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In the present study we investigated the possibility of central convergence of neural pathways coming from distant anatomical regions in modulating the cough response. We addressed this issue by inducing cough from the tracheo-bronchial region on the background of capsaicin-stimulated and mesocain-blocked nasal mucosa in 14 anesthetized guinea pigs. The control group consisted of 6 guinea pigs in which the active agents, capsaicin and mesocain, were substituted for by inert physiological saline. All animals were tracheostomized, and the larynx was disconnected from the proximal part of the trachea with preserved innervations, and all were subjected to the same protocol. Cough, induced by mechanical irritation of the tracheo-bronchial mucosa, was elicited three times: in the control condition, after intranasal capsaicin challenge, and after another capsaicin challenge preceded by intranasal instillation of a local anesthetic, mesocain. The main finding of the study was that the number of cough efforts per bout, assessed from positive deflections on the intrapleural pressure recordings, was significantly enhanced by intranasal capsaicin challenge and this effect was reversed by intranasal pretreatment with the anesthetic mesocain [2.1 ±0.2 (control) vs. 3.5 ±0.4 (capsaicin) vs. 2.2 ±0.2 (capsaicin after mesocain) (P<0.01)], with no appreciable changes in the magnitude of cough efforts. The cough response in the control group remained unchanged. We conclude that tracheo-bronchial cough may be modified by neural sensory input to the brain coming from nasal mucosa. Therefore, cough reflex is subject to central convergence of peripheral neural pathways originating at distant anatomical locations.
Re-evaluation of our earlier c-Fos-like immuno-reactive studies and brainstem transection/lesion experiments in over 40 anaesthetized, non-paralyzed cats allowed comparison of two distinct airway defensive reflexes with the distinct generators for inspiration (I) and expiration (E), described recently in juvenile rats. The spiration reflex (AspR) is characterized by solitary rapid and strong inspiratory effort with a reciprocal inhibition, preventing a subsequent active expiration, while the expiration reflex (ExpR) manifests by rapid and strong expiratory effort, starting without a preceding, inspiration, or reciprocal inhibition of occasional spontaneous inspiration. The retro-trapezoid nucleus/parafacial respiratory group neurones described as the distinct generator for active E in rats, are activated also during the ExpR in adult cats. Brainstem transection 5 mm above the obex eliminates the E generator and the ExpR, but preserves the I generator located in the pre-Bötzinger Complex, and also the AspR. This suggests the existence of a distinct I generator in cats as well as rats, and its contribution to the generation of the AspR. Persistence of the AspR in adult cats during asphyxic gasping, their similar character and the strong activation of I neurones at many places in the medulla and pons, suggest a common brainstem neuronal circuit contributing to generation of both the gasping and the gasp-like AspR. That the AspR and ExpR have distinct multilevel brainstem control mechanisms supports the dual theory of control and provides unique models for testing respiratory rhythm and pattern generation. The AspR may be compared with the powerful "auto-resuscitation effects of asphyxic gasping"; the ExpR may underly the effectiveness of the laryngeal chemoreflexes in prevention of lung diseases.
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