Effects of stimulation of nasal and superior laryngeal inputs on the hindlimb vasculature of anaesthetized cats.

1. In chloralose-anaesthetized artificially ventilated cats, either stimulation of the nasal mucosae with water or electrical stimulation of the superior laryngeal nerve (s.l.n.) resulted in apnoea, as measured from the phrenic nerve activity, and a rise in perfusion pressure of a hindlimb perfused at constant flow. In the absence of changes in venous pressure this vascular response would indicate vasoconstriction in the hindlimb. There was, however, no significant change in either heart rate or arterial blood pressure. 2. Simultaneous stimulation of the nasal mucosae and s.l.n. also resulted in apnoea but with a larger hindlimb vasoconstriction than was obtained with stimulation of only one input. This increased vasoconstriction was not significantly different from the one which in theory could be obtained by summing the two individual responses from stimulation of the nasal mucosae or s.l.n. 3. In cats anaesthetized with chloralose-urethane, stimulation of the nasal mucosae or s.l.n. also evoked an apnoea and hindlimb vasoconstriction. However, in these animals this was accompanied by a bradycardia and small fall in arterial blood pressure. 4. The present results show that whilst stimulation of two parts of the upper respiratory tract evokes qualitatively similar responses in the hindlimb vasculature, simultaneous activation of the two stimuli does not appear to result in facilitation of this hindlimb vasoconstrictor response, simply an addition of those obtained on separate stimulation. The bradycardia evoked in response to upper airway stimulation is dependent on the anaesthetic used and in the present experiments could only be obtained in animals anaesthetized with choralose-urethane.