Nitric oxide and parasympathetic vascular and secretory control of the dog nasal mucosa.

Nasal vascular and secretory responses to local intra-arterial injection of acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) and to electrical stimulation of the nasal parasympathetic nerve fibres were recorded in dogs anaesthetized with pentobarbital. The influence of pretreatment with atropine and propranolol and the nitric oxide synthetase (NOS) inhibitor Nomega-nitro-L-arginine (L-NNA) was analysed. As a marker for NOS, NADPH-diaphorase (NADPH-d) histochemistry was studied in the sphenopalatine ganglion, trigeminal nerve and nasal mucosa. Local intra-arterial infusion of ACh and VIP evoked dose-dependent vasodilatation and nasal secretion which were not modified in the presence of L-NNA. The NO donor nitroprusside induced dose-dependent vasodilatation but no secretion. Atropine did not reduce the vasodilatation evoked by the parasympathetic nerve stimulation, but did reduce the secretory response by 55% (p < 0.05). During L-NNA infusion, the atropine-resistant vasodilatation evoked by parasympathetic nerve stimulation was reduced by a further 80% (p < 0.01) and the non-cholinergic secretory response was reduced by a further 30% (p < 0.05). Simultaneous infusion of the NO donor nitroprusside reversed the secretory response but not the vasodilator response to parasympathetic nerve stimulation. Histochemical studies revealed that NADPH-d activity was co-localized with VIP in parasympathetic axons. These observations suggest that NO could act as a non-cholinergic parasympathetic neurotransmitter in the vascular and secretory control of the dog nasal mucosa.

Modulation by neuropeptide Y of parasympathetic nerve-evoked nasal vasodilatation via Y2 prejunctional receptor.

1. In pentobarbitone anaesthetized dogs, preganglionic stimulation of the superior cervical sympathetic nerve (15V, 1 ms, 10 Hz) induced marked reduction of nasal arterial blood flow, whereas parasympathetic nerve stimulation (5 V, 1 ms, 10-30 Hz) evoked frequency-dependent vasodilatation. 2. Sympathetic nerve stimulation for 3 min at 10 Hz evoked significant (P < 0.05) and prolonged attenuation of the vasodilator response to subsequent parasympathetic stimulation. Pretreatment with phentolamine (0.5 mg kg-1 h-1), propranolol (1 mg kg-1) and atropine (0.5 mg kg-1) reduced the vasoconstrictor effect of sympathetic stimulation by 35 +/- 4% whereas the parasympathetic nerve-evoked vasodilatation was not significantly modified. Atropine-resistant parasympathetic vasodilatation remained significantly attenuated for more than 30 min after non-adrenergic sympathetic nerve-evoked vasoconstriction. 3. Vasodilator effects of exogenous vasoactive intestinal polypeptide and peptide histidine isoleucine and vasoconstrictor effects of exogenous neuropeptide Y (NPY) and the NPY analogue [Leu31, Pro34] NPY (Y1-receptor agonist, 8 nmol kg-1), were not altered by adrenoceptor antagonists and atropine f1p4eas the effects of exogenous noradrenaline and acetylcholine were virtually abolished. Attenuation of parasympathetic-evoked vasodilatation could be mimicked by exogenous NPY (8 nmol kg-1) and the NPY analogue, N-acetyl [Leu28, Leu31] NPY 24-36 (Y2-receptor agonist, 20 nmol kg-1) but not by exogenous Y1-receptor agonist. The Y2-receptor agonist did not show significant vasoconstrictor action. 4. It is concluded that sympathetic nerve stimulation attenuates parasympathetic vasodilatation via NPY release acting on prejunctional Y2 receptors.

Effect of multiple ligations of the external carotid artery and its branches on blood flow in the internal maxillary artery in dogs.

PURPOSE: The effect of occlusion of the external carotid system on blood flow of the internal maxillary artery was investigated in 16 dogs. METHODS: The external carotid system was occluded by ligation or clamping at different levels separately or simultaneously and the blood flow of the internal maxillary artery was measured with an electromagnetic flowmeter before and after each occlusion. RESULTS: The ligation of the external carotid artery below (low ligation) and above (high ligation) the origin of the occipital, lingual, and facial arteries reduced the blood flow by 61.1% and 71.5%, respectively. Low ligation together with ligation of the lingual artery reduced the blood flow by 73.5%. Multiple ligations (high and low ligations combined with ligations of the occipital, lingual, and facial arteries) reduced the blood flow by 81.8%. The internal maxillary artery was sectioned after the multiple ligations, and retrograde flow from the distal segment was studied. The flow was only a trace and could not be measured with the flowmeter. Total blood loss from both ends almost equaled the blood flow of the proximal segment, 18.2% of normal. CONCLUSIONS: Multiple occlusion appears to be the most effective treatment for hemorrhage from the initial part of the internal maxillary artery.

Nutrient and shunt flow responses to vidian nerve stimulation in nasal and facial tissues of the dog.

The potency of parasympathetic vasomotor efferent nerves in controlling blood flow of the face and nose was indicated by the following features attributed to the maxillary artery and their vascular compartments in dogs. Electrical stimulation of the vidian nerve induced a frequency-dependent increase in maxillary flow, which was due to a significant decrease in resistance to flow in nutrient and shunt vessels. Pronounced increases in perfusion rates mainly occurred in evaporative tissues of the nose, in particular the naso-maxilloturbinates and alar fold during vidian nerve stimulation, while those, for example, of the skin remained unchanged. Adrenergic and subsequent cholinergic blockade left the response pattern of maxillary flow to vidian nerve stimulation basically unaffected. Both nutrient and shunt flows contributed to the parasympathetically induced increases in maxillary flow while responses were compartmentalized similar to that found in untreated animals. Apart from sympathetic vasoconstrictor inputs, these results show that cholinergic and non-cholinergic parasympathetic vasodilator inputs contribute to the adjustment of vasomotor tone in the maxillary vascular bed.

The effect of experimental ligation of the external carotid artery and its major branches on haemorrhage from the maxillary artery.

The effect of ligation of the external carotid artery and its major branches on blood flow from the maxillary artery was investigated in four Chacma baboons. The left common carotid artery and its branches were surgically exposed and the maxillary artery was isolated, sectioned and cannulated. Blood flow from the proximal segment of the maxillary artery was determined with and without occlusion of the common carotid artery, the external carotid artery above and below the origin of the linguo-facial trunk and the posterior auricular occipital trunk. Ligation of the external carotid artery below and above the origin of the lingual and facial arteries reduced maxillary artery blood flow by 40% and 73% respectively. Ligation of the external carotid artery above the origin of the lingual and facial vessels, together with ligation of the posterior auricular occipital trunk reduced maxillary artery blood flow by 99.2%. On the basis of these experimental findings, it is suggested that maxillary artery haemorrhage in man may be most effectively controlled by ligation of the external carotid artery in the retromandibular fossa, distal to the origin of the posterior auricular artery, combined with ligation of the superficial temporal artery at the root of the zygoma.

Vascular changes in the pterygopalatine fossa after craniofacial dysjunction surgery.

A study was undertaken to determine vascular changes and the timing of these changes after craniofacial dysjunction surgery. Ten adult male Macaca cynomulgus monkeys were studied with techniques using angiograms and vascular vinyl cast preparations before and after unilateral Le Fort III osteotomy. After surgical disruption of the maxillary artery, the flow of blood was initially maintained by anastomotic branches of the ipsilateral internal carotid artery. Stepwise reconstruction of the disrupted maxillary artery took place via numerous collateral vessels that bridged the site of disruption; continuity of the artery was nearly normal by five weeks.