Regional spinal cord blood flow in rats after severe cord trauma

Rivlin, Alex S.; Tator, Charles H.

doi:10.3171/jns.1978.49.6.0844

Cited by 168 publications

(61 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…35,36 SCBF recordings are also available from studies using comparable trauma models, as in the present study, such as the extradural cu /balloon and clip compression techniques and equivalent autoradiographic techniques. 18,37,38 The SCBF recorded in these studies showed a similar reduction in the blood ow at the site of compression as well as cranial and caudal to the injury zones 1 h after trauma. This indicates that the blood changes recorded in the present study could be compared to the blood¯ow-values obtained using the autoradiographic technique and the same trauma model.…”

Section: Discussionsupporting

confidence: 54%

Spinal cord blood flow changes following systemic hypothermia and spinal cord compression injury: an experimental study in the rat using Laser-Doppler flowmetry

et al. 2001

View full text Add to dashboard Cite

Study design: It is well known that changes of the body temperature as well as trauma in¯uence the blood¯ow in the brain and spinal cord. However, there is still a lack of knowledge concerning the levels of blood¯ow changes, especially during hypothermia. Objectives: This investigation was carried out to examine the e ects of systemic hypothermia and trauma on spinal cord blood¯ow (SCBF). Methods: Twenty-four rats were randomized either to thoracic laminectomy only (Th VII ± IX) or to 35 g spinal cord compression trauma. The animals were further randomized to either constant normothermia (388C) or to a systemic cooling procedure, ie reduction of the esophageal temperature from 38 to 308C. SCBF was recorded 5 mm caudal to the injury zone using Laser-Doppler¯owmetry which allows a non-invasive continuous recording of local changes in the blood¯ow. The autoregulation ability was tested at the end of the experiments by inducing a 30 ± 50 mmHg blood-pressure fall, using blood-withdrawal from the carotid artery. Results: The mean SCBF decreased 2.8% and 3.5% per centigrade reduction of esophageal temperature in the animals sustained to hypothermia with and without trauma, respectively. This could be compared to a decrease of 0.2%/min when only trauma was applied. No signi®cant di erences were seen between the groups concerning auto regulatory ability. Conclusions: Our results indicate that the core temperature has a high impact on the SCBF independent of previous trauma recorded by Laser-Doppler¯owmetry. This in¯uence exceeds the response mediated by moderate compression trauma alone. Sponsorship: The study was supported by grants from the Laerdal foundation. Spinal Cord (2001) 39, 74 ± 84

show abstract

Section: Discussionsupporting

confidence: 54%

Spinal cord blood flow changes following systemic hypothermia and spinal cord compression injury: an experimental study in the rat using Laser-Doppler flowmetry

et al. 2001

View full text Add to dashboard Cite

show abstract

“…After experimental TSCI, a profound reduction in spinal cord blood flow occurs, which progressively worsens (21) and may last for 24 h (22). In a recent study assessing the effects of EPO on the clinical course after subarachnoid hemorrhage in a rabbit model, rhEPO treatment dramatically attenuated the intense intracerebral arterial spasm Extensive white matter preservation can be observed in the rhEPO-treated group.…”

Section: Discussionmentioning

confidence: 99%

Recombinant human erythropoietin counteracts secondary injury and markedly enhances neurological recovery from experimental spinal cord trauma

