花生四烯酸代谢物对呼吸道感受器的作用

迷走神经与神经．免疫交互作用密切相关。在呼吸道中,迷走神经传入纤维末梢上的伤害性感受器能被多种细胞因子、炎性介质和免疫调质激活。在炎症过程中,细胞膜磷脂在磷脂酶A2作用下释放花生四烯酸（arachidonic acid,AA）,后者再经不同的酶促反应产生多种脂类代谢物。与其它的炎性介质一样,这些代谢物在炎症反应中可以激活呼吸道感受器并发挥重要作用。有些AA代谢物直接与感觉神经末梢上的受体结合,产生神经冲动并传向中枢,引起反射性效应;有些作用于感觉末梢周围的组织,改变肺的机械特性,从而刺激感觉传入神经;有些提高感觉神经末梢对机械或化学刺激的敏感性,从而增强其反应;还有些可以产生其它介质或调质而触发反射效应,或者引起炎症细胞的聚集而产生局部效应。总之,AA代谢产物有多种来源,并通过多种途径刺激呼吸道中的伤害性感受器。本综述对此进行了探讨,希望有助于阐明呼吸道炎症反应的机理。

Effects of arachidonic acid metabolites on airway sensors

Arachidonic acid (AA) in the cell membrane produces a variety of metabolites by different enzymatic pathways. These lipid metabolites, along with other mediators, play an important role in the inflammatory processes. Many of them can bind directly to the receptors on the sensory endings and initiate electrical impulses to be transmitted to the central nervous system, causing reflex responses. These bioactive AA metabolites may also alter the lung mechanics (mechanical environment of the sensory ending), and in turn, stimulate sensory afferents. In addition, some metabolites may sensitize the sensory endings and make them more responsive to other mechanical or chemical stimulation. These metabolites may also induce other mediators and modulators to cause physiological effects. Furthermore, some of them may attract inflammatory cells to produce a localized effect. In short, AA metabolites may come from different sources and act through multiple pathways to stimulate airway sensors. This brief review is intended to illustrate the underlying mechanisms and help elucidate the inflammatory process in the airways.