Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Clinical Trial
. 1996 Aug;81(2):964-75.
doi: 10.1152/jappl.1996.81.2.964.

Lung mechanics during induced bronchoconstriction

Affiliations
Clinical Trial

Lung mechanics during induced bronchoconstriction

R Pellegrino et al. J Appl Physiol (1985). 1996 Aug.

Abstract

To elucidate differences in lung mechanics, we investigated the relative changes of partial forced expiratory flows at 50 and 30% of vital capacity, pulmonary resistance (RL), dynamic elastance (Edyn), and the effects of a deep inhalation (DI) on maximal flows, Edyn, and RL in eight asthmatic and eight normal individuals during bronchial challenges with methacholine, histamine, and ATP. RL was partitioned into inspiratory and expiratory resistance. Different constrictor agents did not induce specific patterns of response. For a given decrement of flow at 50 and 30% vital capacity, RL increased significantly more in normal than in asthmatic individuals. The ratio of inspiratory to expiratory RL was always < 1 at baseline but became > 1 in the majority of asthmatic and normal individuals when RL exceeded 12.2 +/- 0.9 cmH2O.1-1.s, suggesting that tidal inspiration may have induced transient bronchodilation in more constricted subjects. In asthmatic individuals, DI had a significantly smaller effect on flow but not on RL compared with normal individuals. The recovery of RL and Edyn after DI was faster than Edyn for both normal and asthmatic individuals. These findings are consistent with the idea that asthmatic individuals have a stronger peripheral response to agonists than normal individuals.

PubMed Disclaimer

Publication types

MeSH terms