scholarly journals On the effects of joining the cervical sympathetic nerve with the chorda tympani.

1904 ◽  
Vol 73 (488-496) ◽  
pp. 99-99
Author(s):  
John Newport Langley ◽  
Hugh Kerr Anderson

It is well known that the cervical sympathetic nerve and the chorda tympani have opposite actions upon the blood-vessels of the sub-maxillary gland, the former causing contraction of the vessels, and the latter, dilatation. Evidence has been given by one of us that the chorda tympani if united with the cervical sympathetic, can in time make connection with the nerve cells of the superior cervical ganglion and become in part vaso-constrictor fibres. Our experiments have been directed to determine whether the cervical sympathetic if allowed an opportunity of becoming connected with the peripheral nerve cells in the course of the chorda tympani will in part change their function from vaso-constrictor to vaso-dilator. Two experiments were made on anæsthetised cats, both give similar results, but one was much more conclusive on the point at issue than the other, and here we shall speak of that only. The superior cervical ganglion was excised and the central end of the cervical sympathetic nerve was joined to the peripheral end of the lingual, which contains the chorda tympani fibres. After allowing time for union and regeneration of the nerves, the cervical sympathetic was stimulated; it caused prompt flushing of the sub-maxillary glands, and the effect was repeatedly obtained.

1960 ◽  
Vol 198 (5) ◽  
pp. 949-954 ◽  
Author(s):  
Shu Chien

The supersensitivity of denervated superior cervical ganglion to acetylcholine was studied in cats at 2 weeks after the section of cervical sympathetic trunk on one side, with the other side as a control. The control ganglion required about four times as much of acetylcholine as the denervated side, in order to release the same amount of norepinephrine at the postganglionic endings. The relative quantity of norepinephrine released on acetylcholine administration to ganglia was determined indirectly by using the in vivo nictitating membrane as an indicator, whose responses to various doses of norepinephrine had been calibrated. The validity of such indirect determination of norepinephrine was shown by experiments in which the eyeballs were removed or the lever magnifications were made unequal. With control cats in which both cervical sympathetic trunks were cut acutely, the sensitivity of the ganglia on two sides to acetylcholine was almost equal.


1890 ◽  
Vol 47 (286-291) ◽  
pp. 379-390 ◽  

It is well known that by stimulating the sympathetic nerve in the neck the following effects can be produced :—(1) Retraction of the nictitating membrane; (2) protrusion of the eyeball and opening of the eye; (3) turning the eye, if previous to stimulation the optic axis is directed nasally, so that the optic axis is directed straight forwards, or it may be forwards and a little outwards


Author(s):  
D. M. DePace

The majority of blood vessels in the superior cervical ganglion possess a continuous endothelium with tight junctions. These same features have been associated with the blood brain barrier of the central nervous system and peripheral nerves. These vessels may perform a barrier function between the capillary circulation and the superior cervical ganglion. The permeability of the blood vessels in the superior cervical ganglion of the rat was tested by intravenous injection of horseradish peroxidase (HRP). Three experimental groups of four animals each were given intravenous HRP (Sigma Type II) in a dosage of.08 to.15 mg/gm body weight in.5 ml of.85% saline. The animals were sacrificed at five, ten or 15 minutes following administration of the tracer. Superior cervical ganglia were quickly removed and fixed by immersion in 2.5% glutaraldehyde in Sorenson's.1M phosphate buffer, pH 7.4. Three control animals received,5ml of saline without HRP. These were sacrificed on the same time schedule. Tissues from experimental and control animals were reacted for peroxidase activity and then processed for routine transmission electron microscopy.


