scholarly journals Sciatic Nerve Stimulation Does Not Increase Endogenous Adenosine Production in Sensory-Motor Cortex

1992 ◽  
Vol 12 (5) ◽  
pp. 835-843 ◽  
Author(s):  
Frances J. Northington ◽  
G. Paul Matherne ◽  
Sharon D. Coleman ◽  
Robert M. Berne
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Motor Cortex ◽  
Sciatic Nerve ◽  
Nerve Stimulation ◽  
Somatosensory Stimulation ◽  
Sensory Motor ◽  
Adenosine Antagonist ◽  
Sciatic Nerve Stimulation

Adenosine participates in the coupling of cerebral blood flow to oxygen consumption in the brain during such stimuli as hypoxia, ischemia, and seizures. It has been suggested that it also participates in the regulation of cerebral blood flow during somatosensory stimulation, a condition during which cerebral blood flow and oxygen consumption appear to be uncoupled. Interstitial adenosine was estimated by the microdialysis technique and cerebral blood flow was measured by hydrogen clearance in the hindlimb sensory-motor cortex during sciatic nerve stimulation. Cerebral blood flow increased from 102 to 188 ml min−1 100 g−1 (p < 0.001) in the cortex contralateral to the stimulated leg without an associated increase in interstitial adenosine (baseline 0.624 μ M, stimulation 0.583 μ M). Infusion of the adenosine antagonist 8-sulfophenyltheophylline failed to block an increase in cerebral blood flow during central sciatic nerve stimulation, but decreased basal cerebral blood flow (69 ml min−1 100 g−1). These results suggest that adenosine does not mediate changes in cerebral blood flow during somatosensory stimulation, but may participate in the regulation of cerebral blood flow in the basal state.

Pial arteriole dilation during somatosensory stimulation is not mediated by an increase in CSF metabolites

2002 ◽  
Vol 282 (3) ◽  
pp. H902-H907 ◽  
Author(s):  
Al C. Ngai ◽  
H. Richard Winn
Keyword(s):  
Sciatic Nerve ◽  
Nerve Stimulation ◽  
Csf Flow ◽  
Pial Surface ◽  
Somatosensory Stimulation ◽  
Flow Rates ◽  
Vasoactive Substances ◽  
Constant Rate ◽  
Pial Arterioles ◽  
Sciatic Nerve Stimulation

Pial arterioles supplying the hindlimb somatosensory cortex dilate in response to contralateral sciatic nerve stimulation. The mechanism of this pial vasodilation is not well understood. One possibility is that vasoactive metabolites released during brain activation may diffuse to subarachnoid cerebrospinal fluid (CSF) to dilate pial vessels. To test this hypothesis, we implanted closed cranial windows in rats and measured pial arteriolar dilation to sciatic nerve stimulation during constant rate superfusion of the pial surface with artificial CSF. We reason that flushing the pial surface with CSF should quickly dissipate vasoactive substances and prevent these substances from dilating pial arterioles. CSF flow (1 and 1.5 ml/min) significantly reduced pial arteriole dilation induced by 5% CO2 inhalation, but the same flow rates did not affect dilator responses to sciatic nerve stimulation. We conclude that brain-to-CSF diffusion of vasoactive metabolites does not play a significant role in the dilation of pial arterioles during somatosensory activity.

L-NNA suppresses cerebrovascular response and evoked potentials during somatosensory stimulation in rats

1995 ◽  
Vol 269 (5) ◽  
pp. H1803-H1810 ◽  
Author(s):  
A. C. Ngai ◽  
J. R. Meno ◽  
H. R. Winn
Keyword(s):  
Sciatic Nerve ◽  
Evoked Potentials ◽  
Nerve Stimulation ◽  
Somatosensory Stimulation ◽  
Vascular Responses ◽  
Cranial Window ◽  
Pial Arterioles ◽  
Sciatic Nerve Stimulation ◽  
Alpha Chloralose

