Effect of ipratropium bromide on airway and pulmonary muscarinic receptors in a rat model of chronic obstructive pulmonary disease
10.3760/j.issn:0366-6999.2001.01.018
- VernacularTitle:大鼠慢性阻塞性肺疾病模型气道和肺组织M受体水平及溴化异丙托品的影响
- Author:
Wanzhen YAO
1
;
Guoyang WANG
;
Hong ZHU
;
Yongchang SUN
;
Mingwu ZHAO
Author Information
1. 北京大学医学部附属第三医院(北医三院)
- Keywords:
receptor;
muscarinic;
chronic obstructive pulmonary disease;
animal model
- From:
Chinese Medical Journal
2001;114(1):80-83
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the level of muscarinic receptors in airway and lung tissues, and the effect of inhaled ipratropium bromide on these receptors in a rat model of chronic obstructive pulmonary disease (COPD). Methods This model was developed by exposure of rats to 250?ppm SO2 gas, 5?h/d, 5?d/wk, for a period of 7?wk. The COPD rats inhaled 0.025% aerosolized iratropium bromide for 20?min, 2 times daily, in an airtight chamber. Muscarinic receptors in airway and lung tissues of normal rats, ipratropium bromide-treated COPD rats and the recovering COPD rats were measured by the radio-ligand binding assay. Results Airway/lung pathology and pulmonary function tests showed that chronic SO2 exposure caused pathophysiologic changes similar to those observed in human COPD. The density (0.038±0.011, pmol/mg protein) and affinity (Kd, 23±11?pmol/L) of muscarinic receptors in airway and lung tissues of COPD rats were not changed compared with those of normal control rats (0.030±0.008 and 29±19, respectively, P>0.05). Densities of the muscarinic receptors were not changed after inhalation of ipratropium bromide for 5 days, but increased significantly after inhalation for 30 days, as compared with those of the untreated COPD rats. The muscarinic receptors returned the normal levels at day 6 after cessation of ipratropium bromide treatment. There were no differences among different groups of rats in equilibrium dissociation constants (Kd). Conclusion A rat model of COPD with pathophysiologic changes similar to the human counterpart was developed using chronic SO2 exposure. There was no significant change in the number and function of muscarinic receptors in airway and lung tissues of the COPD rats, but upregulation of the muscarinic receptors was observed after long-term inhalation of ipratropium bromide.
