scholarly journals Mechanisms of blood flow regulation of in the skin during stimulation of the spinal cord in humans

2019 ◽  
Vol 485 (1) ◽  
pp. 114-116
Author(s):  
G. I. Lobov ◽  
Yu. P. Gerasimenko ◽  
T. R. Moshonkina
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Sensory Nerve ◽  
Nerve Fibers ◽  
Motor Threshold ◽  
Doppler Flowmetry ◽  
Important Mediator ◽  
Antidromic Stimulation ◽  
Cutaneous Blood ◽  
Stimulation Of

Changes of the blood flow in the shin skin in the case of 12 healthy subjects by laser doppler flowmetry were observed under transcutaneous electrical spinal cord stimulation (TSCS) by subthreshold bipolar pulses with a frequency of 30 Hz were detected. It was found that the TSCS in the area of the vertebrae T11 and L1 leads to a significant increase in skin blood flow. With a stimulus intensity of 90% of the motor threshold, the microcirculation rate increased by more than 85% relative to baseline.The results of the study show that the stimulation of blood flow in the skin by TSCS is realized mainly due to the antidromic stimulation of sensory nerve fibers. An important mediator that contributes to vasodilation and increase of cutaneous blood flow in PSCS is nitric oxide (NO), which is predominantly endothelial in origin.

Pearls and pitfalls in experimental in vivo models of migraine: Dural trigeminovascular nociception

Cephalalgia ◽  
2013 ◽  
Vol 33 (8) ◽  
pp. 577-592 ◽  
Author(s):  
Simon Akerman ◽  
Philip R Holland ◽  
Jan Hoffmann
Keyword(s):  
Dura Mater ◽  
Sensory Nerve ◽  
Nerve Fibers ◽  
Trigeminal Nucleus ◽  
Neuronal Activation ◽  
Trigeminovascular System ◽  
In Vivo Models ◽  
Doppler Flowmetry ◽  
Trigeminal Nucleus Caudalis ◽  
Stimulation Of

Background Migraine is a disorder of the brain and is thought to involve activation of the trigeminovascular system, which includes the peripheral afferent projection to the nociceptive specific dura mater, as well as the central afferent projection to the trigeminal nucleus caudalis. Stimulation of the blood vessels of the dura mater produces pain in patients that is referred to the head similar to headache. Headache mechanisms The likely reason for the pain is because the vascular structures of the dura mater, including the superior sagittal sinus and middle meningeal artery, are richly innervated by a plexus of largely unmyelinated sensory nerve fibers from the ophthalmic division of the trigeminal ganglion. Methodology Stimulation of these nociceptive specific nerve fibers is painful and produces neuronal activation in the trigeminal nucleus caudalis. Preclinical models of headache have taken advantage of this primarily nociceptive pathway, and various animal models use dural trigeminovascular nociception to assay aspects of head pain. These assays measure responses at the level of the dural vasculature and the central trigeminal nucleus caudalis as a correlate of trigeminovascular activation thought to be involved in headache. Summary This review will summarize the history of the development of models of dural trigeminovascular nociception, including intravital microscopy and laser Doppler flowmetry at the level of the vasculature, and electrophysiology and Fos techniques used to observe neuronal activation at the trigeminal nucleus caudalis. It will also describe some of pitfalls of these assays and developments for the future.

Cerebrovasodilation elicited by fastigial stimulation is preserved under deep halothane anesthesia

1993 ◽  
Vol 265 (1) ◽  
pp. R187-R194 ◽  
Author(s):  
C. Iadecola ◽  
F. Zhang ◽  
X. Xu
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Glucose Utilization ◽  
Pressor Response ◽  
Dependent Manner ◽  
Halothane Anesthesia ◽  
Doppler Flowmetry ◽  
Dose Dependent ◽  
Deoxyglucose Method ◽  
Stimulation Of

We studied the effect of halothane anesthesia on the increases in cerebral blood flow (CBF) and arterial pressure (AP) elicited by electrical stimulation of the cerebellar fastigial nucleus (FN). Rats were anesthetized (0.75-2% halothane), instrumented for continuous recording of AP, and ventilated. The FN was stimulated through stereotaxically implanted microelectrodes. In CBF experiments the elevations in AP resulting from FN stimulation were eliminated by spinal cord transection at C1. After cord transection AP was maintained by intravenous phenylephrine. CBF or cerebral glucose utilization (CGU) was measured by laser-Doppler flowmetry or the 2-deoxyglucose method, respectively. FN stimulation produced increases in CBF that were graded with the intensity (10-150 microA) or frequency (10-150 Hz) of stimulation. At 1% halothane, FN stimulation (100 microA; 75 Hz; n = 8) increased CBF by 123 +/- 16%. The elevations in CBF were attenuated by increasing levels of halothane anesthesia in a dose-dependent manner. At halothane concentrations of 1.5 and 2% the CBF response to FN stimulation (100 microA; 75 Hz) was reduced by 58 +/- 6 and 77 +/- 4%, respectively (p < 0.05 from 0.75% halothane; analysis of variance and Tukey's test). In contrast, the increases in CBF elicited by hypercapnia were not attenuated (P > 0.05 from 0.75% halothane). At 1% halothane, FN stimulation did not change CGU in neocortex (frontal cortex: unstimulated 48 +/- 6, mumol.100 g-1.min-1, FN stimulation: 47 +/- 11; P > 0.05; n = 5/group). In the group of rats in which the pressor response was studied (n = 7), halothane produced a dose-dependent attenuation of the elevations in AP. The degree of attenuation of the AP response was comparable to that of the CBF response (P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Stellate Ganglion Stimulation on Bilateral Cochlear Blood Flow

