Neuroeffector mechanisms: The interface between inflammation and neuronal responses
Neuroeffector mechanisms: The interface between inflammation and neuronal responses
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DOI：
10.1016/s0091-6749(96)80132-1
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发表时间：
1996-11-01
影响因子：
14.2
通讯作者：
Barnes, PJ
中科院分区：
文献类型：
--
作者：
Barnes, PJ
炎症和气道的神经控制之间有着复杂的关系。炎症介质可增强胆碱能神经传递；胆碱能神经是人类支气管收缩的主要神经通路。抗胆碱能药物对急性重症哮喘比慢性哮喘更有效，提示胆碱能机制可能在哮喘加重中起重要作用。几种可能的哮喘肾上腺素能控制异常已被提出，可能是由炎症过程引起的。肾上腺素能神经不直接控制气道平滑肌，但可能通过几种方式影响支气管运动性张力，如肾上腺素能神经对支气管血管的控制或对胆碱能神经传递的二次作用。非肾上腺素能-非胆碱能（NANC）机制介导支气管收缩和支气管扩张，NANC的支气管扩张缺陷被认为在严重哮喘中起作用。相对而言，我们对人类气道感觉（传入）神经的特性知之甚少。它们被认为与咳嗽和胸闷的症状有关，在慢性炎症的情况下，它们的激活阈值会降低。此外，感觉神经通过局部轴突反射逆行激活，导致多肽的释放，可能有助于气道炎症。然而，神经源性炎症可能与轻度哮喘无关，但在脆性哮喘等严重疾病中可能更为重要。
There is a complex relation between inflammation and neural control of the airways. Cholinergic neurotransmission may be enhanced by inflammatory mediators; cholinergic nerves are the dominant neural pathway for bronchoconstriction in humans. Anticholinergic drugs are more effective in acute severe asthma than in chronic asthma, Suggesting that cholinergic mechanisms may be important in exacerbations. Several possible abnormalities in adrenergic control in asthma have been proposed and may be caused by the inflammatory process. Adrenergic nerves do not have direct control of airway smooth muscle but may influence bronchomotor tone in several ways, such as adrenergic neural control of the bronchial vasculature or a secondary effect on cholinergic neurotransmission. Nonadrenergic noncholinergic (NANC) mechanisms mediate both bronchoconstriction and bronchodilation, and a defect in NANC bronchodilatation has been suggested to operate in severe asthma. Relatively little is known about the properties of airway sensory (afferent) nerves in human beings. They are thought to be involved in symptoms of cough and chest tightness, and the threshold for their activation is lowered in conditions of chronic inflammation. In addition retrograde activation of sensory nerves by a local axon reflex, resulting in the release of peptides, may contribute to inflammation of the airways. Neurogenic inflammation is probably not relevant to mild asthma, however, but it may be more important in severe disease such as brittle asthma.