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.

Estimation of shear and flow rates in pial arterioles during somatosensory stimulation

1996 ◽  
Vol 270 (5) ◽  
pp. H1712-H1717 ◽  
Author(s):  
A. C. Ngai ◽  
H. R. Winn
Keyword(s):  
Shear Stress ◽  
Shear Rate ◽  
Sciatic Nerve ◽  
Nerve Stimulation ◽  
Wall Shear Rate ◽  
Somatosensory Stimulation ◽  
Pial Arterioles ◽  
Wall Shear ◽  
Sciatic Nerve Stimulation ◽  
Stress Dependent

We tested the hypothesis that a shear stress-dependent mechanism is involved in the dilation of pial arterioles during somatosensory stimulation. In alpha-chloralose-anesthetized rats implanted with cranial windows, we simultaneously measured the diameter and flow velocity of pial arterioles with video and dual-slit methods. Stimulation (0.2-0.3 V, 5 Hz, 0.5 ms pulses for 20 s) of the contralateral sciatic nerve evoked consistent dilator responses in pial arterioles (36 +/- 1 micron diam) without affecting blood pressure. The dilator responses consisted of an initial transient peak dilation of 30 +/- 3%, followed by a sustained dilation of 13 +/- 1% (n = 11). Mean velocity increased by 16.4 +/- 5.7% at 5 s after stimulus onset. Wall shear rate and volume flow were calculated from diameter and velocity data by assuming a parabolic flow profile. There was no significant change in wall shear rate, whereas flow rate increased significantly during sciatic nerve stimulation. The present findings suggest that a flow (shear stress)-mediated mechanism does not play an important role in the dilator response of pial arterioles to sciatic nerve stimulation.

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.

scholarly journals Effect of adenosine receptor blockade on pial arteriolar dilation during sciatic nerve stimulation

2001 ◽  
Vol 281 (5) ◽  
pp. H2018-H2027 ◽  
Author(s):  
Joseph R. Meno ◽  
Alison V. Crum ◽  
H. Richard Winn
Keyword(s):  
Sciatic Nerve ◽  
Receptor Antagonist ◽  
Nerve Stimulation ◽  
Adenosine Receptor ◽  
Systemic Administration ◽  
Receptor Subtype ◽  
Somatosensory Stimulation ◽  
Cranial Window ◽  
Artificial Cerebrospinal Fluid ◽  
Sciatic Nerve Stimulation

In the present study, we report the effects of adenosine receptor antagonists on pial vasodilatation during contralateral sciatic nerve stimulation (SNS). The pial circulation was observed through a closed cranial window in α-chloralose-anesthetized rats. In artificial cerebrospinal fluid (CSF), SNS resulted in a 30.5 ± 13.2% increase in pial arteriolar diameter in the hindlimb somatosensory cortex. Systemic administration of the selective adenosine A2A receptor antagonist, 4-(2-{7-amino-2-[2-furyl][3,2,4]triazolol[2,3-a][1,3,5]triazin-5-yl-amino} ethyl)phenol (ZM-241385), significantly ( P < 0.05, n = 6) attenuated the SNS-induced vasodilatation. Systemic administration of 8-( p-sulfophenyl)theophylline (8SPT), a nonselective antagonist that is blood-brain barrier (BBB) impermeable, had no effect on vasodilatation to SNS. In contrast, systemic theophylline, which readily penetrates the BBB, nearly abolished the SNS-induced vasodilatation ( P < 0.01; n = 7). Topical superfusion of 8SPT significantly ( P < 0.01; n = 6) attenuated vasodilatation during SNS. Topical superfusion of 8- cyclopentyl-1,3-dipropylxanthine (DPCPX), a selective adenosine A1 receptor antagonist, significantly potentiated SNS-induced vasodilatation ( P < 0.01; n ≥ 5). Hypercarbic vasodilatation and somatosensory-evoked potentials were not affected by any of the compounds tested. Our findings suggest that luminal endothelial adenosine receptors are not involved in the arteriolar response to SNS, as demonstrated by a lack of effect with systemic 8SPT. Furthermore, the adenosine A2A receptor subtype appears to be involved in the dilator response to SNS. Finally, the neuromodulatory action of adenosine, via the A1 receptor subtype, significantly influences SNS-induced vasodilatation. Thus the present study provides further evidence for a role of adenosine in the regulation of CBF during somatosensory stimulation.

