Characterization of cerebral blood flow response to sciatic nerve stimulation using laser speckle imaging

After complete cerebral ischemia, the postischemic blood flow response to functional activation is severely attenuated for several hours. However, little is known about the spatial and temporal extent of the blood flow response in the acute postischemic period after incomplete cerebral ischemia. To investigate the relative cerebral blood flow (rCBF) response in the somatosensory cortex of rat to controlled vibrissae stimulation after transient incomplete ischemia (15-min bilateral common carotid artery occlusion + hypotension), we employed laser speckle imaging combined with statistical parametric mapping. We found that the ischemic insult had a significant impact on the baseline blood flow ( P <0.005) and the activation area in response to functional stimulation was significantly reduced after ischemia ( P < 0.005). The maximum rCBF response in the activation area determined from the statistical analysis did not change significantly up to 3 h after ischemia ( P > 0.1). However, the time when rCBF response reached its maximum was significantly delayed ( P < 0.0001) from 2.4 ± 0.2 secs before ischemia to 3.6 ± 0.1 secs at 20 mins into reperfusion ( P < 0.001); the delay was reduced gradually to 2.9 ± 0.2 secs after 3 h, which was still significantly greater than that observed before the insult ( P = 0.04).

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Characterization of the Cerebral Blood Flow Response to Balloon Deflation After Temporary Internal Carotid Artery Test Occlusion

Journal of Neurosurgical Anesthesiology ◽

10.1097/00008506-200204000-00006 ◽

2002 ◽

Vol 14 (2) ◽

pp. 123-129 ◽

Cited By ~ 7

Author(s):

Dhanesh K. Gupta ◽

William L. Young ◽

Tomoki Hashimoto ◽

Alexander X. Halim ◽

Randolph S. Marshall ◽

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Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Carotid Artery ◽

Internal Carotid Artery ◽

Internal Carotid ◽

Blood Flow Response ◽

Flow Response

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Characterization of cerebral blood flow response to traumatic brain injury in an animal model using SPECT.

10.25148/etd.fi14052564 ◽

2005 ◽

Author(s):

Michael Capille

Keyword(s):

Traumatic Brain Injury ◽

Animal Model ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Injury ◽

Blood Flow Response ◽

Flow Response

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

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1992.115 ◽

1992 ◽

Vol 12 (5) ◽

pp. 835-843 ◽

Cited By ~ 17

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.

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