Enhanced sensitivity of capsaicin-sensitive afferent airway nerves inthe pathogenesis of cough
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Enhanced sensitivity of capsaicin-sensitive afferent airway nerves inthe pathogenesis of cough

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Published .
Written in English


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Edition Notes

Thesis (M.D.) - University College Dublin, National University of Ireland, 1994.

StatementFinbarr O"Connell.
ID Numbers
Open LibraryOL20222530M

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  The mechanism of cough associated with upper respiratory infection (URI) is poorly understood. This paper reports a study of the role of altered sensitivity of capsaicin-sensitive airway nerves. In a prospective study, baseline (B) capsaicin-induced cough and methacholine-induced airway responsiveness were measured in healthy by:   The hallmark of sensory hyperreactivity is an enhanced capsaicin induced cough reflex. The cough reflex can be modified by activation of nociceptive (capsaicin-sensitive) nerve terminals. The aim of our study was to assess the influence of exposure to CO 2 concentrations up to vol% on capsaicin induced cough reflex on four different by: 6.   Cough sensitivity to capsaicin increased in luteal phase in subjects with normal menstrual cycle, and this functional change was not present in group with contraceptive pills. The cough sensitivity correlates with the Pg/E2 ratio, and relative lack of oestrogen in luteal phase is associated with higher cough sensitivity to by: 3. Sensitization of capsaicin-sensitive lung vagal afferent (CSLVA) fibers by chemical mediators is important in the pathogenesis of hyperreactive airway diseases.

selectively enhances the sensitivity of capsaicin-sensitive C-fibres mediating cough, and increases the neuropeptide content of airway nerves, whilst leaving the bronchocon-strictor response unaffected [7]. At the same time, the cough response to cigarette smoke is unchanged, sug-gesting a selective upregulation of capsaicin-sensitive C-fibres. Airway nerves also may release neurotransmitters, which have proinflammatory effects. Thus neuropeptides such as substance P, neurokinin A, and calcitonin gene–related peptide (CGRP) may be released from sensitized inflammatory nerve endings in the airways or skin to increase and extend the ongoing inflammatory response (Fig. ).There may also be a reduction in the activity of enzymes. Increasing interest and extensive investigations have been focused on uncovering the mechanisms underlying hypersensitivity of these airway afferents, and their role in the manifestation of various symptoms under pathophysiological conditions. Several important and challenging questions regarding these sensory nerves are discussed. However, one of the two types of the afferent nerve conducts of the cough reflex is characterized by rapidly adapting responses to acidification of the large airway epithelium; they are capsaicin-insensitive but may cause coughing, although no heightened response to tussive agents such as capsaicin has been detected.

The capsaicin-sensitive afferent fibers in the airway are considered to be nociceptive-like free nerve endings and have been implicated in the development of lower airway hyperreactivity (29, 62). It has been demonstrated that laryngeal application of capsaicin can trigger several airway reflexes, including bronchoconstriction, cough, apnea. The experimental research in the area of airway sensory nerves suggests that there are two main vagal afferent nerve subtypes that can directly activate cough – extrapulmonary airway C-fibres.   Chronic cough is often associated with an increased response to tussive agents such as capsaicin. Plastic changes in intrinsic and synaptic excitability in the brainstem, spine, or airway nerves can enhance the cough reflex, and can persist in the absence of the initiating cough event. Tachykinin-containing, capsaicin-sensitive C-fibres also innervate the airways and have been implicated in the cough reflex. Capsaicin-sensitive nerves act centrally and synergistically to modify.