Effect of sciatic nerve stimulation on pial arterioles in rats

1988 ◽  
Vol 254 (1) ◽  
pp. H133-H139 ◽  
Author(s):  
A. C. Ngai ◽  
K. R. Ko ◽  
S. Morii ◽  
H. R. Winn
Keyword(s):  
Sciatic Nerve ◽  
Stimulus Intensity ◽  
Nerve Stimulation ◽  
Cerebral Metabolism ◽  
Stimulus Frequency ◽  
Systemic Blood Pressure ◽  
Pial Arterioles ◽  
High Stimulus ◽  
Sciatic Nerve Stimulation ◽  
Sensory Evoked

The present study documents the microvascular response of the pial circulation in sensory hindlimb cortex to sciatic nerve stimulation. Rats, anesthetized with alpha-chloralose and urethan, were equipped with closed cranial windows, and pial arteriolar diameter was measured during stimulation of the contralateral sciatic nerve. The effects of varying stimulus frequency, intensity, and duration were examined. Optimal stimulus frequency was 5 Hz, but response diminished significantly beyond 10 Hz. Optimal stimulus intensity was 0.2 V. At higher stimulus strength, arteriolar dilation was reduced, but systemic blood pressure rose significantly. At low stimulus frequency and intensities, pial arterioles responded to stimulation with a consistent pattern: initial delay of 1.4 s followed by abrupt dilation to a peak magnitude, subsequent decline to a lesser but still dilated state, and recovery to a resting diameter after the cessation of stimulation. No consistent response profile was discernible at high stimulus intensity and/or frequency. This vasodilatory response was discretely restricted to a limited number of arterioles, confined to the hindlimb somatosensory cortex as confirmed by sensory evoked response. The response of the pial circulation provides a well-characterized model for analysis of brain microcirculation, which presumably is linked to cerebral metabolism.

scholarly journals An investigation of arterial insufficiency in the rat hindlimb Correlation of skeletal muscle bloodflow and glucose utilization in vivo

1986 ◽  
Vol 240 (2) ◽  
pp. 395-401 ◽  
Author(s):  
R A Challiss ◽  
D J Hayes ◽  
G K Radda
Keyword(s):  
Skeletal Muscle ◽  
Sciatic Nerve ◽  
Glucose Uptake ◽  
Nerve Stimulation ◽  
Linear Correlation ◽  
Glucose Utilization ◽  
Fold Increase ◽  
Artery Ligation ◽  
Sciatic Nerve Stimulation

Muscle bloodflow and the rate of glucose uptake and phosphorylation were measured in vivo in rats 7 days after unilateral femoral artery ligation and section. Bloodflow was determined by using radiolabelled microspheres. At rest, bloodflow to the gastrocnemius, plantaris and soleus muscles of the ligated limb was similar to their respective mean contralateral control values; however, bilateral sciatic nerve stimulation at 1 Hz caused a less pronounced hyperaemic response in the muscles of the ligated limb, being 59, 63 and 49% of their mean control values in the gastrocnemius, plantaris and soleus muscles respectively. The rate of glucose utilization was determined by using the 2-deoxy[3H]glucose method [Ferré, Leturque, Burnol, Penicaud & Girard (1985) Biochem. J. 228, 103-110]. At rest, the rate of glucose uptake and phosphorylation was statistically significantly increased in the gastrocnemius and soleus muscles of the ligated limb, being 126 and 140% of the mean control values respectively. Bilateral sciatic nerve stimulation at 1 Hz caused a 3-5-fold increase in the rate of glucose utilization by the ligated and contralateral control limbs; furthermore, the rate of glucose utilization was significantly increased in the muscles of the ligated limb, being 140, 129 and 207% of their mean control values respectively. For the range of bloodflow to normally perfused skeletal muscle at rest or during isometric contraction determined in the present study, a linear correlation between the rate of glucose utilization and bloodflow can be demonstrated. Applying similar methods of regression analysis to glucose utilization and bloodflow to muscles of the ligated limb reveals a similar linear correlation. However, the rate of glucose utilization at a given bloodflow is increased in muscles of the ligated limb, indicating an adaptation of skeletal muscle to hypoperfusion.

