the terminal nitrogen rise (closing volume) were measured before and after each agent. Although there was no difference in the degree of overall bronchodilatation after the two drugs, anatomical dead space increased significantly more after atropine than isoetharine (+17% vs. +6%, P less than 0.01), and closing volume increased significantly after isoetharine (P less than 0.005) but did not change with atropine. We interpret these differences to indicate a greater effect of cholinergic antagonists on the more central airways and a greater effect of beta-adrenergic stimulants on peripheral airways.

Bronchial Hyperreactivity in the Peripheral Airways.

“…From the analysis of maximal expiratory flow-volume curves with inspired gases of different densities, Ingram et al (1977) suggested that in normal subjects the predominant sites of atropine aerosol activity are the central airways and sites of isoproterenol are the peripheral airways. Later, using the concept that changes in anatomic dead space reflect changes in central airway dimension, Hensley et al (1978) reached the same conclusion.…”

“…Therefore, in contrast to atropine, there is general agreement that fi adrenergic agents exert their bronchodilating effects on both the central and peripheral airways (Barnes et al 1983). In normal subjects, large airway dilation is produced by atropine, whereas small airway dilation is produced by fl-agonist (Hensley et al 1978). McFadden et al (1977) reported that postexertional asthma with large airway constriction could be abolished by pretreatment with an anticholinergic agent, whereas small airway constriction could be abolished by pretreatment with disodium cromoglycate.…”

Reversible Airflow Obstruction in Lymphangioleiomyomatosis

“…Contrasting with the adrenergic agents, the bronchodilator effects of anticholinergic agents may favor the large airways rather than the small airways. 25 Regardless of the site of action of bronchodilators, as in other lung diseases, 26 some patients with LAM may respond more favorably to one or the other category of drugs.…”

Relationship between Improved Airflow Limitation and Changes in Airway Caliber Induced by Inhaled Anticholinergics in Chronic Obstructive Pulmonary Disease.

“…These efforts have included measuring anatomical dead space as an indicator of central airway changes, [26] generating maximal expiratory flow-volume curves with inspired gases of different densities [27,28] and sensing the lateral pressure of the airway using a catheter-tipped micro manometer. [29] Although these studies were theoretically sound, they could not determine bronchodilatory heterogeneity of in the lung because they are all based on the assumption that lung activity is homogeneous and so overall physiological parameters were measured.…”

“…[29] Although these studies were theoretically sound, they could not determine bronchodilatory heterogeneity of in the lung because they are all based on the assumption that lung activity is homogeneous and so overall physiological parameters were measured. Most of these studies agreed that inhaled anticholinergic agents act mainly on the large central airways in normal individuals as well as in patients with bronchial asthma, [26,28,30] although some disagreed. [27,31] Since resting vagal tone is thought to be maintained under normal circumstances throughout the bronchial tree,[30] the exact site of bronchodilation over the whole lung remains to be elucidated.…”