Spinal cord injury in the rat

Taoka, Yuji; Okajima, Kenji

doi:10.1016/s0301-0082(98)00049-5

Cited by 188 publications

(131 citation statements)

References 163 publications

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“…Rescuing oligodendrocytes and preservation of myelin is expected to have large e ects on the functional outcome after SCI. 3 From our data it is also clear that the signi®cant reduction of the scar/ cavern ratio in the creatine treated group (1.03 in creatine fed animals versus 1.38 in controls, P=0.016) is not due to the di erence of the cavern volume, since this parameter was similar in both groups, but it is rather due to a reduction by creatine of the extent of scar tissue formation.…”

Section: Discussionsupporting

confidence: 57%

“…4 These cells could be responsible for axonal demyelination and further functional impairment. 3,4,9 Considering the protective e ects of the energy precursor creatine on metabolically stressed neural cells in vitro, 18 it is likely that higher intracellular energy levels reached after creatine supplementation in vivo may have saved some of these cells in the penumbra zone around the primary lesion. Rescuing oligodendrocytes and preservation of myelin is expected to have large e ects on the functional outcome after SCI.…”

Section: Discussionmentioning

confidence: 99%

“…Measurements were performed using a 406magni®cation and volumes were given in mm 3 . The contour of the cavern and of the total lesion (cavern and scar) area was highlighted in eight sections spaced 200 mm apart, and the corresponding volumes were calculated.…”

Section: Quanti®cation Of Lesion Volumesmentioning

confidence: 99%

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Protective effects of oral creatine supplementation on spinal cord injury in rats

et al. 2002

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Study design: To evaluate a potential protective e ect of increased creatine levels in spinal cord injury (SCI) in an animal model. Objectives: Acute SCI initiates a series of cellular and molecular events in the injured tissue leading to further damage in the surrounding area. This secondary damage is partly due to ischemia and a fatal intracellular loss of energy. Phospho-creatine in conjunction with the creatine kinase isoenzyme system acts as a potent intracellular energy bu er. Oral creatine supplementation has been shown to elevate the phospho-creatine content in brain and muscle tissue, leading to neuroprotective e ects and increased muscle performance. Setting: Zurich, Switzerland. Methods: Twenty adult rats were fed for 4 weeks with or without creatine supplemented nutrition before undergoing a moderate spinal cord contusion. Results: Following an initial complete hindlimb paralysis, rats of both groups substantially recovered within 1 week. However, creatine fed animals scored 2.8 points better than the controls in the BBB open ®eld locomotor score (11.9 and 9.1 points respectively after 1 week; P=0.035, and 13 points compared to 11.4 after 2 weeks). The histological examination 2 weeks after SCI revealed that in all rats a cavity had developed which was comparable in size between the groups. In creatine fed rats, however, a signi®cantly smaller amount of scar tissue surrounding the cavity was found. Conclusions: Thus creatine treatment seems to reduce the spread of secondary injury. Our results favour a pretreatment of patients with creatine for neuroprotection in cases of elective intramedullary spinal surgery. Further studies are needed to evaluate the bene®t of immediate creatine administration in case of acute spinal cord or brain injury.

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

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Protective effects of oral creatine supplementation on spinal cord injury in rats

et al. 2002

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“…Their persistence in inflamed tissue reflects a balance between recruitment and apoptosis (11) . Neutrophils accumulate within hours after spinal cord injury (17)(18)(19) , reaching a peak at 3 days post-injury followed by a second peak several weeks later (11) (Figure 2). …”

