Flenley D C
Department of Respiratory Medicine, University of Edinburgh, UK.
Respiration. 1989;55 Suppl 2:4-9. doi: 10.1159/000195762.
Airflow limitation results from loss of elastic recoil (as in emphysema), or narrowing of large and small airways from smooth muscle contraction, mucosal swelling and/or oedema, mucous plugging (as in asthma), and loss of small airways (as in COPD). Bronchodilator regimes in asthma include inhaled beta 2-agonists, but these do not reduce bronchial hyper-reactivity but act quickly and synergise with oral slow-release theophyllines (serum level 10-20 micrograms/ml), without potentiating tremor which occurs with oral beta 2-agonists. Airway inflammation as the mechanism of asthma, although fashionable, remains unproven, and clearly requires to be specified for asthma. Inhaled steroids slowly improve FEV1 in asthma and in 10-20% of COPD, and reduce hyper-reactivity. Nedocromil has yet to reveal similar potency. Clinical trial of effective anti-PAF drugs or anti-leukotriene agents are awaited, but understanding the specific asthmatic inflammation is still needed for rational therapy. In COPD combining inhaled beta 2-agonists with ipratropium--both given by a reservoir device--can be effective, along with oral slow-release theophylline and possibly inhaled steroids. New inhalation devices (i.e. modified dry powder inhalers) will be needed as the freon propellents in MDI may soon cease manufacture due to potential environmental hazards.
气流受限源于弹性回缩丧失（如肺气肿），或大小气道因平滑肌收缩、黏膜肿胀和/或水肿、黏液阻塞（如哮喘）以及小气道丧失（如慢性阻塞性肺疾病）而变窄。哮喘的支气管扩张剂治疗方案包括吸入β2激动剂，但这些药物不会降低支气管高反应性，而是起效迅速，并与口服缓释茶碱（血清水平10 - 20微克/毫升）协同作用，且不会增强口服β2激动剂所引发的震颤。气道炎症作为哮喘的发病机制，尽管很流行，但仍未得到证实，显然需要针对哮喘进行明确界定。吸入性糖皮质激素可使哮喘患者以及10% - 20%的慢性阻塞性肺疾病患者的第一秒用力呼气容积（FEV1）缓慢改善，并降低高反应性。奈多罗米的效力尚未得到类似证实。期待有效的抗血小板活化因子（PAF）药物或抗白三烯药物的临床试验，但合理治疗仍需要了解特定的哮喘炎症。在慢性阻塞性肺疾病中，将吸入β2激动剂与异丙托溴铵（均通过储雾装置给药）联合使用可能有效，同时可加用口服缓释茶碱以及可能的吸入性糖皮质激素。由于潜在的环境危害，定量吸入器（MDI）中的氟利昂推进剂可能很快停止生产，因此需要新型吸入装置（即改良干粉吸入器）。
