Experimental Acute Spinal Cord Injury Research Articles

Clinical Evaluation of the Effect of Methylprednisolone Sodium Succinate and Meloxicam in Experimental Acute Spinal Cord Injury

Background: Central nervous system (CNS) has limited repair capacity, and any spinal cord injury (SCI) can cause persistent disability in motor, sensory, and autonomic functions. The harmful reactions around the lesion must be stopped to prevent this consequence. Objectives: The present study compares the clinical effects of methylprednisolone sodium succinate (MPSS) and meloxicam in acute spinal cord injury in an animal model of rats. Methods: We randomly divided 24 male Wistar rats into 4 groups: 1) sham, 2) placebo, 3) SCI+MPSS (30 mg/kg, IV), and 4) SCI+meloxicam (1 mg/kg, SC). We used a Fogarty embolectomy catheter to induce a compression injury to the rats’ T8-T9 spinal cord segment. The drugs were injected one hour after surgery. Neurological evaluation was performed using BBB (Basso, Beattie, and Bresnahan) test immediately after recovery and then once a week for up to 6 weeks. Results: According to the BBB test results, single-dose administration of MPSS one hour after injury improved motor function significantly compared to placebo. But, there was no significant difference between MPSS and meloxicam groups and between meloxicam and placebo groups (P>0.01). Conclusion: In clinical evaluation, single-dose administration of MPSS one hour after injury improved motor function compared to meloxicam.

Neuroprotective Effects of Milrinone on Experimental Acute Spinal Cord Injury: Rat Model

Spinal cord injury (SCI) disrupts nerve axons with devastating neurological consequences, but there is no effective clinical treatment. The secondary damage mechanism is a mainstay process, and it starts within a few minutes after trauma. We aim to investigate the neuroprotective effects of milrinone on the SCI model. A total of 36 Wistar albino rats, each weighing 300-400 g, were randomly split into 4 groups that received different treatments: in group 1 (sham) (n= 9) control, only a laminectomy was performed; in group 2 (SCI) (n= 9), SCI was imitated after laminectomy; in group 3 (SCI+ saline) (n= 9), physiological saline solution was injected intraperitoneally immediately after the SCI; and in group 4 (SCI+ milrinone), milrinone was administered intraperitoneally on lateral decubitus position immediately after the SCI. Spinal cord contusion was established by the weight-drop technique after laminectomy. Neurological examination scores were recorded, and rats were killed 72 hours later. Serum and spinal cord tissue glutathione peroxidase, total antioxidant status, total oxidant status, 8-hydroxiguanosine, interleukin-6 and interleukin-10 levels, histopathological spinal cord damage score, and apoptotic index were examined and compared between groups. Neurological examination scores were significantly better in the milrinone-treated group compared with groups 2 and 3. SCI significantly increased serum and spinal cord tissue glutathione peroxidase, total oxidant status, 8-hydroxiguanosine, and interleukin-6 levels that were successfully reduced with milrinone treatment. Interleukin-10 and total antioxidant status levels decreased as a result of SCI increased with milrinone treatment. Increased histopathological spinal cord damage score and apoptotic index in groups 2 and 3 significantly decreased in group4. Milrinone could reduce apoptosis and increase anti-inflammatory and antioxidative mediators, thus playing a protective role in secondary nerve injury after SCI in rats.

Outcome heterogeneity and bias in acute experimental spinal cord injury: A meta-analysis.

To determine whether and to what degree bias and underestimated variability undermine the predictive value of preclinical research for clinical translation. We investigated experimental spinal cord injury (SCI) studies for outcome heterogeneity and the impact of bias. Data from 549 preclinical SCI studies including 9,535 animals were analyzed with meta-regression to assess the effect of various study characteristics and the quality of neurologic recovery. Overall, the included interventions reported a neurobehavioral outcome improvement of 26.3% (95% confidence interval 24.3-28.4). Response to treatment was dependent on experimental modeling paradigms (neurobehavioral score, site of injury, and animal species). Applying multiple outcome measures was consistently associated with smaller effect sizes compared with studies applying only 1 outcome measure. More than half of the studies (51.2%) did not report blinded assessment, constituting a likely source of evaluation bias, with an overstated effect size of 7.2%. Assessment of publication bias, which extrapolates to identify likely missing data, suggested that between 2% and 41% of experiments remain unpublished. Inclusion of these theoretical missing studies suggested an overestimation of efficacy, reducing the effect sizes by between 0.9% and 14.3%. We provide empirical evidence of prevalent bias in the design and reporting of experimental SCI studies, resulting in overestimation of the effectiveness. Bias compromises the internal validity and jeopardizes the successful translation of SCI therapies from the bench to bedside.