1993 ◽  
Vol 102 (5) ◽  
pp. 378-384 ◽  
Author(s):  
Tianying Ren ◽  
Esa Laurikainen ◽  
Wayne S. Quirk ◽  
Josef M. Miller ◽  
Alfred L. Nuttall
Keyword(s):  
Blood Flow ◽  
Superior Cervical Ganglion ◽  
Stellate Ganglion ◽  
Systemic Blood Pressure ◽  
Nerve Fibers ◽  
Cochlear Blood Flow ◽  
Doppler Flowmetry ◽  
Cervical Ganglion ◽  
Pass Through ◽  
Stimulation Of

The effect of intraneural electrical stimulation of the stellate ganglion (SG) on bilateral cochlear blood flow (CBF) was investigated with laser-Doppler flowmetry. The SG of 15 anesthetized guinea pigs was exposed by a novel surgical approach and stimulated with a specially designed intraneural bipolar platinum-iridium electrode. Bilateral CBF was continuously monitored. Stimulation of 0.25 mA caused a detectable increase of the systemic blood pressure (BP) and a bilateral decrease of the cochlear vascular conductance (R, defined as the ratio CBF/BP). A stimulus of 0.5 mA elicited a statistically significant ipsilateral CBF (CBFi) decrease of 3.6% ± 5.1% from the baseline and a contralateral CBF (CBFc) decrease of 3.1% ± 5.5%. That no statistical difference was found between CBFi and CBFc indicates that a unilateral sympathetic stimulation of the SG can cause equal bilateral responses. These responses were accompanied by a significantly increased BP (8.7% ± 5.2% of baseline) and consequently a greatly decreased R (12.2% ± 6.5%) of the ipsilateral cochlea. Bilateral sections of the cervical sympathetic trunk below the level of the superior cervical ganglion did not alter the evoked changes in CBF, BP, and R. It is concluded that SG stimulation can decrease the conductivity of the cochlear vessels or the supplying vessels of the cochlea. Additionally, the SG nerve fibers that cause these effects do not pass through the superior cervical ganglion.

Modulation of Blood Flow in the Skin of Human Legs during Transcutaneus Electrical Stimulation of the Spinal Cord

2020 ◽  
Vol 46 (4) ◽  
pp. 384-390
Author(s):  
G. I. Lobov ◽  
Yu. P. Gerasimenko ◽  
T. R. Moshonkina
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Electrical Stimulation ◽  
Stimulation Of

Blockade of the pressor response to muscle ischemia by sensory nerve block in man

1979 ◽  
Vol 237 (4) ◽  
pp. H433-H439 ◽  
Author(s):  
P. R. Freund ◽  
L. B. Rowell ◽  
T. M. Murphy ◽  
S. F. Hobbs ◽  
S. H. Butler
Keyword(s):  
Nerve Block ◽  
Pressor Response ◽  
Sensory Nerve ◽  
Sensory Block ◽  
Nerve Fibers ◽  
Dynamic Exercise ◽  
Sensory Blockade ◽  
Muscle Ischemia ◽  
Respiratory Responses ◽  
Stimulation Of

Differential nerve block from peridural anesthesia was used to determine a) if the pressor response to muscle ischemia in man is caused by stimulation of small sensory nerve fibers and b) if these fibers contribute to cardiovascular-respiratory responses during dynamic exercise. Four men exercised at 50-100 W for 5 min. Muscle ischemia and a sustained pressor response were produced by total circulatory occlusion of both legs beginning 30 s before the end of exercise and continuing for 3 min postexercise. During regression of full motor and sensory block, motor strength recovered while sensory block continued; the pressor response was blocked as long as sensory anesthesia persisted (two subjects). During blockade of the pressor response, cardiovascular-respiratory responses to exercise gradually returned from augmented to normal (preblock) levels. Sensory blockade was incomplete in two subjects and the pressor response was not fully blocked. We conclude that stimulation of small sensory fibers during ischemia elicits the pressor response, but that these fibers appear not to contribute to cardiovascular-respiratory responses during mild dynamic exercise with adequate blood flow.

scholarly journals Beneficial Effect of the Traditional Chinese Drug Shu-Xue-Tong on Recovery of Spinal Cord Injury in the Rat

