Correlation of injury severity and tissue Evans blue content, lipid peroxidation and clinical evaluation in acute spinal cord injury in rats

Kaptanoğlu, Erkan; Okutan, Özerk; Akbıyık, Filiz; Solaroğlu, İhsan; Kilinç, Asuman; Beşkonaklı, Etem

doi:10.1016/j.jocn.2004.04.005

Cited by 22 publications

(13 citation statements)

References 49 publications

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“…While a variety of surrogate markers have been used to examine the BSCB, including radiolabeled AIB (Popovich et al, 2006) and Evans Blue (Kaptanoglu et al, 2004; Benton et al, 2008), a study by Whetstone et al (2003) demonstrated beautifully in the mouse that luciferase can be used to document the temporal changes in the BSCB following a standard thoracic moderately severe contusion injury. Their data shows that, in addition to the rapid and dramatic increase in luciferase extravasation at 24 h post-injury, a second peak of permeability can be observed during the 3–7-day period that includes not only the injury epicenter but also extends rostrocaudally for up to 6 mm (Whetstone et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Swim Training Initiated Acutely after Spinal Cord Injury Is Ineffective and Induces Extravasation In and Around the Epicenter

Smith

Brown

Shum-Siu

et al. 2009

Journal of Neurotrauma

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Activity-based rehabilitation is a promising strategy for improving functional recovery following spinal cord injury (SCI). While results from both clinical and animal studies have shown that a variety of approaches can be effective, debate still exists regarding the optimal post-injury period to apply rehabilitation. We recently demonstrated that rats with moderately severe thoracic contusive SCI can be re-trained to swim when training is initiated 2 weeks after injury and that swim training had no effect on the recovery of overground locomotion. We concluded that swim training is a task-specific model of post-SCI activity-based rehabilitation. In the present study, we ask if re-training initiated acutely is more or less effective than when initiated at 2 weeks post-injury. Using the Louisville Swim Scale, an 18-point swimming assessment, supplemented by kinematic assessment of hindlimb movement during swimming, we report that acute re-training is less effective than training initiated at 2 weeks. Using the bioluminescent protein luciferase as a blood-borne macromolecular marker, we also show a significant increase in extravasation in and around the site of SCI following only 8 min of swimming at 3 days post-injury. Taken together, these results suggest that acute re-training in a rat model of SCI may compromise rehabilitation efforts via mechanisms that may involve one or more secondary injury cascades, including acute spinal microvascular dysfunction.

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Section: Discussionmentioning

confidence: 99%

Swim Training Initiated Acutely after Spinal Cord Injury Is Ineffective and Induces Extravasation In and Around the Epicenter

Smith

Brown

Shum-Siu

et al. 2009

Journal of Neurotrauma

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“…BBB was assessed by EB method. Tissue EB content is further accepted by some researchers as a parameter that indicates the intensity of the injury [45]. In the early term of sepsis, riluzole reduced BBB permeability in the brain, but failed in the cerebellum.…”

Section: Degeneration Of Neurons (0 -3) 2 Pericellular and Vascularmentioning

confidence: 99%

The Effects of Riluzole on Neurological, Brain Biochemical, and Histological Changes in Early and Late Term of Sepsis in Rats

Toklu

Uysal

Kabasakal

et al. 2009

Journal of Surgical Research

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“…The expression of cPLA 2 in spinal cord neurons and oligodendrocytes suggests that the two cell types may be particularly vulnerable to cPLA 2 -mediated cell death following SCI (Liu et al, 2006). Oxidative damage is a key early event that contributes to cell death and functional deficits in SCI (Kaptanoglu et al, 2004;Xu et al, 2005), and the reduction of such damage by cPLA 2 inhibition could be a contributor to the neuroprotective effects seen. Our observations also indicate that the inhibitor may reduce neuroinflammation and the recruitment of macrophages and activated microglia after SCI.…”

mentioning

confidence: 99%

Arachidonyl Trifluoromethyl Ketone Is Neuroprotective after Spinal Cord Injury

Huang

Bhavsar

Ward

et al. 2009

Journal of Neurotrauma

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In spinal cord injury (SCI), neuronal and oligodendroglial loss occurs as a result of the initial trauma and the secondary damage that is triggered by excitotoxicity, free radicals, and inflammation. There is evidence that SCI ellicits increased cytosolic phospholipase A(2) (cPLA(2)) activity. The cleavage of phospholipids by cPLA(2) leads to release of fatty acids, and in particular arachidonic acid (AA), the metabolites of which have been associated with increased inflammation and oxidative stress. The aim of our study was to investigate whether the inhibition of cPLA(2) following SCI leads to tissue protection and an improved functional outcome. Adult rats received compression SCI and 30 min after injury they were treated intravenously with either saline or the cPLA(2) inhibitor arachidonyl trifluoromethyl ketone (AACOCF3) (7.13 mg/kg). The animals were sacrificed at 7 days post-injury and the lesioned tissue was labeled using markers for neurons, oligodendrocytes, and macrophages/activated microglia. We also assessed locomotor recovery using the Basso-Beattie-Bresnahan (BBB) score. The number of surviving neurons and oligodendrocytes was significantly increased in animals treated with the cPLA(2) inhibitor compared to saline controls. The behavioral analysis mirrored the neuroprotective effects and showed that the inhibitor-treated group had better locomotor recovery compared to saline controls. Our results show that AACOCF3 has neuroprotective potential, and support the idea that cPLA(2) is critically involved in acute spinal injury.

show abstract

Correlation of injury severity and tissue Evans blue content, lipid peroxidation and clinical evaluation in acute spinal cord injury in rats

Cited by 22 publications

References 49 publications

Swim Training Initiated Acutely after Spinal Cord Injury Is Ineffective and Induces Extravasation In and Around the Epicenter

Swim Training Initiated Acutely after Spinal Cord Injury Is Ineffective and Induces Extravasation In and Around the Epicenter

The Effects of Riluzole on Neurological, Brain Biochemical, and Histological Changes in Early and Late Term of Sepsis in Rats

Arachidonyl Trifluoromethyl Ketone Is Neuroprotective after Spinal Cord Injury

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