Evaluation of the effects of erythropoietin and interleukin-6 in rats submitted to acute spinal cord injury

OBJECTIVE:To evaluate the effects of interleukin-6 (IL-6) and erythropoietin (EPO) in experimental acute spinal cord injury (SCI) in rats.METHODS:Using standardized equipment, namely, a New York University (NYU) Impactor, a SCI was produced in 50 Wistar rats using a 10-g weight drop from a 12.5-mm height. The rats were divided into the following 5 groups of 10 animals each: “Group EPO”, treated with erythropoietin only; “Group EPO + IL-6”, treated with both substances; “Group IL-6”, receiving IL-6 administration only; “Group Placebo”, receiving a placebo solution; and “Group Sham”, submitted to an incomplete procedure (only laminectomy, without SCI). All drugs and the placebo solution were administered intraperitoneally for three weeks. The animals were followed up for 42 days. Functional motor recovery was monitored by the Basso, Beattie, and Bresnahan (BBB) scale on days 2, 7, 14, 21, 28, 35 and 42. Motor-evoked potential tests were performed on the 42nd day. Histological analysis was performed after euthanasia.RESULTS:The group receiving EPO exhibited superior functional motor results on the BBB scale. IL-6 administration alone was not superior to the placebo treatment, and the IL-6 combination with EPO yielded worse results than did EPO alone.CONCLUSIONS:Using EPO after acute SCI in rats yielded benefits in functional recovery. The combination of EPO and IL-6 showed benefits, but with inferior results compared to those of isolated EPO; moreover, isolated use of IL-6 resulted in no benefit.

Therapeutic effects of simultaneous Photobiomodulation therapy (PBMT) and Meloxicam administration on experimental acute spinal cord injury: Rat animal model

Study designApplication of Photobiomodulation therapy (PBMT) and meloxicam in acute spinal cord injury, functional recovery and histological evaluation. ObjectiveEvaluation of the effect of simultaneous PBMT and meloxicam on treatment of acute experimental spinal cord injury and comparing it with the effect of application of each of them separately. SettingThe study was conducted at the Department of Surgery & Radiology, Faculty of Veterinary Medicine and Institute of Biomedical Research, University of Tehran, Tehran, Iran. MethodsTwenty four rats were used in this study. A compression injury was induced to the T8-T9 segment of the spinal cord of rats using a Fogarty embolectomy catheter. Rats were randomly divided into 4 groups including: Control group, PBMT (810 nm-200 mw-8 s-2 weeks) group, Meloxicam (1 mg/kg) group, and PBMT and Meloxicam (mixed) group. After inducing injury, hind limb performance of the rats was evaluated, using BBB test and then treatment intervention was performed and continued for 2 weeks. ResultsFour weeks after injury induction, BBB test results were significantly higher in all treatment groups in comparison to control group, however, there were no significant differences among the treatment groups. In addition, histological findings revealed no significant difference between all 4 study groups. ConclusionAccording to the results of this study we can conclude that simultaneous and separate application of PBMT and Meloxicam play an effective role in treatment of acute spinal cord injuries.

