In a feline model, tracheal blood flow is increased by vagal nerve stimulation and sensory C-fiber activation, and decreased by sympathetic stimulation.
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Should not change airway management; extends preclinical evidence on autonomic tracheal vascular control.
Nervous control of tracheal blood flow in the cat measured by the laser Doppler technique. Acta Physiol Scand 130 , 409–417. Received 2 December 1986, accepted 9 February 1987. ISSN 0001–6772. Department of Anaesthesia. Karolinska Hospital and Departments of Pharmacology and Endodontics, Karolinska Institute, Stockholm, Sweden. The tracheal blood flow as determined by the laser Doppler technique was continuously monitored in anaesthetized cats. Electrical stimulation of the right superior laryngeal nerve caused an atropine‐resistant increase in blood flow of the upper trachea. Unilateral vagal nerve stimulation at the cervical level in the presence of atropine induced a frequency‐dependent increase in blood flow of the lower trachea. Intermittent stimulation with bursts of impulses at a high frequency resulted in a considerably larger blood flow increase than a continuous low frequency stimulation giving the same total number of impulses. The ganglionic blocking agent chlorisondamine abolished most of the vagally induced increase in tracheal blood flow when using low threshold parameters (2 V, 0.2 ms) presumably activating preganglionic nerves. High threshold stimulation (10 V, 5 ms) however, still resulted in an increased blood flow suggesting antidromic activation of sensory C fibres. Local mechanical irritation or chemical irritation by capsaicin also increased tracheal blood flow. Furthermore, local application of calcitonin gene‐related peptide on to the mucosa caused a slowly developing, long‐lasting increase in blood flow. Electrical stimulation of the cervical sympathetic trunk and local application of adrenaline reduced tracheal blood flow. In conclusion, vagal nerve stimulation induces an atropine‐resistant increase in tracheal blood flow probably mainly by activating preganglionic parasympathetic nerves and possibly also by antidromic stimulation of C‐fibre afferents.
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Martling et al. (1987) studied this question.
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