scholarly journals Contribution of astrocytes to neurovascular coupling in the spinal cord of the rat

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Thierry Paquette ◽  
Mathieu Piché ◽  
Hugues Leblond
Keyword(s):  
Spinal Cord ◽  
Field Potential ◽  
Neurovascular Coupling ◽  
Noxious Stimulation ◽  
Hemodynamic Changes ◽  
Spinal Cord Blood Flow ◽  
Before And After ◽  
Local Field Potential Lfp ◽  
Stimulation Of

AbstractFunctional magnetic resonance imaging (fMRI) of the spinal cord relies on the integrity of neurovascular coupling (NVC) to infer neuronal activity from hemodynamic changes. Astrocytes are a key component of cerebral NVC, but their role in spinal NVC is unclear. The objective of this study was to examine whether inhibition of astrocyte metabolism by fluorocitrate alters spinal NVC. In 14 rats, local field potential (LFP) and spinal cord blood flow (SCBF) were recorded simultaneously in the lumbosacral enlargement during noxious stimulation of the sciatic nerve before and after a local administration of fluorocitrate (N  = 7) or saline (N  = 7). Fluorocitrate significantly reduced SCBF responses (p  < 0.001) but not LFP amplitude (p  = 0.22) compared with saline. Accordingly, NVC was altered by fluorocitrate compared with saline (p  < 0.01). These results support the role of astrocytes in spinal NVC and have implications for spinal cord imaging with fMRI for conditions in which astrocyte metabolism may be altered.

Acetaminophen Inhibits Spinal Prostaglandin E2Release after Peripheral Noxious Stimulation 

1999 ◽  
Vol 91 (1) ◽  
pp. 231-239 ◽  
Author(s):  
Uta S. Muth-Selbach ◽  
Irmgard Tegeder ◽  
Kay Brune ◽  
Gerd Geisslinger
Keyword(s):  
Spinal Cord ◽  
Urinary Excretion ◽  
Dorsal Horn ◽  
Formalin Test ◽  
Intraperitoneal Administration ◽  
Noxious Stimulation ◽  
Cyclooxygenase Inhibitor ◽  
Nociceptive Processing ◽  
Pge2 Release

Background Prostaglandin play a pivotal role in spinal nociceptive processing. At therapeutic concentrations, acetaminophen is not a cyclooxygenase inhibitor. inhibitor. Thus, it is antinociceptive without having antiinflammatory or gastrointestinal toxic effects. This study evaluated the role of spinal prostaglandin E2 (PGE2) in antinociception produced by intraperitoneally administered acetaminophen. Methods The PGE2 concentrations in the dorsal horn of the spinal cord were measured after formalin was injected into the hind paw of rats. The effect of antinociceptive doses of acetaminophen (100, 200, and 300 mg/kg given intraperitoneally) on PGE2 levels and flinching behavior was monitored Spinal PGE2 and acetaminophen concentrations were obtained by microdialysis using a probe that was implanted transversely through the dorsal horn of the spinal cord at L4. Furthermore, the effects of acetaminophen on urinary prostaglandin excretion were determined. Results Intraperitoneal administration of acetaminophen resulted in a significant decrease in spinal PGE2 release that was associated with a significant reduction in the flinching behavior in the formalin test Acetaminophen was distributed rapidly into the spinal cord with maximum dialysate concentrations 4560 min after intraperitoneal administration. Urinary excretion of prostanoids (PGE2, PGF2alpha, and 6-keto-PGF1alpha) was not significantly altered after acetaminophen administration. Conclusions The data confirm the importance of PGE2 in spinal nociceptive processing. The results suggest that antinociception after acetaminophen administration is mediated, at least in part, by inhibition of spinal PGE2 release. The mechanism, however, remains unknown. The finding that urinary excretion of prostaglandins was not affected might explain why acetaminophen is antinociceptive but does not compromise renal safety.

Drastic Decrease in Isoflurane Minimum Alveolar Concentration and Limb Movement Forces after Thoracic Spinal Cooling and Chronic Spinal Transection in Rats

2005 ◽  
Vol 102 (3) ◽  
pp. 624-632 ◽  
Author(s):  
Steven L. Jinks ◽  
Carmen L. Dominguez ◽  
Joseph F. Antognini
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Minimum Alveolar Concentration ◽  
Tail Flick ◽  
Noxious Stimulation ◽  
Partial Recovery ◽  
Spinal Transection ◽  
Thoracic Spinal ◽  
Cord Injury ◽  
Stimulation Of