Granulocyte Colony-Stimulating Factor Combined with Methylprednisolone Improves Functional Outcomes in Rats with Experimental Acute Spinal Cord Injury

OBJECTIVES:To evaluate the effects of combined treatment with granulocyte colony-stimulating factor (G-CSF) and methylprednisolone in rats subjected to experimental spinal cord injury.METHODS:Forty Wistar rats received a moderate spinal cord injury and were divided into four groups: control (no treatment); G-CSF (G-CSF at the time of injury and daily over the next five days); methylprednisolone (methylprednisolone for 24 h); and G-CSF/Methylprednisolone (methylprednisolone for 24 h and G-CSF at the time of injury and daily over the next five days). Functional evaluation was performed using the Basso, Beattie and Bresnahan score on days 2, 7, 14, 21, 28, 35 and 42 following injury. Motor-evoked potentials were evaluated. Histological examination of the spinal cord lesion was performed immediately after euthanasia on day 42.RESULTS:Eight animals were excluded (2 from each group) due to infection, a normal Basso, Beattie and Bresnahan score at their first evaluation, or autophagy, and 32 were evaluated. The combination of methylprednisolone and G-CSF promoted greater functional improvement than methylprednisolone or G-CSF alone (p<0.001). This combination also exhibited a synergistic effect, with improvements in hyperemia and cellular infiltration at the injury site (p<0.001). The groups displayed no neurophysiological differences (latency p=0.85; amplitude p=0.75).CONCLUSION:Methylprednisolone plus G-CSF promotes functional and histological improvements superior to those achieved by either of these drugs alone when treating spinal cord contusion injuries in rats. Combining the two drugs did have a synergistic effect.

Effects of Local Transplantation of Autologous Bone Marrow Mesenchymal Stem Cells in Combination with Low Level Laser Therapy in Repair of Experimental Acute Spinal Cord Injury in Rats

Objective- The aim of this study was to demonstrate the efficacy MSCs transplantation in combination with low level laser irradiation (low level laser irradiation) in repair of experimental acute spinal cord injury. Design- Experimental study. Animals- 28 adult male Wistar Rats. Procedures- A ballon- compression technique was used to produce an injury at the T8-T9 level of spinal cord applying Fogarty embolectomy catheter. In group-1, the autologous MSCs were transplanted to the spinal cord lesion; and followed by treatment with low level laser irradiation during 15 consecutive days in group-2. The injured rats in third group were treated by LLLI alone. The functional recovery was assessed using the Basso-Beattie-Bresnahan (BBB) locomotion scoring along 5 weeks. Results-In these three treatment groups, the score was significantly higher than control group. The differences among group-2 and two other treatment groups were statistically significant during all five weeks after treatment. There were no significant differences in BBB score between group-1(MSCs) and group-3(LLLI) at 3rd, 4th and 5th weeks of treatment. According to histopathological findings, the best response was observed in group-2(MSCs+LLLI) that repair of injured parts of dorsal funiculi and less cavitation were occurred by proliferation of mesenchymal stem cells and their differentiation to glial cells especially oligodendrocytes resulting in axon regeneration and relatively spinal cord recovery. Conclusion and Clinical Relevance- The findings of present study, demonstrate that concurrent use of LLLI and local transplantation of MSCs exhibits profound effects on axon regeneration and revealed remarkable functional improvement. These results suggest that MSCs characteristics could be influenced by low level laser irradiation, so this treatment may be as a useful procedure for neural regeneration, although further detailed investigations needs to be carried out particularly in clinical cases.

Associations Between Anesthetic Variables and Functional Outcome in Dogs With Thoracolumbar Intervertebral Disk Extrusion Undergoing Decompressive Hemilaminectomy.

BackgroundOutcome of acute experimental spinal cord injury is strongly associated with tissue perfusion and oxygenation. Cardiopulmonary depression could affect outcome in dogs undergoing general anesthesia for surgical treatment of thoracolumbar intervertebral disk extrusion (IVDE).Hypothesis/ObjectivesTo evaluate the effects of general anesthesia on functional outcome in dogs undergoing surgery to treat thoracolumbar IVDE.AnimalsEighty‐four client‐owned dogs with acute thoracolumbar IVDE treated by decompressive hemilaminectomy.MethodsExploratory, retrospective observational study. Medical records were reviewed for clinical presentation and anesthetic monitoring variables, including duration of anesthesia and surgery, hypotension, bradycardia, temperature, and respiratory parameters. Multivariable regression tree analysis was performed to explore associations between anesthetic variables and functional outcome scores after 6 weeks, as well as return to ambulatory status.ResultsEpisodes of bradycardia (69%) and hypotension (57%) were frequent. Across all outcome measures, regression tree analysis highlighted functional grade at presentation as the primary determining factor, and among pain perception negative dogs, there was a possible association between increased duration of surgery and poorer outcome. In dogs with intact pain perception, duration of bradycardia, mean body temperature, and mean end‐tidal carbon dioxide were highlighted.Conclusions and Clinical ImportanceExploratory statistical methods can facilitate hypothesis‐generating studies to inform prospective investigations in veterinary medicine. Although the mechanism is uncertain, increased duration of surgery might be associated with poorer outcome in pain perception negative dogs with thoracolumbar IVDE.