1999 ◽  
Vol 86 (4) ◽  
pp. 1236-1246 ◽  
Author(s):  
Ling Chen ◽  
Anthony L. Sica ◽  
Steven M. Scharf

This study was designed to evaluate the importance of sympathoadrenal activation in the acute cardiovascular response to apneas and the role of hypoxemia in this response. In addition, we evaluated the contribution of the vagus nerve to apnea responses after chemical sympathectomy. In six pigs preinstrumented with an electromagnetic flow probe and five nonpreinstrumented pigs, effects of periodic nonobstructive apneas were tested under the following six conditions: room air breathing, 100% O2 supplementation, both repeated after administration of hexamethonium (Hex), and both repeated again after bilateral vagotomy in addition to Hex. With room air apneas, during the apnea cycle, there were increases in mean arterial pressure (MAP; from baseline of 108 ± 4 to 124 ± 6 Torr, P < 0.01), plasma norepinephrine (from 681 ± 99 to 1,825 ± 578 pg/ml, P < 0.05), and epinephrine (from 191 ± 67 to 1,245 ± 685 pg/ml, P < 0.05) but decreases in cardiac output (CO; from 3.3 ± 0.6 to 2.4 ± 0.3 l/min, P < 0.01) and cervical sympathetic nerve activity. With O2supplementation relative to baseline, apneas were associated with small increases in MAP (from 112 ± 4 to 118 ± 3 Torr, P < 0.01) and norepinephrine (from 675 ± 97 to 861 ± 170 pg/ml, P< 0.05). After Hex, apneas with room air were associated with small increases in MAP (from 103 ± 6 to 109 ± 6 Torr, P < 0.05) and epinephrine (from 136 ± 45 to 666 ± 467 pg/ml, P < 0.05) and decreases in CO (from 3.6 ± 0.4 to 3.2 ± 0.5 l/min, P < 0.05). After Hex, apneas with O2 supplementation were associated with decreased MAP (from 107 ± 5 to 100 ± 5 Torr, P < 0.05) and no other changes. After vagotomy + Hex, with room air and O2 supplementation, apneas were associated with decreased MAP (from 98 ± 6 to 76 ± 7 and from 103 ± 7 to 95 ± 6 Torr, respectively, both P < 0.01) but increased CO [from 2.7 ± 0.3 to 3.2 ± 0.4 l/min ( P < 0.05) and from 2.4 ± 0.2 to 2.7 ± 0.2 l/min ( P < 0.01), respectively]. We conclude that sympathoadrenal activation is the major pressor mechanism during apneas. Cervical sympathetic nerve activity does not reflect overall sympathoadrenal activity during apneas. Hypoxemia is an important but not the sole trigger factor for sympathoadrenal activation. There is an important vagally mediated reflex that contributes to the pressor response to apneas.


1987 ◽  
Vol 7 (1) ◽  
pp. 45-57 ◽  
Author(s):  
L. Edvinsson ◽  
J. R. Copeland ◽  
P. C. Emson ◽  
J. McCulloch ◽  
R. Uddman

Perivascular nerve fibers containing neuropeptide Y (NPY)-like immunoreactivity were identified around cerebral blood vessels of human, cat, guinea pig, rat, and mouse. The major cerebral arteries were invested by dense plexuses; veins, small arteries, and arterioles were accompanied by few fibers. Removal of the superior cervical ganglion resulted in a reduction of NPY-like material in pial vessels and dura mater. Pretreatment with 6-hydroxydopamine or reserpine reduced the number of visible NPY fibers and the concentration of NPY in rat cerebral vessels. Sequential immuno-staining with antibodies toward dopamine-β-hydroxylase (DBH) (an enzyme involved in the synthesis of noradrenaline) and NPY revealed an identical localization of DBH and NPY in nerve cell bodies in the superior cervical ganglion and in perivascular fibers of pial blood vessels, suggesting their coexistence. Administration of NPY in vitro resulted in concentration-dependent contractions that were not modified by a sympathectomy. The contractions induced by noradrenaline, 5-hydroxytryptamine, and prostaglandin F2α and the dilator responses to calcitonin gene-related peptide were not modified by NPY in rat cerebral arteries. However, the constrictor response to NPY was reduced by 70% in the presence of the calcium entry blocker nifedipine, and abolished following incubation in a calcium-free buffer. These data suggest an interaction of NPY at a postsynaptic site, which for induction of contraction may open calcium channels in the sarcolemma of cerebral arteries.


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