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Upper airway neurogenic mechanisms.

机译:上呼吸道神经发生机制。

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摘要

Stimulation of the nasal sensory nerves leads to sensations of pain and stuffiness. Type C nociceptive nerve releases neuropeptides including substance P and calcitonin gene related peptides that increase plasma extravasation and glandular secretion. This axonal response acts as an immediate protective mucosal defense mechanism. Recruited parasympathetic reflexes cause submucosal gland secretion via acetylcholine and muscarinic M(3) receptors. Itching, sneezing, and other avoidance behaviors rapidly clear the offending agents from the upper airways and protect the lower airways. Dysfunction of these nerves may contribute to allergic rhinitis, infectious rhinitis, nasal hyperresponsiveness, and possibly sinusitis. Sympathetic arterial vasoconstriction reduces mucosal blood flow, sinusoidal filling, and mucosal thickness, and so restores nasal patency. Loss of sympathetic tone may contribute to some chronic, nonallergic rhinopathies. Human axon responses differ from those in animals, an important distinction that limits extrapolation from other species.
机译:刺激鼻部感觉神经导致疼痛和闷闷不乐的感觉。 C型伤害感受神经释放神经肽,包括P物质和降钙素基因相关肽,从而增加血浆外渗和腺体分泌。该轴突反应充当直接的保护性粘膜防御机制。募集的副交感神经反射通过乙酰胆碱和毒蕈碱M(3)受体引起粘膜下腺分泌。瘙痒,打喷嚏和其他回避行为会迅速清除上呼吸道的有害物质,并保护下呼吸道。这些神经功能障碍可能会导致变应性鼻炎,感染性鼻炎,鼻腔过敏和鼻窦炎。交感性动脉血管收缩可减少粘膜血流量,正弦曲线充盈和粘膜厚度,从而恢复鼻腔通畅性。失去同情心可能会导致一些慢性非过敏性鼻病。人轴突反应与动物反应不同,这是一个重要的区别,它限制了其他物种的外推作用。

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