The Effect of Quetiapine on Treatment of Experimental Acute Spinal Cord Injury.

It is well known that treatment modalities against secondary damage due to spinal cord injury (SCI) are very important. This phase has been researched in many experimental studies. Apoptosis is one of the major mechanisms of secondary damage on spinal cord. The present study was undertaken to determine if quetiapine, a 5-HT2 receptor blocker atypical antipsychotic agent can rescue neuronal cells from apoptosis in a SCI model. Thirty-two female Wistar rats were separated to 4 equal groups. Total laminectomy was performed at T5-7 level and spinal cord injury was produced by using the clip compression technique. Each rat from groups "1 day" (D-I) and "7 days" (D-II) was daily injected intraperitoneally with Quetiapine (10 mg/kg/day). No treatment was administered to the control groups "1 day" (K-I) and "7 days" (K-II). At the end of follow-up periods, all animals were sacrificed and spinal cords were removed. Apoptotic cells were evaluated by using immunohistochemical technique (TUNEL) in injured spinal cord specimens. There was a statistically significant difference while counting ApopTag positive cells, both at 1 day groups of K-I and D-I (p=0.00000008) and at 7 day groups of K-II and D-II (p=0.000005). Unlike the 1-day period, a statistically significant difference was found between grey and white matter ApopTag positive cells at the 7 < sup > th < /sup > day (p=0.0001). Quetiapine has a protective effect on secondary damage caused by SCI, while also can be used in post-traumatic stress disorder, depression and agitation as a versatile agent.

Therapeutic Efficacy of E-64-d, a Selective Calpain Inhibitor, in Experimental Acute Spinal Cord Injury.

This study aims to investigate the therapeutic effect of calpain inhibitor E-64-d on SCI and to find a new approach to treat SCI. When an SCI rat model was established, it was immediately administered with E-64-d. RT-PCR and Western blotting were used to determine the protein and mRNA levels of calpain 1 and 68-kD NFP. TUNEL staining and NeuN labeling were performed to analyze neuronal apoptosis in the lesion. Immunohistochemistry assay was carried out to observe the expressions of calpain 1 and GFAP. Cyclooxygenase-2 activity was measured to show the immune response status. Locomotor function was evaluated by inclined plane test and Basso, Beattie, and Bresnahan locomotor rating scale. The results showed that calpain 1 was activated after SCI occurred. Treatment with E-64-d decreased expressions of calpain 1 and GFAP, alleviated neuronal apoptosis, inhibited cyclooxygenase-2 activity, and resulted in the promoted locomotor function. Furthermore, combination of E-64-d and MP had better efficacy than did E-64-d or MP alone. E-64-d is expected to be applied to treat SCI, and its alliance with MP may provide a valid strategy for SCI therapy.

The Pressure Distribution of Cerebrospinal Fluid Responds to Residual Compression and Decompression in an Animal Model of Acute Spinal Cord Injury

