The cervical sympathetic nerve trunks contain a large number of preganglionic and postganglionic sympathetic nerve fibres which innervate a variety of structures in the head and neck, with a potential to influence ventilation and upper airway resistance. These include the sympathetic innervation to the carotid body [1], carotid sinus [2], thyroid gland [3] and the vasculature of the upper airway mucosa [4].Several studies have examined the effects of cervical sympathetic nerve stimulation on carotid body function and on ventilation in anaesthetized and decerebrate cats but results have been conflicting. Thus, although sympathetic stimulation can cause small increases or decreases in chemoreceptor activity in the sinus nerve [5], it usually induces a large increase in ventilation [6] which is abolished by sinus nerve section. Therefore, the ventilatory effects appear unrelated to chemoreceptor afferent activity, yet cutting the sinus nerves abolishes the ventilatory effect. The sinus nerves also contain carotid sinus baroreceptor afferents which can influence ventilation and the activity of which can be increased by sympathetic stimulation [7]. However, this appears to be an unlikely explanation for the ventilatory excitation caused by sympathetic stimulation since baroreceptor activity is inhibitory to breathing [8].Recently, it has been shown that cutting the ganglioglomerular nerves containing the sympathetic nerve supply to the carotid body causes a decrease in ventilation in normoxia but has no effect on the ventilatory responses to hypoxia and hypercapnia in awake goats [9]. However, in anaesthetized cats, ganglioglomerular nerve section enhances the carotid chemoreceptor response to sustained hypoxia [10]. Cervical sympathetic nerve stimulation affects thyroid hormone secretion in mice [3] and removal of the superior cervical ganglion decreases thyroid hormone secretion in the rat [11]. However, in these studies, the effects on metabolic rate and breathing were not examined.Since the cervical sympathetic nerves exert an influence on ventilation and thyroid function and since the activity in these nerves has a respiratory modulation and is stimulated by systemic hypoxia and hypercapnia [12], it was hypothesized that cutting the cervical sympathetic trunks should affect ventilation and the ventilatory responses to hypoxia and hypercapnia. Therefore, the purpose of the present investigation was to examine the effects of cervical sympathetic nerve section on ventilation in normoxia, hypoxia and hypercapnia in conscious rats. In addition, because of the controversial findings concerning the effects of cervical sympathetic nerve stimulation on breathing, the ventilatory effects of cervical sympathetic nerve stimulation in anaesthetized rats were also examined in order to establish the ventilatory effects of the activation of these nerves in this species.It has previously been demonstrated that passing cool air through the isolated upper airway causes a fall in upper A constant airflow was applied to the upper ai...

The upper airway (UA) of adult animals is known to contain carbon dioxide‐sensitive receptors and UA CO2 reflexly affects breathing, UA dilator muscle activity and UA resistance. These effects may function in the control of UA patency. There is evidence that some UA reflexes are stronger in young than in adult animals, but it is not known whether CO2‐sensitive receptors are present in the UA of young animals, and the effects of UA CO2 on UA resistance and on UA dilator muscle activity have not been investigated in young animals. The responses of ventilation, UA resistance and geniohyoid muscle electromyographic activity to warm air containing 10% CO2 applied to the isolated UA were measured in anaesthetized, vagotomized young guinea‐pigs breathing spontaneously through a low‐cervical tracheostomy. Upper airway carbon dioxide caused an increase in ventilation (46.7±16.3 to 49.9±16.8 mL·min‐1·100 g body weight‐1) and upper airway resistance (56.8±14.8 to 63.7±17.7 cmH2O·L‐1·s‐1·kg body weight‐1). Similar effects were obtained following vagotomy. Geniohyoid activity became apparent following vagotomy and this activity was reduced by upper airway carbon dioxide. These responses were abolished by topical anaesthesia of the upper airway. This suggests that the reflexes seen are due to carbon dioxide‐sensitive receptors in the upper airway.

No abstract

No abstract

No abstract