Reflex Control of Nasal Blood Vessels

1987 ◽  
Vol 96 (3) ◽  
pp. 273-277 ◽  
Author(s):  
Shigeki Nishihira ◽  
Thomas V. Mccaffrey

The effect of stimulation of vagal afferent fibers on nasal blood vessels was studied in 36 cats. Volume change of the nasal capacitance vessels was measured by plethysmographic balloons inserted into the nose. Electrical stimulation of the vagus nerve produced a vasodilatation of nasal mucosa. Pulmonary stretch receptor stimulation by veratridine alkaloid and progressive lung inflation in open-chest cats also produced a vasodilatation of the nasal mucosa. These reflexes were abolished by sectioning the vagus nerves. These results suggest a reflex arc between the lung and nasal capacitance vessels which arises from pulmonary stretch receptors.

1993 ◽  
Vol 265 (4) ◽  
pp. R733-R738 ◽  
Author(s):  
H. Izumi ◽  
K. Karita

Local application of capsaicin (threshold dose 150 microM) or nicotine (threshold dose 15 mM) to the nasal mucosa as well as electrical stimulation (threshold intensity 10 V) of the nasal mucosa elicited dose- or intensity-dependent blood flow increases in the ipsilateral lower lips of the anesthetized cats. Pretreatment with 3 mM capsaicin applied locally to the nasal mucosa abolished or reduced the vasodilation in response to capsaicin, nicotine, and ammonia vapor but not to light mechanical or electrical stimulation of the nasal mucosa. The blood flow increases elicited by all above stimuli were greatly reduced by pretreatment with hexamethonium, an autonomic ganglion blocker. These results suggest that stimulation of the nasal mucosa by chemical (capsaicin, nicotine, ammonia), mechanical, or electrical methods elicits the autonomic reflex vasodilatation in the cat lower lips. Furthermore, there seem to be at least two types of afferent fibers in the nasal mucosa of the cats: one type is capsaicin-sensitive fibers, while another type is capsaicin-resistant fibers involved in reflex vasodilatation.


1980 ◽  
Vol 88 (4) ◽  
pp. 434-438 ◽  
Author(s):  
Richard T. Jackson

An in vitro method for testing vasoactive drugs on nasal blood vessels is described. Isolated dog nasal mucosa contracts when treated with nasal decongestant or stimulated electrically. Vasodilating drugs inhibit this contraction. Atropine blocks the effects of acetylcholine on this tissue.


1988 ◽  
Vol 97 (3) ◽  
pp. 289-293 ◽  
Author(s):  
Keiichi Ichimura ◽  
Hiroyuki Mineda ◽  
Atsuro Seki

We used dog nasal blood vessels and an in vitro muscle tension-detecting technique to examine the vascular effects of several neuropeptides: Vasoactive intestinal polypeptide, substance P, neurotensin, somatostatin, and neuropeptide Y (NPY). Electrically induced vasoconstriction was inhibited by every peptide except neurotensin, which enhanced this response. Every preparation treated with somatostatin, and one tissue treated with NPY, showed an enhanced noradrenaline-induced contraction. Only NPY caused a tissue contraction. Preparations precontracted by methoxamine were relaxed by every peptide. These results indicate that all peptides examined have marked but varied vasoactivities.


1983 ◽  
Vol 91 (6) ◽  
pp. 648-652 ◽  
Author(s):  
Daniel J. Blum ◽  
Thomas V. McCaffrey

To define the relationship between central control of upper airway muscles and respiratory muscle function, the electromyographic responses of the dilator nares muscles to stimulation of chemoreceptors and pulmonary receptors were studied in six anesthetized dogs. Only at maximal levels of hypoxia was the inspiratory activity of the dilator nares significantly increased. Hypercapnic stimulation increased the inspiratory activity with each incremental increase in CO2. Pulmonary stretch receptor stimulation produced by lung inflation inhibited dilator nares activity. Pulmonary irritant receptor stimulation by intravenously administered histamine increased dilator nares activity, as did pulmonary J receptor stimulation by the intravenous administration of capsaicin.


1980 ◽  
Vol 89 (5) ◽  
pp. 462-466 ◽  
Author(s):  
Thomas V. McCaffrey ◽  
Eugene B. Kern

The response of laryngeal airway resistance to pulmonary receptor stimulation was studied in 20 mongrel dogs anesthetized with α-chloralose (80 mg/kg). Stimulation of pulmonary stretch receptors by lung inflation inhibited the phasic variation of laryngeal resistance during respiration and produced a sustained reduction of laryngeal resistance, which was related to lung inflation pressure. Stimulation of pulmonary J-receptors with capsaicin produced apnea and a large increase in laryngeal resistance. Capsaicin produced this reflex when injected into the pulmonary circulation but not when injected into the systemic circulation. Irritant receptor stimulation with histamine hydrochloride produced tachypnea and a reduction in inspiratory laryngeal resistance. Pulmonary receptor reflexes were abolished by dividing the vagus nerves distal to the origin of the recurrent laryngeal nerves. Laryngeal reflexes may be important in the regulation of respiration and the production of physiologic and pathologic alterations in pulmonary function.


1964 ◽  
Vol 207 (2) ◽  
pp. 303-307 ◽  
Author(s):  
B. J. Prout ◽  
J. H. Coote ◽  
C. B. B. Downman

In cats anesthetized with chloralose-urethane mixture, stimulation of an afferent nerve evoked a vasoconstrictor reflex (VCR) and a galvanic skin response (GSR) in the pads of the feet. Stimulation of the ventromedial medullary reticular substance at the level of the obex abolished the VCR and the GSR. VCR could also be reduced by occlusion during prolonged stimulation of another spinal or visceral afferent pathway. Medulla stimulation was effective without itself causing a sympathetic discharge to the paw, showing that inhibition rather than occlusion was operative. Anterior cerebellar stimulation also inhibited the VCR. Carotid sinus nerve stimulation did not abolish the VCR. It is concluded that the effective mechanism includes a bulbospinal inhibitory path projecting on a spinal vasoconstrictor reflex arc. This arrangement is similar to the descending pathways inhibiting other spinal reflexes but the VCR-inhibitory path can be activated independently of them.


1959 ◽  
Vol 148 (2) ◽  
pp. 437-449 ◽  
Author(s):  
E. L. Blair ◽  
A. A. Harper ◽  
C. Kidd ◽  
T. Scratcherd
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