In vivo large animal (pig) model study of cerebrospinal fluid (CSF) pressures after acute experimental spinal cord injury (SCI). To determine how the CSF pressure (CSFP) and CSF pulse pressure amplitude (CSFPPA) cranial and caudal to the injury site change after an acute SCI with subsequent thecal occlusion and decompression. Lowering intrathecal pressure via CSF drainage is currently instituted to prevent ischemia-induced SCI during thoracoabdominal aortic aneurysm surgery and was recently investigated as a potential intervention for acute traumatic SCI. However, in SCI patients, persistent extradural compression commonly occludes the subarachnoid space. This may generate a CSFP differential across the injury site, which cannot be appreciated with lumbar catheter pressure measurements. Anesthetized pigs were subjected to an acute contusive SCI at T11 and 8 hours of sustained compression (n = 12), or sham surgery (n = 2). CSFP was measured cranial and caudal to the injury site, using miniature pressure transducers, during compression and for 6 hours after decompression. The cranial-caudal CSFP differential increased (mean, 0.39 mm Hg/h), predominantly due to increased cranial pressure. On decompression, cranial CSFP decreased (mean, -1.16 mm Hg) and caudal CSFP increased (mean, 0.65 mm Hg). The CSFP differential did not change significantly after decompression. Cranial CSFPPA was greater than caudal CSFPPA, but this differential did not change during compression. On decompression, the caudal CSFPPA increased in some but not all animals. Although extradural compression exists at the site of injury, lumbar CSFP may not accurately indicate CSFP cranial to the injury. Decompression may provide immediate, though perhaps partial, resolution of the pressure differential. CSFPPA was not a consistent indicator of decompression in this animal model. These findings may have implications for the design of future clinical protocols in which CSFP is monitored after acute SCI.

Gross Morphological Changes of the Spinal Cord Immediately After Surgical Decompression in a Large Animal Model of Traumatic Spinal Cord Injury

Quantitative in vivo ultrasound imaging study of spinal cord and dura morphology after acute experimental spinal cord injury (SCI) and decompression in a pig model. To study the morphological changes of the spinal cord and dura immediately after surgical decompression for acute SCI. Surgical decompression for traumatic SCI is currently a topic of debate. After decompression, relief of bony impingement on the thecal sac and spinal cord can be confirmed intraoperatively. However, postoperative imaging often reveals that the cord has swollen to fill the subarachnoid space. Little is known about the extent and timing of this morphological response. Yucatan miniature pigs received sham surgery (N = 1) or a moderate (N = 6, 20 g, 2.3 m/s) or high (N = 6, 20 g, 4.7 m/s) severity weight-drop SCI followed by 8 hours of sustained compression (100 g) and 6 hours of postdecompression monitoring. Sagittal-plane ultrasound images were used to quantify spinal cord, dura, and subarachnoid space dimensions preinjury and once per hour after decompression. Animals with a moderate SCI exhibited a residual cord deformation of up to 0.64 mm within 10 minutes of decompression, which tended to resolve during 6 hours because of tissue relaxation and swelling. For animals with high-severity SCIs, cord swelling was immediate and resulted in occlusion of the subarachnoid space within 10 minutes to 5 hours, whereas this occurred for only half of the moderate injury group. Decompression of an acute SCI may result in residual cord deformation followed by gradual swelling or immediate swelling leading to subarachnoid occlusion. The response is dependent on initial injury severity. These observations may partly explain the lack of benefit of decompression in some patients and suggest a need to reduce cord swelling to optimize the clinical outcome after acute SCI.

Early Administration of l-Arginine in Experimental Acute Spinal Cord Injury Impairs Long-Term Motor Function Recovery

Recently, we reported that L-arginine, a nitric oxide precursor, reverses altered drug disposition induced by acute spinal cord injury (SCI) by increasing hepatic blood flow, without affecting mean arterial pressure and heart rate, whereas others have shown that it produces neuroprotection in several models of acute neurologic damage. Its use as a therapeutic agent for microcirculatory alterations associated with spinal shock seems promising. Therefore, here we have tested its influence on long-term morphofunctional neurologic outcome. Intravenous L-arginine (300 mg/kg per dose) was administered to adult rats after SCI of moderate intensity according to the following schemes (n=6): (1) single dose at 1 hour, (2) single dose at 24 hour, and (3) repeated doses first at 24 hour and then daily for 7 days. Control injured rats received the vehicle (saline solution). Contrary to our expectations, locomotor function, assessed using the Basso-Beattie-Bresnahan scale for 8 weeks, was significantly worse in the L-arginine treated groups compared with the control group. Areas of both spared white matter and myelin stain at the epicenter seemed reduced in rats that received L-arginine as a single dose at 1 hour after injury but were not significantly different from the control group. L-arginine as used here interfered with the functional outcome of rats subjected to SCI, suggesting that L-arginine or its metabolic products may be neurotoxic. Because of its potential utility for acute SCI suggested in the past, strategies should be designed to block its apparent neurotoxicity.

