Some Observations on the Sympathetic Nervous System

1939 ◽  
Vol 85 (358) ◽  
pp. 902-902
Author(s):  
E. Arnold Carmichael

Outline of physiology of sympathetic nervous system and its effect on the cerebral blood-vessels. Other factors controlling cerebral blood-vessels, such as local intra-arterial pressure and gas tension. The action of adrenalin-like and cholin-like substances on the cerebral blood-vessels. Alteration in cerebral blood flow during a convulsion, and the accompanying changes in cerebro-spinal fluid pressure. Evidence for systemic sympathetic disturbance during a convulsion. Discussion of “vaso-vagal” attacks and “diencephalitic” epilepsy.

1979 ◽  
Vol 378 (3) ◽  
pp. 189-195 ◽  
Author(s):  
Eric T. MacKenzie ◽  
Anne P. McGeorge ◽  
David I. Graham ◽  
William Fitch ◽  
Lars Edvinsson ◽  
...  

1988 ◽  
Vol 255 (3) ◽  
pp. H563-H568
Author(s):  
C. D. Kurth ◽  
L. C. Wagerle ◽  
M. Delivoria-Papadopoulos

We examined cerebral blood flow (CBF) regulation by the sympathetic nerves in 12 newborn lambs (3–11 days old) during seizures, a potent reflex stimulator of the sympathetic nervous system. CBF was measured with microspheres, and seizures were induced with bicuculline. In six of these lambs, one hemibrain was denervated (D) chronically by interrupting the ipsilateral cervical sympathetic trunk; the other hemibrain remained innervated (I). Before and after 10, 35, and 70 min of seizures, cerebral gray matter blood flow (mean +/- SE ml.min-1.100 g-1) was, respectively, 12 +/- 3 (9%), 71 +/- 12 (21%), 120 +/- 15 (38%), and 54 +/- 5 (14%) greater (P less than 0.05) in the D than in the I hemibrain. In the cerebral white matter, hippocampus, caudate, and thalamus blood flows to the D and I hemibrains were similar before seizures but during seizures they were 10–39% greater (P less than 0.05) in the D than in the I hemibrain. Midbrain, brainstem, and cerebellum D and I blood flows were always similar. In the other six lambs, acute denervation during seizures increased ipsilateral cerebral gray and hippocampus blood flow by 10–31%, but unilateral electrical stimulation decreased ipsilateral cerebral gray, cerebral white, hippocampus, thalamus, and caudate blood flow by 17–27%. The data demonstrate that, during seizures, sympathetic nerve activity modifies regional CBF and the effect is sustained, suggesting a role for the sympathetic nervous system in newborn CBF regulation.


Neonatology ◽  
1990 ◽  
Vol 58 (4) ◽  
pp. 192-199 ◽  
Author(s):  
Pierre Monin ◽  
François Feillet ◽  
Jean-Michel Hascoet ◽  
Paul Vert

1960 ◽  
Vol 15 (1) ◽  
pp. 23-24 ◽  
Author(s):  
G. E. Burch ◽  
N. DePasquale

Simultaneous digital plethysmographic and brachial arterial pressure recordings in 11 normal subjects at rest in bed in a comfortable atmosphere showed that the spontaneous variations in digital volume (alpha and beta deflections) were independent of variations in arterial blood pressure. This indicates that the regulation of the caliber of the peripheral blood vessels as well as the spontaneous variations in the volume of the digital vessels is not passively produced by fluctuations in arterial blood pressure, including the Traube-Hering waves, but must be controlled by different centers and pathways of the sympathetic nervous system. Submitted on July 27, 1959


Cephalalgia ◽  
1987 ◽  
Vol 7 (6_suppl) ◽  
pp. 287-288
Author(s):  
M. L. Fasano ◽  
Marcello Mancini ◽  
L. A. Ferrara ◽  
M. Mancini

2016 ◽  
Vol 311 (3) ◽  
pp. H837-H848 ◽  
Author(s):  
Saqib Saleem ◽  
Paul D. Teal ◽  
W. Bastiaan Kleijn ◽  
Philip N. Ainslie ◽  
Yu-Chieh Tzeng

The dynamic regulation of cerebral blood flow (CBF) is thought to involve myogenic and chemoreflex mechanisms, but the extent to which the sympathetic nervous system also plays a role remains debated. Here we sought to identify the role of human sympathetic neurovascular control by examining cerebral pressure-flow relations using linear transfer function analysis and multivariate wavelet decomposition analysis that explicitly accounts for the confounding effects of dynamic end-tidal Pco2 (PetCO2) fluctuations. In 18 healthy participants randomly assigned to the α1-adrenergic blockade group ( n = 9; oral Prazosin, 0.05 mg/kg) or the placebo group ( n = 9), we recorded blood pressure, middle cerebral blood flow velocity, and breath-to-breath PetCO2. Analyses showed that the placebo administration did not alter wavelet phase synchronization index (PSI) values, whereas sympathetic blockade increased PSI for frequency components ≤0.03 Hz. Additionally, three-way interaction effects were found for PSI change scores, indicating that the treatment response varied as a function of frequency and whether PSI values were PetCO2 corrected. In contrast, sympathetic blockade did not affect any linear transfer function parameters. These data show that very-low-frequency CBF dynamics have a composite origin involving, not only nonlinear and nonstationary interactions between BP and PetCO2, but also frequency-dependent interplay with the sympathetic nervous system.


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