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Updated: Aug 11, 2026
A Reversible, Non-invasive Method for Airway Resistance Measurements and Bronchoalveolar Lavage Fluid Sampling in Mice
Published on: April 14, 2010
[Image analysis of airway remodeling and responsiveness in asthmatic guinea pig]
1Respiratory Department, The Third School of Clinical Medicine, Beijing University, Beijing 100083, China.
Objective:
To observe the mechanism of airway remodeling and changes of airway responsiveness in guinea pig model of asthma.
Methods:
40 guinea pigs were randomly divided into two groups: control (20) and asthmatic group (20). After incubating with different stimulus, bilateral lung tissue section were stained with HE. Using image analysis system to measure the airway internal perimeter, wall area, external perimeter, etc. and calculate percentage of muscle shortening (PMS) according to formula.
Results:
(1) The airway wall thickness (WA/Pi) in asthmatic group and control group were (10.0 +/- 2.0) and (7.9 +/- 2.1) micrometer(2)/micrometer, respectively. The bronchial smooth muscle thickness in asthmatic group and control group were (4.8 +/- 1.5) and (3.1 +/- 2.0) micrometer(2)/micrometer, respectively. Both were statistically significant (P < 0.01). The number of bronchial smooth muscle nucleus in asthmatic group (0.012 3 +/- 0.002 7/micrometer) was higher compared with control (0.010 +/- 0.003/micrometer) (P < 0.05). (2) Responsiveness of airway smooth muscle to adenosine (represented by PMS) in asthmatic group and control were 0.34 +/- 0.07 and 0.29 +/- 0.08, respectively (P < 0.05). When combined with aminophyline, PMS in asthmatic group was 0.26 +/- 0.07. There was statistically significant difference when compared with adenosine alone (0.34 +/- 0.07) (P < 0.01). (3) PMS to acetylcholine in asthmatic group and control were 0.24 +/- 0.04 and 0.19 +/- 0.06, respectively (P < 0.05). When combined with heparin, PMS in asthmatic group was 0.20 +/- 0.04. There was statistically significant difference when compared with acetylcholine alone (0.24 +/- 0.04) (P < 0.05).
Conclusions:
The main reason of airway remodeling in asthma is due to bronchial smooth muscle hyperplasia. Aminophylline and heparin may inhibit the responsiveness of airway to adenosine and acetylcholine respectively.
