Alterations in spinal cord norepinephrine levels following experimentally produced trauma in normal and adrenalectomized cats

Schoultz, Ture W.; DeLuca, Donald C.

doi:10.1016/0024-3205(74)90123-4

Cited by 13 publications

(4 citation statements)

References 9 publications

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Section: Discussionmentioning

confidence: 99%

“…After SCI, in fact, there is a prompt activation of both the adrenal medulla and the sympathetic nervous system, as well as the parasympathetic and the hypothalamic-hypophyseal-adrenal systems. [57][58][59][60][61][62][63][64][65][66] This response results in rises of blood pressure, heart rate and blood glucose. 57,59 Unexpectedly, in Experiment 1 blood glucose levels never exceed normoglycemic levels, and many of the rats were rather moderately hypoglycemic.…”

Section: Methodsmentioning

confidence: 99%

“…We did not study catecholamine concentrations in the blood; nevertheless it is highly probable that this metabolic response is secondary to the sympathoadrenal response, as extensively demonstrated by others. 65,[67][68][69][70] Finally, because both lesion volume and glucose response correlated with injury severity, this experiment did not clarify whether or not blood glucose levels directly affect spinal cord damage.…”

Section: Methodsmentioning

confidence: 99%

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Role of Glycemia in Acute Spinal Cord Injury: Data from a Rat Experimental Model and Clinical Experience

Sala

Menna

Bricolo

et al. 1999

Annals of the New York Academy of Sciences

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While experimental and clinical evidence indicates that in brain injury blood glucose increases with injury severity and hyperglycemia worsens neurological outcome, the role of blood glucose in secondary mechanisms of neuronal damage after acute spinal cord injury has not yet been investigated. Data from spinal cord ischemia models suggests a deleterious effect of hyperglycemia, likely due to enhanced lactic acidosis, which is primarily dependent on the amount of glucose available to be metabolized. The purpose of this study is to summarize preliminary experimental and clinical observations on the role of blood glucose in acute spinal cord injury. Between 1995 and 1996 we used the New York University (NYU) rat spinal cord injury model to test the following hypotheses: 1) Blood glucose levels increase with injury severity. 2) Fasting protects from hyperglycemia and prevents secondary damage to the spinal cord. 3) Postinjury-induced hyperglycemia (dextrose 5% 2 gm/Kg) enhances spinal lesion volume. From a clinical perspective, we reviewed blood glucose records of 47 patients admitted to the Department of Neurosrgery in Verona, between 1991 and 1995, within 24 hours of acute spinal cord injury in order to determine: a) the incidence of hyperglycemia (> 140 mg/dl); b) the correlation between blood glucose and injury severity; and c) the role of methylprednisolone in affecting blood glucose. Results indicate that in a graded spinal cord injury model: 1) Early after injury, more severe contusions support significantly higher blood glucose levels. 2) Fasting overnight does not directly affect spinal cord lesion volume but influences blood gases, and we observed that a slightly systemic acidosis plays a minor neuroprotective role. Fasting also ensures more consistent normoglycemic baseline blood glucose values. 3) Postinjury-induced moderate hyperglycemia (160-190 mg/dl) does not significantly affect spinal cord injury. In the clinical study, we observed that during the first 24 hours after spinal cord injury: a) Glycemia ranges between 90 and 243 mg/dl (mean value 143 mg/dl), and close to 50% of the patients present blood glucose values higher than normal. b) Methylprednisolone administration is not associated to significantly higher blood glucose levels. c) There is a trend for larger glucose rises with more severe injury.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Role of Glycemia in Acute Spinal Cord Injury: Data from a Rat Experimental Model and Clinical Experience

Sala

Menna

Bricolo

et al. 1999

Annals of the New York Academy of Sciences

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“…The experiments in the present study were performed to determine whether an artificially induced spinal cord injury had similar effects on noradrenaline uptake and release as the simulation of ischaemic conditions in healthy tissues in vitro (Uchihashi et al, 1998;Nakai et al, 1999;Sumiya et al, 2001;Sircuta et al, 2016) and in vivo (Globus et al, 1989). In contrast to the above-mentioned studies, normal Krebs perfusion solution was used in the present study, but the spinal cord tissue was isolated caudally and in close proximity (2-5 mm) to an artificial injury (Schoultz and DeLuca, 1974). After surgical hemisection, the rats showed typical signs of hemiplegia, with no movement of the right hindlimb.…”

Section: Discussionmentioning

confidence: 99%

Effect of rat spinal cord injury (hemisection) on the ex vivo uptake and release of [ 3 H]noradrenaline from a slice preparation

Borbély

Csomó

Kittel

et al. 2017

Brain Research Bulletin

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We measured the ex vivo uptake and release of [H]noradrenaline ([H]NA) from perfused rat spinal cord slice preparations at 1, 3 and 14days after unilateral hemisection-induced spinal cord injury (SCI) compared with control slice preparations. After surgical hemisection under anaesthesia, the rats showed characteristic signs of hemiplegia, with no movement of the ipsilateral hindlimb. After 3days, the electron microscopy images showed overall degeneration of neuronal organelles and the myelin sheath, but the synapses seemed to be intact. In ex vivo experiments, the spinal cord injury did not influence uptake but increased [H]NA release at rest and in response to axonal stimulation. The effect of a selective noradrenaline reuptake inhibitor, nisoxetine, was studied to identify the mechanisms underlying the increase in NA release. Nisoxetine potentiated stimulation-evoked [H]NA release from the non-injured tissue, but it gradually lost its effectiveness after injury, depending on the time (1 and 3days) elapsed after hemisection, indicating that the noradrenaline transporter binding sites of the terminals become impaired after decentralisation.

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Effect of Pharmacological Agents on Normalization of Molecular and Histologic Dysfunction Following Traumatic Injury to the Spinal Cord

Naftchi¹,

Demeny²,

Demopoulos³

et al. 1982

Spinal Cord Injury

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Alterations in spinal cord norepinephrine levels following experimentally produced trauma in normal and adrenalectomized cats

Cited by 13 publications

References 9 publications

Role of Glycemia in Acute Spinal Cord Injury: Data from a Rat Experimental Model and Clinical Experience

Role of Glycemia in Acute Spinal Cord Injury: Data from a Rat Experimental Model and Clinical Experience

Effect of rat spinal cord injury (hemisection) on the ex vivo uptake and release of [ 3 H]noradrenaline from a slice preparation

Effect of Pharmacological Agents on Normalization of Molecular and Histologic Dysfunction Following Traumatic Injury to the Spinal Cord

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