We studied the local cerebrovascular response and somatosensory-evoked potentials (SEPs) to stimulation of the sciatic nerve during both short- (< 30 min) and long-term (90-150 min) exposure to topically applied NG-nitro-L-arginine (L-NNA). The pial circulation was visualized through a cranial window in alpha-chloralose-anesthetized rats. The diameter of pial arterioles (25-45 microns) and laser-Doppler flow (LDF) in the hindlimb sensory cortex were simultaneously measured during sciatic nerve stimulation. Short-term (< 30 min) treatment with L-NNA (1 mM) abolished the dilation of pial arterioles induced by acetylcholine, whereas the response to sciatic nerve stimulation was not affected. When applied for > 30 min, L-NNA induced severe vasomotion and attenuated the vascular responses to sciatic nerve stimulation. Long-term exposure to topically (1 mM) or systemically (10 mg/kg i.v.) applied L-NNA also attenuated cortical SEPs to sciatic nerve stimulation. Thus L-NNA-induced inhibition of vascular responses may be secondary to suppression of neuronal activity and an L-arginine metabolite, such as nitric oxide, may be involved in neurotransmission in the cerebral cortex during somatosensory activity.

scholarly journals Effect of Caffeine on Cerebral Blood Flow Response to Somatosensory Stimulation

2005 ◽  
Vol 25 (6) ◽  
pp. 775-784 ◽  
Author(s):  
Joseph R. Meno ◽  
Thien-son K. Nguyen ◽  
Elise M. Jensen ◽  
G. Alexander West ◽  
Leonid Groysman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sciatic Nerve ◽  
Intravenous Administration ◽  
Cortical Activation ◽  
Somatosensory Stimulation ◽  
Adenosine Receptor Antagonist ◽  
Arteriolar Diameter

Despite caffeine's wide consumption and well-documented psychoactive effects, little is known regarding the effects of caffeine on neurovascular coupling. In the present study, we evaluated the effects of caffeine, an adenosine receptor antagonist, on intracerebral arterioles in vitro and subsequently, on the pial circulation in vivo during cortical activation induced by contralateral sciatic nerve stimulation (SNS). In our in vitro studies, we utilized isolated intracerebral arterioles to determine the effects of caffeine (10 or 50 μmol/L) on adenosine-induced vasodilatation. At the lower concentration, caffeine was without effect, but at the higher concentration, caffeine produced significant attenuation. In our in vivo studies, we determined the cerebrospinal fluid (CSF) caffeine concentrations at 15, 30, and 60 mins after intravenous administration of 5, 10 and 40 mg/kg. At the latter two concentrations, CSF levels exceeded 10 μmol/L. We then evaluated the pial arteriolar response during cortical activation caused by contralateral SNS after administering caffeine intravenously (0, 5, 10, 20 30, and 40 mg/kg). The pial circulation was observed through a closed cranial window in chloralose-anesthetized Sprague—Dawley rats. The contralateral sciatic nerve was isolated, positioned on silver electrodes and stimulated for 20 secs (0.20 V, 0.5 ms, and 5 Hz). Arteriolar diameter was quantified using an automated video dimension analyzer. Contralateral SNS resulted in a 23.8%±3.9% increase in pial arteriolar diameter in the hindlimb sensory cortex under control conditions. Intravenous administration of caffeine at the lowest dose studied (5 mg/kg) had no effect on either resting arteriolar diameter or SNS-induced vasodilatation. However, at higher doses (10, 20, 30, and 40 mg/kg, intravenously), caffeine significantly ( P<0.05; n=6) attenuated both resting diameter and cerebral blood flow (CBF) responses to somatosensory stimulation. Intravenous administration of theophylline (10, 20, and 40 mg/kg), another adenosine receptor antagonist, also significantly reduced SNS-induced vasodilatation in a dose-dependent manner. Hypercarbic vasodilatation was unaffected by either caffeine or theophylline. The results of the present study show that caffeine significantly reduces cerebrovascular responses to both adenosine and to somatosensory stimulation and supports a role of adenosine in the regulation of CBF during functional neuronal activity.

The effect of sciatic nerve stimulation on spinal cord blood flow

1978 ◽  
Vol 38 (3) ◽  
pp. 435-439 ◽  
Author(s):  
Arthur I. Kobrine ◽  
Delbert E. Evans ◽  
Hugo V. Rizzoli
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Sciatic Nerve ◽  
Cord Blood ◽  
Nerve Stimulation ◽  
Spinal Cord Blood Flow ◽  
Sciatic Nerve Stimulation
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