SUMMARY1. In pentobarbitone-anaesthetized dogs with constant-flow vascular perfusion of nasal mucosa on both sides, nasal airway resistance, vascular resistance, vascular capacitance (via changes in total venous outflow) and blood flow in the anterior and posterior venous systems were measured.2. Electrical stimulation of the cut peripheral ends of the cervical sympathetic trunk, caudal nasal nerve, or major palatine nerve increased vascular resistance and decreased vascular capacitance and airway resistance. Propranolol and atropine had no effect on the responses while bretylium completely abolished them; phentolamine greatly lessened the vascular resistance response and partially decreased the vascular capacitance and airway responses. Hence, sympathetic stimulation causes constriction of the resistance vessels via a-adrenergic mechanism and constriction of capacitance vessels via a-adrenergic as well as some non-adrenergic and noncholinergic mechanisms.3. Denervation of the cervical sympathetic trunk, caudal nasal nerve and major palatine nerve decreased nasal vascular resistance and increased vascular capacitance and airway resistance, suggesting tonic sympathetic discharge to nasal mucosa via caudal nasal and major palatine nerves.4. Electrical stimulation of the nerve of pterygoid canal decreased vascular resistance but increased vascular capacitance (in the posterior venous system) and airway resistance to low-voltage stimulation (below 10 V), and decreased vascular capacitance (in the anterior venous system) and airway resistance to high-voltage stimulation (above 10 V). Hexamethonium reversed the vascular resistance response as well as vascular capacitance and airway responses to high-voltage stimulation. Bretylium and phentolamine enhanced the vascular resistance response and reversed vascular capacitance and airway resistance responses to high-voltage stimulation. Hence, low-voltage stimulation results in parasympathetic dilatation of resistance and capacitance vessels whereas high-voltage stimulation results in parasympathetic dilatation of resistance vessels and sympathetic constriction of capacitance vessels. The parasympathetic vasodilatation was atropine resistant and the sympathetic vasoconstriction was partially via az-adrenergic mechanisms.5. Denervation of the nerve of pterygoid canal did not affect vascular resistance, vascular capacitance or airway resistance suggesting negligible tonic parasympathetic and sympathetic discharges to nasal blood vessels via the nerve.MS 7611 M. A. LUNG AND J. C. C. WANG 6. Simultaneous optimal stimulation of sympathetic and parasympathetic nerves resulted in vasoconstriction, especially in capacitance vessels, suggesting sympathetic predominance over parasympathetic control.

SUMMARY1. Nasal vascular and airflow resistances have been measured in dogs, simultaneously on both sides separately.2. Vascular resistance was measured either by constant flow perfusion of the terminal branch of the maxillary artery (which supplies, via the sphenopalatine artery, the nasal septum, most of the turbinates and the nasal sinuses) or by measuring blood flow through this artery, maintained by the dog's own blood pressure.3. Airflowresistancewasassessedbyinsertingballoon-tippedendotrachealcatheters into the back of each nasal cavity via the nasopharynx, and measuring transnasal pressure at constant airflow through each side of the nose simultaneously.4. Preliminary experiments indicated that there was 5-10 % collateral anastomosis between the two sides.5. Close-arterial injection of drugs showed different patterns of response. 6. Adrenaline, phenylephrine, chlorpheniramine and low doses of prostaglandin F2a increased vascular resistance and lowered airway resistance.7. Salbutamol, methacholine and histamine lowered vascular resistance and increased airway resistance.8. Dobutamine decreased airway resistance with a small increase in vascular resistance.9. Prostaglandins E1, E2 and F2a (high dose) decreased both vascular and airway resistances.10. Substance P, eledoisin-related peptide and vasoactive intestinal polypeptide lowered vascular resistance with little change in airway resistance.11. The results are interpreted in terms of possible drug actions on precapillary resistance vessels, sinusoids and venules, and arteriovenous anastomoses. It is concluded that nasal airway resistance cannot be correlated with vascular resistance or blood flow, since the latter has a complex and ill-defined relationship with nasal vascular blood volume. M. A. LUNG AND OTHERS

SUMMARY1. Continuous stimulation of the preganglionic parasympathetic nerve (the ramus communicans of the mandibular ganglion) for 1-2 min at supramaximal voltage (5 V) and pulse duration (1 ms) increased salivary gland arterial inflow and this was accompanied by copious salivary secretion. The responses were recorded continuously during the period of stimulation. The frequency for initiating the responses was 0 5 Hz. Maximal responses occurred at 16 Hz. The response coefficient of arterial inflow to stimulus frequency was 0417 ml min-1 g-' Hz-1 and that of secretion to stimulus frequency was 0-016 ml min-' g-1 Hz-'.2. The secretory response to low and moderate levels of parasympathetic nerve stimulation (below 8 Hz) was not affected by a reduction or cessation in arterial inflow whereas the response to high level parasympathetic nerve stimulation (above 8 Hz) was significantly alleviated if blood flow to the gland was maintained (via controlled vascular perfusion) at a level less than that of the resting arterial inflow. However, when the gland was already secreting near-maximally (stimulated at 8 Hz), sudden cessation of blood flow for a short period of time (0-5-2 min) had no effect on the salivary flow.3. Continuous stimulation of the cervical sympathetic nerve for 1-2 min at supramaximal voltage (20 V) and pulse duration (1 ms) decreased arterial inflow and this was accompanied by scanty salivary secretion. The vascular response persisted during the period of stimulation. The secretory response was 15 s late in onset and might continue for 1 min after stimulation. The frequency for initiating the responses was 1-4 Hz. Maximal responses occurred at 16-32 Hz. The response coefficient of arterial inflow to stimulus frequency was -0-04 ml min-' g-1 Hz-' and that of salivary secretion to stimulus frequency was 0 001 ml min-' g-1 Hz-l.4. The secretory response to sympathetic nerve stimulation at different frequencies in glands with blood flow maintained at resting rate (via controlled vascular perfusion) resembled that in glands with spontaneous blood flow.5. Sympathetic nerve stimulation was found to retard salivary secretion caused by parasympathetic stimulation, irrespective of whether the gland received spontaneous arterial inflow or controlled vascular perfusion at a resting flow rate.6. The results suggest that the salivary secretion to stimulation of para- MS 8340 sympathetic nerve is independent of blood flow over a wide range of stimulus frequencies; however, the response to high frequency stimulation of the parasympathetic nerve may be affected by fluctuations in blood flow. Retardation of parasympathetic-induced salivary flow by superimposed sympathetic nerve stimulation may not be related to blood flow changes.

Patients suffering from allergic or vasomotor rhinitis usually show nasal mucosal hyperaemia, engorgement, hyperrhinorrhoea and obstruction of the nasal airway. The nasal mucosa is drained by two venous systems which are anatomically and functionally separate. The nasal mucosa receives tone discharges from the sympathetic nerves but not from the parasympathetic nerves. Sympathetic nerve stimulation causes constriction of the resistance vessels via the α -adrenergic mechanism and constriction of the capacitance vessels via the α -adrenergic mechanism and some non-adrenergic and non-cholinergic mechanism; the capacitance vessels are under more prominent sympathetic influence than the resistance vessels. Parasympathetic nerve stimulation causes non-cholinergic dilatation of both resistance and capacitance vessels; dilatation is more pronounced in the posterior venous system. Simultaneous optimal stimulation of the autonomic nerves resulted in vasoconstriction, especially of the capacitance vessels. Hence, nasal congestion may be related more to a withdrawal of sympathetic discharge than to an overactivity of the parasympathetic nerves.