Background Individuals with spinal cord injury may undergo multiple surgical procedures; however, it is not clear how spinal cord injury affects anesthetic requirements and movement force under anesthesia during both acute and chronic stages of the injury. Methods The authors determined the isoflurane minimum alveolar concentration (MAC) necessary to block movement in response to supramaximal noxious stimulation, as well as tail-flick and hind paw withdrawal latencies, before and up to 28 days after thoracic spinal transection. Tail-flick and hind paw withdrawal latencies were measured in the awake state to test for the presence of spinal shock or hyperreflexia. The authors measured limb forces elicited by noxious mechanical stimulation of a paw or the tail at 28 days after transection. Limb force experiments were also conducted in other animals that received a reversible spinal conduction block by cooling the spinal cord at the level of the eighth thoracic vertebra. Results A large decrease in MAC (to &lt;/= 40% of pretransection values) occurred after spinal transection, with partial recovery (to approximately 60% of control) at 14-28 days after transection. Awake tail-flick and hind paw withdrawal latencies were facilitated or unchanged, whereas reflex latencies under isoflurane were depressed or absent. However, at 80-90% of MAC, noxious stimulation of the hind paw elicited ipsilateral limb withdrawals in all animals. Hind limb forces were reduced (by &gt;/= 90%) in both chronic and acute cold-block spinal animals. Conclusions The immobilizing potency of isoflurane increases substantially after spinal transection, despite the absence of a baseline motor depression, or "spinal shock." Therefore, isoflurane MAC is determined by a spinal depressant action, possibly counteracted by a supraspinal facilitatory action. The partial recovery in MAC at later time points suggests that neuronal plasticity after spinal cord injury influences anesthetic requirements.

Role of the sympathetic nervous system in CCl4 hepatotoxicity

1960 ◽  
Vol 198 (3) ◽  
pp. 669-676 ◽  
Author(s):  
Deane N. Calvert ◽  
Theodore M. Brody
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Liver Mitochondria ◽  
Central Vein ◽  
Fat Depots ◽  
Sympathetic Nervous ◽  
Adrenergic Blocking ◽  
Stimulation Of

An hypothesis is proposed which states that the characteristic hepatic changes seen after the administration of carbon tetrachloride are the result of stimulation of central sympathetic areas which produce a massive discharge of the peripheral sympathetic nervous system. Stimulation of the sympathetic supply to the blood vessels of the liver results in restriction of blood flow in the liver, leading to anoxia and the characteristic necrosis around the central vein of the hepatic lobule. Similarly the discharge causes the release of unesterified fatty acids from the peripheral fat depots and the consequent deposition of lipid in the liver. This hypothesis is based upon experimental evidence using the following physiologic and pharmacologic maneuvers: adrenergic blocking agents, pretreatment with reserpine, adrenalectomy and section of the spinal cord—all are effective to a greater or lesser extent in preventing the changes characteristically seen in oxidative phosphorylation of the liver mitochondria, activation of a Mg-dependent ATPase and deposition of lipid in the liver. Transection of the spinal cord is the most effective treatment and prevents entirely the characteristic changes seen in the above-mentioned functions.

Leptin response to short-term fasting in sympathectomized men: role of the SNS

2003 ◽  
Vol 284 (3) ◽  
pp. E634-E640 ◽  
Author(s):  
Justin Y. Jeon ◽  
Vicki J. Harber ◽  
Robert D. Steadward
Keyword(s):  
Body Mass Index ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Short Term ◽  
Cord Injury ◽  
Before And After ◽  
Sympathetic Nervous ◽  
Plasma Leptin

We studied plasma leptin levels in six people with high-lesion spinal cord injury [SCI; body mass index (BMI) 25.9 ± 1.5 kg/m2, age 37 ± 3.0 yr] and six able-bodied (AB) controls (BMI 29.1 ± 1.9 kg/m2, age 35 ± 3.5 yr) before and after 12, 24, and 36 h of fasting. The plasma leptin levels significantly decreased during 36 h fasting by 48.8 ± 4.5% (pre: 11.3 ± 2.3, post: 6.2 ± 1.5 ng/ml) and 38.6 ± 7.9% (pre: 7.6 ± 5.0, post: 4.2 ± 1.0 ng/ml) in SCI and AB, respectively. Plasma leptin started to decrease at 24 h of fasting in the SCI group, whereas plasma leptin started to decrease at 12 h of fasting in the AB group. The current study demonstrated that plasma leptin decreased with fasting in both SCI and AB groups, with the leptin decrease being delayed in the SCI group. The delayed leptin response to fasting in the SCI group may be because of increased fat mass (%body fat, SCI: 33.8 ± 3.0, AB: 24.1 ± 2.9) and sympathetic nervous system dysfunction.