Section: Leukocytes Microglia/macrophages and Dendritic Cells As Mementioning

confidence: 99%

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Trivedi

Olivas

Noble-Haeusslein

2006

Clinical Neuroscience Research

179

138

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The immune response that accompanies spinal cord injury contributes to both injury and reparative processes. It is this duality that is the focus of this review. Here we consider the complex cellular and molecular immune responses that lead to the infiltration of leukocytes and glial activation, promote oxidative stress and tissue damage, influence wound healing, and subsequently modulate locomotor recovery. Immunomodulatory strategies to improve outcomes are gaining momentum as ongoing research carefully dissects those pathways, which likely mediate cell injury from those, which favor recovery processes. Current therapeutic strategies address divergent approaches including early immunoblockade and vaccination with immune cells to prevent early tissue damage and support a wound-healing environment that favors plasticity. Despite these advances, there remain basic questions regarding how inflammatory cells interact in the injured spinal cord. Such questions likely arise as a result of our limited understanding of immune cell/neural interactions in a dynamic environment that culminates in progressive cell injury, demyelination, and regenerative failure.

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“…2 Neutrophils have also been suggested to contribute and aggravate this socalled`ischemia-reperfusion (IR) injury' to the spinal cord. 3,4 Many agents such as iloprost, 2 nitroglycerin, 5 phenytoin, 6 steroids, 7 memantine, 8 trimetazidine, 9 riluzole, 10 aprotinin 11 and various treatment modalities such as ischemic pretreatment 12,13 and hypothermia 14,15 have been suggested to prevent this complication. Another pharmacological agent with the potential for altering the ischemia-reperfusion injury is the methylxanthine derivate, Pentoxifylline (PTX); this has been used in many types of cerebrovascular disease including transient ischemic attacks, sequelae of cerebral thrombosis and hemorrhage, and chronic ischemic disorders beside the experiments on IR injury.…”

Section: Introductionmentioning

confidence: 99%

Pentoxifylline reduces biochemical markers of ischemia-reperfusion induced spinal cord injury in rabbits

et al. 2002

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Study design: Occlusion of the infrarenal abdominal aorta with administration of pentoxifylline was applied to adult rabbits, followed by removal of aortic clamp and reperfusion. Tissue levels of cytokines, lipid peroxides, and antioxidant enzymes were assayed and compared within groups. Objectives: To examine the e ect of pentoxifylline (PTX) on cytokine levels, lipid peroxidation, and antioxidant enzymes in a rabbit model of spinal cord ischemia-reperfusion injury induced by aortic occlusion. Setting: Isparta, Turkey. Methods: Rabbits were randomly allocated into four groups of sham laparotomy (SHAM), sham laparotomy with PTX administration (SHAM+PTX), aortic occlusion and reperfusion (AOR), aortic occlusion and reperfusion with PTX administration (AOR+PTX). An intravenous bolus of 50 mg/kg PTX was given just before aortic cross clamping. An atraumatic microvascular clamp was then placed on the abdominal aorta immediately distal to the left renal artery for 30 min. PTX was infused at a rate of 0.5 mg/kg/min during the aortic occlusion. Animals were subjected to 120 min of reperfusion after removal of the aortic clamp. All animals were sacri®ced at the end of reperfusion. The lumbosacral segments of spinal cords were quickly harvested and stored at 7788C for biochemical assays of IL-6, TNF-a, MDA, SOD, and CAT levels. Di erences among groups were analyzed by one-way analysis of variance followed by a post hoc Tukey's honestly signi®cant di erence test. Results: No di erences in mean levels of IL-6, TNF-a, MDA, SOD, and CAT were noted between SHAM and SHAM+PTX groups (P40.05). There was a signi®cant increase in all biochemical parameters in the AOR group (P50.05). Administration of PTX signi®cantly attenuated the levels of all biochemical parameters in the AOR+PTX group (P50.05). Conclusion: PTX pretreatment attenuated ischemia-reperfusion induced spinal cord injury in a rabbit model, in terms of biochemical parameters of ischemia and reperfusion.

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Spinal cord injury in the rat

Cited by 188 publications

References 163 publications

Protective effects of oral creatine supplementation on spinal cord injury in rats

Protective effects of oral creatine supplementation on spinal cord injury in rats

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Pentoxifylline reduces biochemical markers of ischemia-reperfusion induced spinal cord injury in rabbits

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