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Li-Yun Jia ◽  
An-Hui Yao ◽  
Fang Kuang ◽  
Yu-Kai Zhang ◽  
Xue-Feng Shen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Histological Analysis ◽  
Lesion Size ◽  
Chinese Drug ◽  
Sprague Dawley ◽  
Spinal Cord Blood Flow ◽  
Doppler Flowmetry ◽  
Cord Injury

Shu-Xue-Tong (SXT) is a traditional Chinese drug widely used to ameliorate stagnation of blood flow, such as brain or myocardial infarction. Whether SXT may have therapeutic value for spinal cord injury (SCI), during which ischemia plays an important role in its pathology, remains to be elucidated. We hypothesized that SXT may promote SCI healing by improving spinal cord blood flow (SCBF), and a study was thus designed to explore this possibility. Twenty-five male Sprague-Dawley rats were used. SCI was induced by compression, and SXT was administrated 24 h postinjury for 14 successive days. The effects of SXT were assessed by means of laser-Doppler flowmetry, motor functional analysis (open-field walking and footprint analysis), and histological analysis (hematoxylin-eosin and thionin staining and NeuN immunohistochemistry). SXT significantly promoted SCBF of the contused spinal cord and enhanced the recovery of motor function. Histological analysis indicated that the lesion size was reduced, the pathological changes were ameliorated, and more neurons were preserved. Based on these results we conclude that SXT can effectively improve SCI.

scholarly journals Reductions in Focal Ischemic Infarctions Elicited from Cerebellar Fastigial Nucleus Do Not Result from Elevations in Cerebral Blood Flow

1993 ◽  
Vol 13 (6) ◽  
pp. 1020-1024 ◽  
Author(s):  
Seiji Yamamoto ◽  
Eugene V. Golanov ◽  
Donald J. Reis
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Parietal Cortex ◽  
Occipital Cortex ◽  
Fastigial Nucleus ◽  
Ventrolateral Medulla ◽  
Ischemic Lesion ◽  
Doppler Flowmetry ◽  
Mca Occlusion ◽  
Stimulation Of

To determine whether the neuroprotection elicited from electrical stimulation of the cerebellar fastigial nucleus (FN) is attributable to the elevation in regional cerebral blood flow (rCBF), we compared the effects in spontaneously hypertensive rats of stimulation of the rostral ventrolateral medulla (RVL) or FN on (a) a focal ischemic lesion produced by middle cerebral artery (MCA) occlusion, and (b) the changes in rCBF, measured by laser-Doppler flowmetry for 1.5 h, over regions corresponding to the ischemic core (parietal cortex), penumbra (occipital cortex), and nonischemic area (contralateral parietal cortex). Stimulation of FN for 1 h following MCA occlusion reduced infarction 24 h later by 52%. Stimulation of RVL was ineffective. Changes in the lesion were confined to the penumbra. FN and RVL stimulation comparably and significantly increased rCBF up to 185% in unlesioned animals. Following MCA occlusion, stimulation of FN or RVL and hypercarbia failed to elevate rCBF in the ischemic area but did so in the nonischemic area, even though in the same animals only FN stimulation reduced infarction 24 h later. We conclude that (a) the neuroprotection elicited from FN is not the result of an increase in rCBF but results from another mechanism, possibly reduction of metabolism in penumbra, and (b) the pathways mediating central neurogenic vasodilation and neuroprotection are, in part, distinct.

Inhibition of spinal afferent nerve-mediated gastric hyperemia by nicotine: role of ganglionic blockade

1993 ◽  
Vol 264 (4) ◽  
pp. H1087-H1092
Author(s):  
F. W. Leung
Keyword(s):  
Blood Flow ◽  
Afferent Nerve ◽  
Gastric Blood Flow ◽  
Doppler Flowmetry ◽  
Afferent Nerves ◽  
Vasodilatory Effect ◽  
Blocking Property ◽  
Intravenous Nicotine ◽  
Ganglionic Blocking ◽  
Stimulation Of

The hypothesis that intravenous nicotine modulates gastric spinal afferent nerve function by its ganglionic-blocking property is tested. Stimulation of the gastric spinal afferent nerves in anesthetized rats is accomplished by intragastric capsaicin irrigation. Gastric blood flow is monitored by laser-Doppler flowmetry. The increase in gastric blood flow during intragastric capsaicin irrigation is significantly reduced by 4 and 40 micrograms.kg-1.min-1 of intravenous nicotine. The inhibition appears to be specific for the spinal afferent nerves as the increase in gastric blood flow induced by electrical stimulation of the vagal afferent nerves is unaltered by these doses of intravenous nicotine. A ganglionic-blocking dose (10 mg/kg) of intraperitoneal hexamethonium also significantly attenuates the gastric vasodilatory effect of intragastric capsaicin. Intravenous nicotine (40 micrograms.kg-1.min-1) combined with intraperitoneal hexamethonium (10 mg/kg) completely abolishes the gastric vasodilatory effect of intragastric capsaicin. These data suggest that intravenous nicotine offers a specific inhibition of the gastric spinal afferent nerve-mediated hyperemia, possibly as a consequence of its ganglionic-blocking property.

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