ELECTROACUPUNCTURE DECREASES C-FOS EXPRESSION IN THE SPINAL CORD INDUCED BY NOXIOUS STIMULATION OF THE RAT BLADDER

1998 ◽  
pp. 2274-2279 ◽  
Author(s):  
CARL J. CHANG ◽  
SHIH-TSUNG HUANG ◽  
KENNETH HSU ◽  
AUSTIN LIN ◽  
MARSHALL L. STOLLER ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Noxious Stimulation ◽  
Rat Bladder ◽  
Fos Expression ◽  
Stimulation Of

scholarly journals Transcranial doppler sonography in two patients who underwent decompressive craniectomy for traumatic brain swelling: report of two cases

2004 ◽  
Vol 62 (3a) ◽  
pp. 715-721 ◽  
Author(s):  
Edson Bor-Seng-Shu ◽  
Manoel Jacobsen Teixeira ◽  
Roberto Hirsch ◽  
Almir Ferreira de Andrade ◽  
Raul Marino Jr
Keyword(s):  
Blood Flow ◽  
Decompressive Craniectomy ◽  
Transcranial Doppler ◽  
Doppler Sonography ◽  
Transcranial Doppler Sonography ◽  
Brain Swelling ◽  
Hemodynamic Changes ◽  
Before And After ◽  
Intracranial Arteries

The role of decompressive craniectomy in the treatment of severe posttraumatic cerebral swelling remains quite a controversial issue. To the best of our knowledge, there is no study demonstrating the effect of decompressive craniectomy on cerebral blood flow (CBF) velocity by means of transcranial Doppler sonography (TCD). We present two patients who developed traumatic brain swelling and uncontrollable intracranial hypertension with coma and signs of transtentorial herniation. One patient underwent bifrontal, while the second, unilateral, frontotemporoparietal decompressive craniectomy with dural expansion. In both patients, TCD examinations were performed immediately before and after surgery to study the cerebral hemodynamic changes related to the operations. Pre and postoperative TCD examinations demonstrated a significant increase in blood flow velocity in the intracranial arteries in both subjects. In conclusion, our cases suggest that decompressive craniectomy with dural expansion may result in elevation of CBF velocity in patients with massive brain swelling. The increase in CBF velocity appears to occur not only in the decompressed hemisphere, but also on the opposite side.

The effect of norepinephrine on the spinal cord circulation and its possible implications in the pathogenesis of acute spinal trauma

1977 ◽  
Vol 47 (4) ◽  
pp. 567-576 ◽  
Author(s):  
Robert A. Crawford ◽  
Ian R. Griffiths ◽  
James McCulloch
Keyword(s):  
Spinal Cord ◽  
Bolus Injection ◽  
Spinal Injury ◽  
Spinal Cord Blood Flow ◽  
Arterial Infusion ◽  
Content Type ◽  
Barrier Disruption ◽  
Before And After ◽  
Hydrogen Clearance ◽  
Fine Print

✓ The effect of intra-arterially administered norepinephrine (NE) upon spinal cord blood flow (SCBF), before and after disruption of the blood-cord barrier was studied in dogs. Barrier disruption was accomplished with an intra-arterial bolus injection of 2.5 M urea. Multiple ligations of branches of the posterior aorta and cannula placements ensured that the urea was directed to the lumbar and sacral segments of the cord. The SCBF was measured by the hydrogen clearance method. Intra-arterial urea by itself had no significant effect on SCBF. The intra-arterial infusion of NE (12 µg/min and 30 µg/min) was without overall effect on SCBF. However, if the blood-cord barrier had been previously disrupted with hypertonic urea, both concentrations of NE resulted in large reductions in SCBF. No such reductions in SCBF were seen with blood-cord barrier disruption and NE if the animals had been pre-treated with the α-blocker, phenoxybenzamine (1.5 mg/kg). Some aspects of the possible involvement of NE in the pathophysiology of acute spinal injury are discussed.

The effect of percutaneous electrical stimulation of the spinal cord on autonomic reactions in the acute period of rehabilitation after ischemic stroke

2021 ◽  
Author(s):  
Y.Y. Bikbaeva ◽  
D.A. Pavlov ◽  
A.S. Kuznetsov ◽  
E.S. Balykina ◽  
I.V. Antipov
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Electrical Stimulation ◽  
Ischemic Stroke ◽  
Neurological Disorders ◽  
Acute Period ◽  
Before And After ◽  
Parasympathetic Influences ◽  
Circulatory Disorders ◽  
Stimulation Of

The effect of percutaneous electrical stimulation of the spinal cord on the reactions of the autonomic nervous system in patients after acute cerebral circulatory disorders was evaluated. Patients in the acute period of rehabilitation treatment underwent a course of percutaneous electrical stimulation for 10 days. Before and after rehabilitation, vegetative reactions were assessed using an orthoclinostatic test, an A.M.Wein questionnaire, and neurological disorders on the Scandinavian scale. The inclusion of the course of percutaneous electrical stimulation in the program of physical rehabilitation of patients who have suffered an ischemic stroke indicates an improvement in the motor status of patients and a decrease in the imbalance of sympathetic and parasympathetic influences Keywords: ischemic stroke, percutaneous electrical stimulation of the spinal cord, vegetative reactions

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