scholarly journals Electroacupuncture Reduces the Effects of Acute Noxious Stimulation on the Electrical Activity of Pain-Related Neurons in the Hippocampus of Control and Neuropathic Pain Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Jun-Ying Wang ◽  
Renbo Chen ◽  
Shu-Ping Chen ◽  
Yong-Hui Gao ◽  
Jian-Liang Zhang ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Electrical Activity ◽  
Nerve Stimulation ◽  
Mek Inhibitor ◽  
Mitogen Activated Protein Kinase ◽  
Noxious Stimulation ◽  
Ca1 Region ◽  
Mitogen Activated Protein ◽  
Hippocampal Area ◽  
Sciatic Nerve Stimulation

To study the effects of acupuncture analgesia on the hippocampus, we observed the effects of electroacupuncture (EA) and mitogen-activated protein kinase (MEK) inhibitor on pain-excited neurons (PENs) and pain-inhibited neurons (PINs) in the hippocampal area CA1 of sham or chronic constrictive injury (CCI) rats. The animals were randomly divided into a control, a CCI, and a U0126 (MEK1/2 inhibitor) group. In all experiments, we briefly (10-second duration) stimulated the sciatic nerve electrically and recorded the firing rates of PENs and PINs. The results showed that in both sham and CCI rats brief sciatic nerve stimulation significantly increased the electrical activity of PENs and markedly decreased the electrical activity of PINs. These effects were significantly greater in CCI rats compared to sham rats. EA treatment reduced the effects of the noxious stimulus on PENs and PINs in both sham and CCI rats. The effects of EA treatment could be inhibited by U0126 in sham-operated rats. The results suggest that EA reduces effects of acute sciatic nerve stimulation on PENs and PINs in the CA1 region of the hippocampus of both sham and CCI rats and that the ERK (extracellular regulated kinase) signaling pathway is involved in the modulation of EA analgesia.

scholarly journals Sciatic nerve stimulation activates the retrotrapezoid nucleus in anesthetized rats

2016 ◽  
Vol 116 (5) ◽  
pp. 2081-2092 ◽  
Author(s):  
Roy Kanbar ◽  
Ruth L. Stornetta ◽  
Patrice G. Guyenet
Keyword(s):  
Sciatic Nerve ◽  
Nerve Stimulation ◽  
Motor Nucleus ◽  
Sprague Dawley ◽  
Neuron Firing ◽  
Afferent Stimulation ◽  
Retrotrapezoid Nucleus ◽  
Facial Motor Nucleus ◽  
Stimulation Experiments ◽  
Sciatic Nerve Stimulation

Retrotrapezoid nucleus (RTN) neurons sustain breathing automaticity. These neurons have chemoreceptor properties, but their firing is also regulated by multiple synaptic inputs of uncertain function. Here we test whether RTN neurons, like neighboring presympathetic neurons, are excited by somatic afferent stimulation. Experiments were performed in Inactin-anesthetized, bilaterally vagotomized, paralyzed, mechanically ventilated Sprague-Dawley rats. End-expiratory CO2 (eeCO2) was varied between 4% and 10% to modify rate and amplitude of phrenic nerve discharge (PND). RTN and presympathetic neurons were recorded extracellularly below the facial motor nucleus with established criteria. Sciatic nerve stimulation (SNstim, 1 ms, 0.5 Hz) slightly increased blood pressure (6.6 ± 1.6 mmHg) and heart rate and, at low eeCO2 (<5.5%), entrained PND. Ipsi- and contralateral SNstim produced the known biphasic activation of presympathetic neurons. SNstim evoked a similar but weaker biphasic response in up to 67% of RTN neurons and monophasic excitation in the rest. At low eeCO2, RTN neurons were silent and responded more weakly to SNstim than at high eeCO2. RTN neuron firing was respiratory modulated to various degrees. The phasic activation of RTN neurons elicited by SNstim was virtually unchanged at high eeCO2 when PND entrainment to the stimulus was disrupted. Thus RTN neuron response to SNstim did not result from entrainment to the central pattern generator. Overall, SNstim shifted the relationship between RTN firing and eeCO2 upward. In conclusion, somatic afferent stimulation increases RTN neuron firing probability without altering their response to CO2. This pathway may contribute to the hyperpnea triggered by nociception, exercise (muscle metabotropic reflex), or hyperthermia.

Sign in / Sign up

Export Citation Format

Share Document