Sympathetic vascular control of the pig nasal mucosa: (I) increased resistance and capacitance vessel responses upon stimulation with irregular bursts compared to continuous impulses

An in vivo model is described in which pentobarbital anaesthetized pigs were used to study the sympathetic nervous control of the nasal mucosal vascular bed. Changes in blood flow in the sphenopalatine artery (representing nasal blood flow) and in the volume of the nasal cavity (mainly reflecting blood content in venous sinusoids), upon electrical stimulation of the cervical sympathetic trunk, were recorded simultaneously. Single impulses (15V, 5 ms) reduced both the arterial flow and the volume of the nasal mucosa. The effects of nerve stimulation with a continuous train of impulses at 0.59, 2 and 6.9 Hz were compared with those caused by stimulation with the irregular bursting pattern, triggered by recorded human sympathetic vasoconstrictor nerve activity, with the same average frequencies. Both types of stimulation reduced nasal blood flow and volume, but the responses were significantly larger with burst stimulation at 0.59 Hz. The volume reduction was already maximal at 0.59 Hz while the blood flow response increased further higher frequencies. Local intra‐arterial pretreatment with the α‐adrenoceptor antagonist phenoxybenzamine significantly attenuated the flow and volume responses to single impulses, while clear‐cut reductions in blood flow (by 40%) and volume (by 80%) remained, upon stimulation, at 6.9 Hz. Noradrenaline given intra‐arterially caused a dose‐dependent reduction in nasal blood flow and volume. The noradrenaline effects were blocked by phenoxybenzamine treatment. The results show that the pig nasal mucosa represents a model where both blood flow and volume changes can be studied in parallel in vivo. Furthermore, stimulation with the firing pattern of human vasoconstrictor nerves, i.e. irregular bursts, causes larger vascular responses in the pig nasal mucosa compared to a continuous stimulation. The large residual vascular responses to sympathetic nerve stimulation at high frequency after a‐adrenoceptor blockage may be mediated by some other non‐adrenergic transmitter substance(s).