Abraham W M, Perruchoud A P
Division of Pulmonary Disease, Mount Sinai Medical Center, Miami Beach, Fla.
Respiration. 1989;56(1-2):48-56. doi: 10.1159/000195777.
The sheep model of allergic airway disease shares many pathophysiological similarities with allergic airway disease in humans. Studies performed in this animal model present strong evidence that the release of arachidonic acid metabolites plays an important role in the development of late bronchial responses to antigen challenge. The release of leukotrienes through the lipoxygenase pathway during the acute bronchial obstruction after inhalation of Ascaris suum antigen represents the key factor for the initiation of the subsequent events, namely the late phase response and the bronchial hyperreactivity. If this hypothesis can be substantiated in patients with bronchial asthma then pharmacologic modification of the lipoxygenase pathway and/or products may be important in the treatment of asthma.
过敏性气道疾病的绵羊模型与人类过敏性气道疾病在许多病理生理方面具有相似性。在这个动物模型中进行的研究提供了强有力的证据，表明花生四烯酸代谢产物的释放在抗原激发后迟发性支气管反应的发展中起重要作用。吸入猪蛔虫抗原后急性支气管阻塞期间通过脂氧合酶途径释放白三烯是引发后续事件（即迟发性反应和支气管高反应性）的关键因素。如果这一假说能在支气管哮喘患者中得到证实，那么对脂氧合酶途径和/或其产物进行药物修饰可能在哮喘治疗中具有重要意义。
