Modulation of airway sensitivity to inhaled irritants: Role of inflammatory mediators
Modulation of airway sensitivity to inhaled irritants: Role of inflammatory mediators
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DOI：
10.2307/3454674
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发表时间：
2001-08-01
影响因子：
10.4
通讯作者：
Widdicombe, JG
中科院分区：
文献类型：
--
作者：
Lee, LY;Widdicombe, JG
支气管肺 C 纤维末梢和快速适应肺受体 (RAR) 主要负责引发防御反射，保护肺部免受吸入刺激物的侵害。在麻醉动物中，将香烟烟雾（常见的吸入刺激物之一）吸入肺部会引发通过刺激肺 C 纤维介导的肺化学反射。当迷走神经中的 C 纤维传导被选择性阻断时，同一只动物吸入相同的烟雾只会引发呼吸增强，这是激活 RAR 的反射效应。事实上，电生理学研究表明，吸入烟雾对两种类型的传入神经都有直接刺激作用。越来越多的证据表明，气道粘膜炎症会增强这些传入神经的兴奋性，从而增强它们的反射作用。其中一个例子是急性接触臭氧引起的气道高反应性。虽然炎症引起的 C 纤维末端超敏反应的机制尚未完全清楚，但应考虑某些炎症介质（例如组胺和前列腺素 E-2 (PGE(2))）的局部释放可能参与其中。据信，这些神经末梢膜上某些特定受体蛋白的激活所介导的膜特性的变化参与其中，因为 PGE2 的敏化作用也可以在培养的肺 C 神经元中得到证明。
Bronchopulmonary C-fiber endings and rapidly adapting pulmonary receptors (RARs) are primarily responsible for eliciting the defense reflexes in protecting the lungs against inhaled irritants. In anesthetized animals, inhalation of cigarette smoke, one of the common inhaled irritants, into the lungs elicits pulmonary chemoreflexes that are mediated through the stimulation of pulmonary C fibers. When the C-fiber conduction is selectively blocked in the vagus nerves, the same smoke inhalation triggered only augmented breaths, a reflex effect of activating RARs, in the same animals. Indeed, electrophysiologic study shows that inhaled smoke exerts a direct stimulatory effect on both types of afferents. Increasing evidence indicates that the excitability of these afferents and therefore their reflex actions are enhanced by airway mucosal inflammation; one such example is the airway hyperresponsiveness induced by acute exposure to ozone. Although the mechanism underlying the inflammation-induced hypersensitivity of C-fiber endings is not fully understood, the possible involvement of local release of certain inflammatory mediators, such as histamine and prostaglandin E-2 (PGE(2)), should be considered. It is believed that changes in the membrane properties mediated by the activation of certain specific receptor proteins located on the membrane of these nerve terminals are involved, as the sensitizing effects of PGE2 can be also demonstrated in cultured pulmonary C neurons.