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目的观察吸入溴化异丙托品对大鼠慢性阻塞性肺疾病（ＣＯＰＤ）模型气道和肺组织Ｍ受体的影响及其规律。方法通过长期吸入高浓度ＳＯ２气体的方法建立大鼠ＣＯＰＤ模型４７只，ＣＯＰＤ大鼠在密闭箱内吸入雾化的０．０２５％溴化异丙托品溶液１０ｍｌ（２次／天，２０分钟／次），应用放射配基结合法测定大鼠气道和肺组织Ｍ受体。结果与对照组相比，ＣＯＰＤ大鼠吸入溴化异丙托品５天，气道和肺组织Ｍ受体密度无明显增加，吸入异丙托品３０天，Ｍ受体的密度显著升高（Ｐ＜０．０５），停药６天后，Ｍ受体的密度基本恢复正常。各组平衡离解常数（Ｋｄ）值差异均无显著性。结论长期吸入溴化异丙托品可上调气道毒蕈碱Ｍ受体，但停药后能较快恢复，气道Ｍ受体的上调可能与长期应用异丙托品患者停药后所出现的暂时性的支气管痉挛及肺功能恶化有关。
Objective To investigate the effects and mechanisms of ipratropium bromide inhalation on M receptor in airway and lung tissue of chronic obstructive pulmonary disease (COPD) model rats. Methods Forty-seven COPD rats were established by long-term inhalation of high concentration of SO2 gas. In COPD rats, 10 ml of 0.025% ipratropium bromide solution was inhaled in airtight containers (2 times / day, 20 minutes / Times), and radioimmunoassay was used to determine M receptor in airway and lung tissue of rats. Results Compared with the control group, COPD rats inhaled ipratropium bromide for 5 days and there was no significant increase in M receptor density in airway and lung tissue. After ipratropium inhalation for 30 days, the density of M receptor was significantly increased P <0.05). After 6 days withdrawal, the density of M receptor returned to normal. There was no significant difference in the equilibrium dissociation constants (Kd) between groups. Conclusions Long-term inhalation of ipratropium bromide can up-regulate muscarinic M receptor in the airway, but it can recover quickly after discontinuation. The up-regulation of airway M receptor may be associated with long-term use of ipratropium after discontinuation Of the temporary bronchospasm and lung function deterioration.