Mechanical consequences of airway smooth muscle relaxation.
J Appl Physiol 1971 May; 30(5):670-676
The nature of airway smooth muscle relaxation was studied in humans. The study group consisted of 22 healthy volunteers, 21 males, 9 to 42 years old. They inhaled an aerosol of isoproterenol (7683592) and phenylephrine (59427) from a pocket nebulizer. Lung volume and airway conductance were measured immediately before and after bronchodilator challenge. Maximum expiratory flow volume, isovolume pressure flow (IVPF), and static lung recoil curves were recorded at these times. Bronchodilation induced a 34.7 percent increase in airway conductance at 50 percent vital capacity (VC), a 33.9 percent increase in the airway conductance/thoracic gas volume ratio, a 9.0 percent increase in maximum expiratory flow at 50 percent VC, and a 3.6 increase in 1 second forced vital expiratory volume. Maximum flows as determined from IVPF curves decreased in two subjects. Bronchodilation did not significantly affect total lung capacity, VC, peak expiratory flow, or static lung recoil pressure. The authors conclude that the observed responses can be explained by the fact that isoproterenol stimulates beta adrenergic receptors, leading to a relaxation of airway smooth muscle. Normal airway smooth muscular tone may allow the large airways to withstand compression forces during forced expiration, thereby allowing dynamic compression to extend further upstream than would be the case if the muscles were less rigid. The significance of the increased compressibility of large airways as a clinical side effect of bronchodilator therapy is not known.
NIOSH-Publication; NIOSH-Grant; Pulmonary-system-disorders; Inhalation-studies; Physiological-response; Muscle-function; Pulmonary-function-tests; Laboratory-testing; Drugs
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Journal of Applied Physiology
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