Non‐Resolving Aspects of Acute Inflammation after Spinal Cord Injury (SCI): Indices and Resolution Plateau

Inflammatory resolution is an active, highly regulated process already encoded at the onset of inflammation and required to prevent the transition into chronic inflammation associated with spreading of tissue injury and exacerbated scarring. We introduce objective, quantitative measurements [resolution indices (R(i) ) and resolution plateau (R(P) )] to characterize inflammatory resolution and to determine the persistence ("dwell time") of differential leukocyte subpopulations at the lesion site after acute experimental spinal cord injury (SCI). The cell type-specific resolution interval R(i) (time between maximum cell numbers and the point when they are reduced to 50%) ranges from 1.2 days for neutrophils, 1.5 days for T lymphocytes, to 55 days for microglia/macrophages. As the resolution interval neglects exiting cell trafficking in the later period of resolution (49%-0% of lesional cells), we introduced the R(P) , a marker for the persisting, chronified leukocyte subsets, which are likely to participate in late degeneration and non-resolving inflammation. Here, we identify the acute inflammatory response in central nervous system (CNS) lesions as partly non self-limiting. Both extended resolution intervals (reduced leukocyte clearance) and elevated plateaus (permanent lesional cell numbers) provide quantitative measures to characterize residual, sustained inflammation and define cognate timeframes of impaired resolution after acute SCI.

W1918 Mesenteric Hypoperfusion Following Acute Experimental Spinal Cord Injury

W1918 Mesenteric Hypoperfusion Following Acute Experimental Spinal Cord Injury

Methylprednisolone fails to improve functional and histological outcome following spinal cord injury in rats

Currently, methylprednisolone sodium succinate (MPSS) is the standard treatment following acute spinal cord injury (SCI) as a consequence of the results obtained from the National Acute Spinal Cord Injury Studies. However, many have questioned the efficacy of MPSS because of its marginal effects. Additionally there has been criticism of both study design and statistical interpretation. The functional consequences of experimental SCI have been assessed in many ways. The purpose of this investigation was to determine the effects of MPSS vs. saline solution (SS) following moderate T10 contusion injury in rat. Functional recovery was evaluated using the 21-point Basso, Beattie and Bresnahan (BBB) locomotor recovery scale, the inclined plane, the beam walk, footprint analysis and the horizontal ladder. To optimize the precision and accuracy of functional results we examined the locomotion on a treadmill using three-dimensional (3D) analysis. Stereology was used to estimate the amount of damaged tissue. The results of the traditional functional methods showed that administration of the NASCIS dosage of MPSS following acute spinal cord contusion did not lead to any significant differences in the functional recovery of MPSS- vs. SS-treated animals. More importantly, the results of the 3D kinematic showed that the MPSS administration did not affect the flexion/extension of the hip, knee and ankle joints during the step cycle. Finally, stereological results revealed no statistically significant differences between the two experimental groups. Altogether, our results support data previously reported by several authors, suggesting that MPSS does not lead to improved functional outcome following experimental acute SCI.

Immunomodulation of acute experimental spinal cord injury with human immunoglobulin G

Immunomodulation of acute spinal cord injury may inhibit the activity of specific inflammatory cascades and result in recovery of motor function. In this study, evaluation of the protective effect of a well-known anti-inflammatory immunomodulator, immunoglobulin G (IgG), was conducted in rats after a 50 g/cm contusion spinal cord injury. Following injury, 400 mg/kg of IgG was administered to the treatment group. Twenty-four hours later, animals were assessed functionally via an inclined plane and the Basso-Beattie-Bresnahan motor scale and compared to controls. Tissue was reviewed for myeloperoxidase activiy (MPO) and lipid peroxidation (LPO), and electron microscopy was conducted to assess tissue ultrastructure. Significant functional preservation was observed in the IgG treatment group. In addition, biochemical assays revealed decreased MPO activity, and electron microscopic views of tissue showed preserved ultrastructure. IgG treatment following acute contusion injury to the rat spinal cord confers functional and structural neuroprotection.