Gorio

Gökmen

Erbayraktar

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

357

260

View full text Add to dashboard Cite

Erythropoietin (EPO) functions as a tissue-protective cytokine in addition to its crucial hormonal role in red cell production. In the brain, for example, EPO and its receptor are locally produced, are modulated by metabolic stressors, and provide neuroprotective and antiinflammatory functions. We have previously shown that recombinant human EPO (rhEPO) administered within the systemic circulation enters the brain and is neuroprotective. At present, it is unknown whether rhEPO can also improve recovery after traumatic injury of the spinal cord. To evaluate whether rhEPO improves functional outcome if administered after cord injury, two rodent models were evaluated. First, a moderate compression of 0.6 N was produced by application of an aneursym clip at level T3 for 1 min. RhEPO (1,000 units per kg of body weight i.p.) administered immediately after release of compression was associated with partial recovery of motor function within 12 h after injury, which was nearly complete by 28 days. In contrast, saline-treated animals exhibited only poor recovery. In the second model used, rhEPO administration (5,000 units per kg of body weight i.p. given once 1 h after injury) also produced a superior recovery of function compared with saline-treated controls after a contusion of 1 N at level T9. In this model of more severe spinal cord injury, secondary inflammation was also markedly attenuated by rhEPO administration and associated with reduced cavitation within the cord. These observations suggest that rhEPO provides early recovery of function, especially after spinal cord compression, as well as longerlatency neuroprotective, antiinflammatory and antiapoptotic functions.T raumatic spinal cord injury (TSCI) occurs frequently and is devastating for the individual patient and costly to society by requiring substantial long-term health care expenditures. Currently, methylprednisolone administered at high dose within 8 h after injury is the only therapy with any recognized benefit (1), which, unfortunately, is relatively minor. Any new treatment of TSCI that allows for major recovery of function would be a significant advance in clinical care.Injury of the nervous system provokes a complex cascade of proinflammatory cytokines and other molecules that ultimately result in apoptosis and necrosis of neurons, oligodendrocytes, and endothelial cells (2-4). Recent studies have demonstrated that one general response of the brain to injury is the increased local production of the erythropoietin (EPO) and its receptor (5, 6). These proteins are members of the cytokine type I superfamily that provide beneficial effects including inhibition of apoptosis, reduction of inflammation, modulation of excitability (7-11), and mobilization and proliferation of neuronal stem cells (12). Prior study has shown that recombinant human EPO (rhEPO) administered directly into the brain dramatically reduces hypoxic or ischemic injury and conversely, that neutralization of endogenous EPO amplifies injury (8). We have extended these observations by sho...

show abstract

“…With respect to impacting devices, efforts in this direction have resulted in SCI models in adult rodents where multiple parameters of the impact such as speed, force and duration can be manipulated (reviewed by 44 ). Another approach, involving less equipment, employs a modification of the Kerr-Lougheed aneurysm clip 45,46 . These 2 approaches are complementary as the impactor mimics a contusion injury whereas the clip mimics a compression injury with some degree of concurrent ischemia.…”

Section: Discussionmentioning

confidence: 99%

A Neonatal Mouse Spinal Cord Compression Injury Model

Züchner

Glover

Boulland

2016

JoVE

View full text Add to dashboard Cite

Spinal cord injury (SCI) typically causes devastating neurological deficits, particularly through damage to fibers descending from the brain to the spinal cord. A major current area of research is focused on the mechanisms of adaptive plasticity that underlie spontaneous or induced functional recovery following SCI. Spontaneous functional recovery is reported to be greater early in life, raising interesting questions about how adaptive plasticity changes as the spinal cord develops. To facilitate investigation of this dynamic, we have developed a SCI model in the neonatal mouse. The model has relevance for pediatric SCI, which is too little studied. Because neural plasticity in the adult involves some of the same mechanisms as neural plasticity in early life 1 , this model may potentially have some relevance also for adult SCI. Here we describe the entire procedure for generating a reproducible spinal cord compression (SCC) injury in the neonatal mouse as early as postnatal (P) day 1. SCC is achieved by performing a laminectomy at a given spinal level (here described at thoracic levels 9-11) and then using a modified Yasargil aneurysm mini-clip to rapidly compress and decompress the spinal cord. As previously described, the injured neonatal mice can be tested for behavioral deficits or sacrificed for ex vivo physiological analysis of synaptic connectivity using electrophysiological and high-throughput optical recording techniques 1 . Earlier and ongoing studies using behavioral and physiological assessment have demonstrated a dramatic, acute impairment of hindlimb motility followed by a complete functional recovery within 2 weeks, and the first evidence of changes in functional circuitry at the level of identified descending synaptic connections 1 .

show abstract

Regional spinal cord blood flow in rats after severe cord trauma

Cited by 168 publications

References 14 publications

Spinal cord blood flow changes following systemic hypothermia and spinal cord compression injury: an experimental study in the rat using Laser-Doppler flowmetry

Spinal cord blood flow changes following systemic hypothermia and spinal cord compression injury: an experimental study in the rat using Laser-Doppler flowmetry

Recombinant human erythropoietin counteracts secondary injury and markedly enhances neurological recovery from experimental spinal cord trauma

A Neonatal Mouse Spinal Cord Compression Injury Model

Contact Info

Product

Resources

About