Nasonasal reflex mechanisms in anaesthetized dogs.

In dogs anaesthetized with pentobarbitone, we recorded bilateral vascular and secretory responses to unilateral stimulation of intranasal afferent nerves. Nasonasal reflexes evoked by intranasal light mechanical stimulation, intranasal application of cold saline (2 ml at 3 degrees C), capsaicin (0.003-0.3 mmol) and antidromic electrical stimulation (15 V, 0.2 ms) of the trigeminal nerve at 10 Hz for 45 s were recorded. Vascular and secretory responses were studied before and after atropine pre-treatment, after ipsilateral section of the post-ganglionic parasympathetic fibres and the trigeminal nerve, and after administration of the ganglionic nicotinic receptor antagonist chlorisondamine. All stimuli studied induced bilateral increases in nasal arterial blood flow and secretion, although the contralateral responses were smaller under control conditions (p < 0.05). Bilateral vasodilatation evoked by mechanical stimulation, capsaicin and antidromic trigeminal nerve stimulation was resistant to atropine. The ipsilateral non-cholinergic vasodilatation evoked by mechanical stimulation or capsaicin was reduced by 50% (p < 0.05) after section of both trigeminal and post-ganglionic parasympathetic fibres. The remaining ipsilateral vasodilatation induced by these two stimuli was significantly reduced after chlorisondamine. The ipsilateral secretory responses to all stimuli studied were significantly reduced (p < 0.05), but not abolished by atropine. Contralateral secretory responses to all stimuli studied were not affected by atropine, the section of either the parasympathetic or trigeminal nerves, or chlorisondamine, suggesting the activation of local axon reflexes only. We conclude that unilateral intranasal stimulation of primary afferent neurons with light pressure, cold saline and capsaicin induces bilateral vascular and secretory responses via axon reflex mechanisms, as well as the activation of local and central sensory-parasympathetic reflex arcs.