Gastric dysreflexia after acute experimental spinal cord injury in rats

Gastric reflexes are mediated mainly by vago-vagal reflex circuits in the caudal medulla. Despite the fact that brainstem vago-vagal circuitry remains intact after spinal cord injury (SCI), patients with SCI at the cervical level most often present gastric stasis with an increased risk of reflux and aspiration of gastric contents. Using a miniature strain gauge sutured to the gastric surface; we tested gastric motility and reflexive gastric relaxation following oesophageal distension (oesophageal-gastric relaxation reflex) in animals 3 days after a severe spinal contusion at either the third or ninth thoracic spinal segment (acute T3- or T9 SCI, respectively). Both basal gastric motility and the oesophageal-gastric relaxation reflex were significantly diminished in animals with T3 SCI. Conversely, both basal gastric motility and the oesophageal-gastric relaxation reflex were not significantly reduced in T9 SCI animals compared to controls. The reduced gastric motility and oesophageal-gastric reflex in T3 SCI rats was not ameliorated by celiac sympathectomy. Our results show that gastric stasis following acute SCI is independent of altered spinal sympathetic input to the stomach caudal to the lesion. Our data suggest that SCI may alter the sensitivity of vagal reflex function, perhaps by interrupting ascending spinosolitary input to brainstem vagal nuclei.

Serum Leptin Levels Following Acute Experimental Spinal Cord Injury

Background/Objective: Spinal cord injury influences many hormones that are known to be involved in the modulation of neurotrophic, neurogenic, and neuroprotective events. Recent studies showed that leptin could be neuroprotective, enhancing neuronal survival in vitro and in vivo. The objective of this study was to evaluate the pattern of the serum leptin levels in rats during acute traumatic SCI.Methods: Forty male Sprague-Dawley rats were divided randomly into 4 groups. In the control group, neither laminectomy nor SCI was performed; only laminectomy was performed without SCI in the sham group. In the cervical and thoracic spinal trauma groups, laminectomies were performed following the same trauma procedure. Blood samples were drawn 2, 6, 12, and 24 hours after the procedures and assayed immediately.Results: In the first 2 hours, levels of leptin were similar in control and sham-operated groups and higher in neurotrauma groups (P < 0.05). At the sixth hour, leptin levels increased in the sham-operated group, decreased in the neurotrauma groups (P < 0.05), and did not change in the control group (P > 0.05). At the 12th hour, the levels of leptin increased in all groups (P > 0.05). At the 24th hour, they decreased in the control, sham-operated, and cervical groups (P < 0.05); levels did not change in the thoracic group (P > 0. 05). The decrease was higher in the control group than in the other groups (P < 0.05).Conclusions: Activation of endogenous leptin secretion started immediately after the SCI. The level of neurologic lesion (either cervical or thoracic regions) affected the levels of serum leptin differently, but with the exception of the first 12-hour period, this difference did not reach a statistically significant level.

Elevation of neuron-specific enolase and S-100β protein level in experimental acute spinal cord injury

We evaluated the protein levels of neuron-specific enolase (NSE) and S-100β in serum and cerebrospinal fluid (CSF) in an animal model of acute spinal cord injury and ascertained their relevance. Spinal cord injury was induced at the T8 level in rats. Enzyme-linked immunosorbent assay was used to measure the protein levels of NSE and S-100β in both serum and CSF at different time points (30 min, 2 h, 6 h, 12 h and 24 h after induction of spinal cord injury). There existed a significant correlation between neurological deficits and the severity of spinal cord injury ( p < 0.05). Compared with the control group, the protein levels of NSE and S-100β in serum and CSF significantly increased from 2 h after injury ( p < 0.05) and reached a maximum at 6 h. Within a certain time window, the protein levels of NSE and S-100β in serum and CSF were closely related to the severity of injury level ( p < 0.05). The protein levels of NSE and S-100β in serum and CSF significantly increased after experimental spinal cord injury in a time-dependent manner and thus may be considered specific biomarkers for acute spinal cord injury.