Nasal vasoconstriction induced by electrical stimulation of the cat hypothalamus [proceedings].
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Biomedical subjects
Publications and source records attributed to R Eccles.
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1 Contractions of the cat nictitating membrane were elicited on stimulation of the internal carotid nerve, and the effects were studied of desipramine and two inhibitors of catechol-O-methyltransferase, U-0521 and pyrogallol, on the subsequent relaxation of the muscle. 2 The relaxation of the nictitating membrane occurred in at least two phases. The late phase of relaxation was prolonged after increase in the period of nerve stimulation and the duration of this phase was further prolonged after treatment with pyrogallol. 3 After inhibition of neuronal uptake of noradrenaline with desipramine both the early and late phases of relaxation were increased in duration, and subsequent administration of pyrogallol or U-0521 caused a further increase in the duration of the late phase of relaxation. 4 The results suggest that the late phase of relaxation of the nictitating membrane is influenced by efflux of noradrenaline from an extraneuronal pool.
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1. A method for studying in vivo the process of neuroeffector transmission in the nictitating membrane and nasal blood vessels of the cat is described. 2. Administration of desmethylimipramine or cocaine caused increases in both the amplitude and duration of the nasal and membrane responses which may be explained by inhibition of neuronal uptake of noradrenaline. 3. Phenoxybenzamine depressed the responses to nerve stimulation, but had little effect on the relationship between response amplitude and rate of recovery. 4. The relationship between response amplitude and rate of recovery is discussed and related to the sigmoid shape of a log concentration-response curve.
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Vasomotor responses from the nasal mucosa and tongue, and contractions of the nictitating membrane, were recorded on stimulation of the cervical sympathetic or internal carotid nerves. Preganglionic sympathetic nerve fibres which elicited a membrane response possessed a lower threshold than those which evoked nasal vasoconstriction, while the latter displayed a lower threshold than fibres which evoked tongue vasoconstriction. The sympathetic vasodilator fibres to the tongue whose activity was revealed after alpha-receptor blockade, had a similar threshold to the vasoconstrictor fibres. Membrane contraction, nasal vasoconstriction and occasionally tongue vasoconstriction could be evoked by stimulating the internal carotid nerve. The postganglionic fibres innervating the nasal mucosa had a similar threshold to those of the nictitating membrane, which may indicate that there are small myelinated fibres innervating the mucosa. The preganglionic compound nerve action potential had four major components, S1-S4. S1, S2 and usually S3 fibres were associated with membrane contraction; S2, S3 and sometimes S1 fibres were associated with nasal vasoconstriction; and S3, usually S2 and occasionally S1 fibres were associated with vasoconstriction in the tongue. It is concluded that each of these three groups of nerve fibres, but not S4 fibres, may include fibres associated functionally with the three effectors. There was a considerable difference between the relative amplitude of the responses of the three effectors elicited by stimulation of the cervical sympathetic nerve at frequencies between 0.2 and 2 Hz. Vasoconstrictor responses were relatively larger than membrane contractions suggesting differences in the mechanisms of neurotransmission at the neuroeffector junctions.
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1. A study has been made in the anaesthetized cat of the stimulation parameters required to separate the vasodilator and vasoconstrictor responses evoked in the nose by stimulating the cut peripheral end of the Vidian nerve.2. The extent of the vasodilation and vasoconstriction was found to be dependent on the stimulation frequency, but whereas vasodilation reached a maximum at 25 Hz, vasoconstriction occurred at lower frequencies and was maximum between 10 and 15 Hz.3. Atropine, in a dose much greater than that which inhibits nasal secretion, did not abolish the vasodilator responses evoked by Vidian nerve stimulation. This suggests that the Vidian nerve may convey atropine resistant fibres to the nasal vasculature.
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Incubation of cat nasal secretion with cat plasma releases a substance which will contract the cat isolated jejunum, a tissue specifically sensitive to bradykinin and similar peptides. The smooth muscle stimulating activity of the incubate is potentiated and prolonged 'by the addition of the kininase inhiibitor, EDTA. From the results it is concluded that the incubation of cat nasal secretion and plasma releases a kinin-like substance, and that this kinin may have a role in the secretory and vasomotor activity of the nasal mucosa.
1. A flow of watery nasal secretion can be induced in the anaesthetized cat either by electrical stimulation of the brain stem or by the simpler procedure of stimulating the cut peripheral end of the Vidian nerve. In both instances the rate of flow of secretion was dependent on the stimulation frequency. Because brain stem stimulation caused an increase in arterial blood pressure, nasal secretion was evoked in subsequent experiments by Vidian nerve stimulation.2. The application of nicotine to the sphenopalatine ganglion shows that the secretory fibres in the Vidian nerve relay in this ganglion and reach the nasal mucosa by way of the posterior nasal nerve.3. Inhibition by atropine of the secretion induced by Vidian nerve stimulation indicates that the secretory fibres are cholinergic.4. It is suggested that the induction of nasal secretion by Vidian nerve stimulation may be useful in assessing the effects of drugs on this secretion.
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Codeine is generally accepted as a standard or reference antitussive against which new antitussive medications can be compared. However there are very few studies which have investigated the antitussive efficacy of codeine using cough associated with upper respiratory tract infection (URTI) and there is little if any evidence to support the antitussive efficacy of codeine in this model. This paper discusses the mechanism of cough in man and describes some clinical investigations on the effects of codeine on cough associated with URTI. The recent clinical investigations do not provide any evidence to support an antitussive action of codeine in the treatment of cough associated with URTI yet there is evidence in the literature which indicates that codeine inhibits fictive cough in animal models and also has antitussive activity against both induced and chronic cough models in man. In order to explain these different effects of codeine on the different models of cough, a hypothesis is put forward that there are two cough pathways in man. A voluntary pathway associated with cough related to URTI which is not affected by codeine, and a reflex pathway associated with induced and chronic cough which is inhibited by codeine.
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