Barnes P J
Department of Thoracic Medicine, National Heart & Lung Institute, London, UK.
Br Med Bull. 1992 Jan;48(1):149-68. doi: 10.1093/oxfordjournals.bmb.a072531.
Neural control of the airways may be abnormal in asthma and neurogenic mechanisms may contribute to the pathophysiology of asthma. Cholinergic nerves are the predominant bronchoconstrictor pathway in airways and cholinergic neurotransmission may be increased in asthma by the effects of inflammatory mediators on afferent nerves (reflex effect) and on prejunctional receptors on postganglionic nerves. In addition there may be a defect in prejunctional M2-receptors on cholinergic nerves resulting in increased cholinergic neural effects. beta-Adrenoceptor function may be abnormal in asthmatic airways as a result of chronic inflammation, but alpha-receptors are probably unimportant in regulation of human airway tone. Inhibitory NANC nerves are the only bronchodilator pathway in human airways, and there is some evidence that the neurotransmitter is predominantly nitric oxide, although vasoactive intestinal peptide may be contributory. It is possible that i-NANC function may be abnormal in asthma as a consequence of inflammation. Unmyelinated sensory nerves contain a variety of potent inflammatory peptides, including substance P and neurokinin A, which might be released in chronic inflammation, particularly if there is a proliferation of these nerves, increased neuropeptide synthesis or reduced metabolism by neutral endopeptidase.
哮喘患者气道的神经控制可能异常，神经源性机制可能参与哮喘的病理生理过程。胆碱能神经是气道中主要的支气管收缩途径，在哮喘中，炎症介质对传入神经（反射效应）和节后神经节前受体的作用可能会增加胆碱能神经传递。此外，胆碱能神经节前M2受体可能存在缺陷，导致胆碱能神经效应增强。由于慢性炎症，哮喘气道中的β-肾上腺素能受体功能可能异常，但α受体在调节人类气道张力方面可能并不重要。抑制性非肾上腺素能非胆碱能（NANC）神经是人类气道中唯一的支气管舒张途径，有证据表明其神经递质主要是一氧化氮，尽管血管活性肠肽可能也有作用。炎症可能导致哮喘患者的抑制性NANC功能异常。无髓感觉神经含有多种强效炎症肽，包括P物质和神经激肽A，这些炎症肽可能在慢性炎症中释放，特别是在这些神经增殖、神经肽合成增加或中性内肽酶代谢减少的情况下。
