The role of RARs and SARs, as a structural elements of the cough reflex, is rather limited, they probably regulate the duration and magnitude of the inspiratory and expiratory phases of coughing but do not usually initiate the reflex itself ( Canning et al. They are not sensitive to chemicals, unless these substances cause airway edema, increase mucus secretion or induce the changes in airway muscle tone. These fibers participate in the regulation of breathing pattern, bronchomotor response and other reflex responses in the respiratory tract ( Mazzone 2005, Widdicombe 1995). The main stimuli for these receptors include lung volume changes, contraction of airway smooth muscles and the airway wall edema. These fibers have relatively fast conduction speed (10–20 m/s) and their endings are classified as rapidly or slowly adapting receptors (RARs and SARs, respectively) based on the adaptation pattern to the lung inflation. Airway mechanosensors are derived from the nodose ganglion and terminate in airways and lungs. Airway afferents relevant for cough are classified into mechano- and chemosensitive terminals depending on their activation profile. ![]() The bodies of the neurons innervating airways are located in the nodose and jugular ganglia of the vagal nerve ( Mazzone 2005). The vagotomy or vagal nerve cooling in animals completely abolishes cough ( Canning et al. There is indisputable evidence on the close relationship between cough and vagal nerve function. First, the effect of cough on heart function is presented and then, the mechanisms of “cardiac cough” or “cough triggered by heart function disorders” are discussed. Both directions of the heart-cough interactions are reviewed. Therefore, the main objective of this review is to discuss the available data on possible heart-cough relations. Nonetheless, the mechanisms of heart disorder-related cough still remain not completely elucidated. Although the prevalence of arrhythmia-related cough seems to be rather low, the mutual interactions have been recently recognized by national and international cough guidelines ( Kardos et al. heart diseases, mainly arrhythmias, being a trigger of cough ( Hargreaves and Channon 1994, Odeh and Oliven 1996, Niimi et al. However, there is a number of case reports documenting an opposite relation, e.g. Also, the impact of cough on heart hemodynamics associated with the robust changes of intraabdominal and intrathoracic pressure, influencing preload or afterload, is well known ( Sharpey-Schafer 1953, Lo Mauro and Aliverti 2018). the alterations in sinus heart rhythm during breathing and the hypoxemia causing the increase in blood pressure and supraventricular arrhythmias in obstructive sleep apnea ( Shepherd 1981, Shivkumar et al. Strong physiological interactions between respiration and heart function have been well described, including e.g. trigeminal, glossopharyngeal) nerves modulate the final cough motor pattern ( Canning et al. These neuronal circuits are subjects of neuronal plasticity, where simple neuronal interaction or more complex neuroplastic relationships between vagal and other than vagal (e.g. ![]() Although the vagal nerve plays a fundamental role in cough, the significance of convergence of other than vagal afferent inputs to the neuronal clusters in the brainstem - known as the cough pattern generator - cannot be ignored. ![]() 2014, Widdicombe 1995), because the cough is related to stimulation of vagal afferents, irrespective of the organ localization ( Widdicombe 1995). esophagus or external auditory canal ( Canning et al. Even though cough is triggered exclusively by vagal reflex and is aimed at the airway defence, it can be elicited and modulated by afferent inputs from extrapulmonary organs, e.g. It is also a common symptom of various pulmonary diseases. Cough is a defensive mechanism of the airways evoked by stimulation of nerve endings localized in larynx, trachea and main bronchi ( Canning et al.
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