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目的 观察大鼠慢性阻塞性肺疾病 (COPD)模型气道和肺组织M受体水平 ,以及吸入溴化异丙托品对M受体的影响及其规律。方法 通过长期吸入高浓度SO2气体的方法 ( 2 50ppm ,5h d ,5d wk ,共 7wk)建立COPD模型 ,大鼠在密闭箱内吸入雾化的 0 0 2 5%溴化异丙托品溶液 10ml( 2次 d ,2 0min 次 ) ,采用放射配基结合法 ,分别测定正常大鼠、吸入和未吸入异丙托品大鼠气道和肺组织的M受体。结果 支气管肺病理学及肺功能检查显示 ,大鼠长期吸入高浓度SO2气体可引起与人类COPD相似的病理生理改变。COPD大鼠气道和肺组织M受体的密度 ( 0 0 38± 0 0 11pmol mg蛋白质 )及亲和力 (Kd ,2 3± 11pmol L)与正常大鼠相比 (分别为 0 0 30± 0 0 0 8,2 9± 19)无明显变化 (P >0 0 5)。吸入异丙托品 30天后 ,气道和肺组织M受体密度显著升高 (P <0 0 5) ,停药 6天后 ,M受体的密度恢复正常。结论 长期吸入高浓度SO2可制备与人类COPD病理生理改变相似的大鼠模型。COPD大鼠气道和肺组织M受体的数量及功能无异常改变 ,但长期应用异丙托品可使M受体上调。
Objective To observe the levels of M receptor in airway and lung tissue of chronic obstructive pulmonary disease (COPD) model rats and the effects of inhaled ipratropium bromide on M receptor. Methods The model of COPD was established by long-term inhalation of high concentration of SO2 gas (2 50ppm, 5h d, 5d wk, total 7wk). The rats were inhaled in a closed box with 10ml of 025% ipratropium bromide solution (2 d, 20 min). Radioimmunoassay was used to determine M receptor in airway and lung of normal rats, inhaled and non-infused ipratropium rats respectively. Results Bronchopulmonary histopathology and pulmonary function tests showed that long-term inhalation of high concentrations of SO2 in rats caused similar pathophysiological changes in human COPD. The density of M receptor (0 38 ± 0 0 11 pmol mg protein) and affinity (Kd 2 3 ± 11 pmol L) in airway and lung tissue of COPD rats were significantly higher than those in normal rats (0 0 30 ± 0 0 0 8,2 9 ± 19) showed no significant change (P> 0.05). After 30 days of inhalation of ipratropium, the density of M receptor in airway and lung tissue was significantly increased (P <0 05). After 6 days withdrawal, the density of M receptor returned to normal. Conclusion Long-term inhalation of high concentrations of SO2 can be prepared with human COPD pathophysiological changes similar to the rat model. COPD rats airway and lung tissue M receptor number and function without abnormal changes, but long-term use of ipratropium can up-regulate M receptors.