RESUMEN

BACKGROUND: Cervical spinal cord injury usually results in cardiorespiratory dysfunctions due to interruptions of the bulbospinal pathways innervating the cervical phrenic motoneurons and thoracic sympathetic preganglionic neurons. PURPOSE: The present study aimed to evaluate the therapeutic effects of adrenergic agents on systemic and spinal hemodynamics during acute cervical spinal cord injury. STUDY DESIGN: In vivo animal study. METHODS: The cardiorespiratory function and spinal cord blood flow and oxygenation level were monitored in response to cervical spinal cord contusion and intravenous infusion of three types of adrenergic agents (phenylephrine, dobutamine, and norepinephrine). RESULTS: Cervical spinal cord contusion resulted in immediate reduction of respiratory airflow, arterial blood pressure, and spinal cord blood flow. The arterial blood pressure and spinal cord blood flow remained lower than the pre-injury value in contused animals infused with saline at 60 min post-injury. Infusion of phenylephrine (500, 1000, and 2000 µg/kg) and norepinephrine (125, 250, and 500 µg/kg) significantly increased the arterial blood pressure, while only norepinephrine augmented the spinal cord blood flow. Conversely, dobutamine (1000 and 2000 µg/kg) reduced both arterial blood pressure and spinal cord blood flow. Notably, administration of adrenergic agents tended to increase spinal cord hemorrhage in contused animals. CONCLUSIONS: Infusion of norepinephrine can effectively maintain the blood pressure and improve spinal cord blood flow during acute spinal cord injury. CLINICAL SIGNIFICANCE: Norepinephrine may be a superior medicine for hemodynamic management; however, the potential hemorrhage should be considered when utilizing the vasopressor to regulate systemic and spinal hemodynamics at the acute injured stage.

RESUMEN

Background: During thoracoabdominal aortic surgery, the spinal cord is placed under ischemic conditions. Elevation of systemic blood pressure is thus recommended as a method of increasing the blood supply from collateral networks. This study examined the mechanisms by which noradrenaline administration increases spinal cord blood flow (SCBF) by elevating systemic blood pressure. Methods: In beagles (n = 7), the thoracoabdominal aorta and L2-L7 spinal cord segmental arteries (SAs) were exposed and a distal perfusion bypass was created to simulate clinical practice. SCBF was measured by laser flowmetry at the L5 dura mater and spinal cord perfusion pressure (SCPP) was measured inside the clamped aorta. The six pairs of SAs from L2 to L7 were clamped, and mean systemic blood pressure (mSBP), SCBF, and SCPP were measured before and after clamping and after starting continuous infusion of noradrenaline at 0.5 µg/kg/min. Rates of change in systemic vascular resistance (SVR) and spinal cord vascular resistance (SCVR) were calculated from the measured values. Results: With no SA clamping (control), the rate of increase in SCVR was 0.74 times the rate of increase in SVR (y = 0.2 + 0.74x, r = 0.889, r2 = 0.789; P < 0.01). When all six pairs of SAs were clamped, a weak correlation was evident between rate of change in SCVR and rate of change in SVR, and the rate of increase in SCVR was lower than the rate of increase in SVR (y = 0.39 + 0.07x, r = 0.209, r2 = 0.039; P < 0.01). When all six pairs of SAs were clamped in the absence of distal perfusion, a weak correlation was also evident between rate of change in SCVR and rate of change in SVR, and the rate of increase in SCVR was lower than the rate of increase in SVR (y = 0.19 + 0.08x, r = 0.379, r2 = 0.144; P < 0.01). Conclusions: The rate of increase in SCVR induced by noradrenaline administration was lower than the rate of increase in SVR in the control group with no spinal cord SA clamping and in both experimental groups with clamped SAs (with and without distal perfusion), creating an environment conducive to spinal cord flow distribution.

RESUMEN

This study investigates the effect of extended laminectomy (EL) on spinal cord injury (SCI) caused by spinal shortening, and further, the timing and the optimal length of removal. Dogs received spinal column shortening at T13 segment, following which the control group underwent regular laminectomy while other groups underwent laminectomy with an additional 1-lamina length removed 6h after shortening ("1-lamina EL 6 h"), an extra 1.5-lamina length resected at 6 h or 12 h after shortening ("1.5-lamina EL 6 h" and "1.5-lamina EL 12 h"), and an extra 2-lamina length removed at 6 or 12 h after shortening ("2-lamina EL 6 h" and 2-lamina EL 12 h"), respectively. Somatosensory evoked potential (SSEP) and neurological function were recorded periodically; spinal cord blood flow (SCBF) and nerve cell apoptosis were detected. The results showed that resection of an additional 1-lamina length appeared inadequate to relieve the sharp kinking of the spinal cord, whereas the kinking disappeared with an additional 2-lamina length resection. The "1-lamina EL 6 h" and "1.5-lamina EL 12 h" groups showed no significant differences from the control in latency of SSEP, SCBF, hindlimb function and apoptosis. By contrast, significant recovery of SSEP, SCBF and hindlimb function as well as reduction of apoptosis were presented in other three groups. The "2-lamina EL 6 h" group, in particular, showed the most prominent recovery. In conclusion, an additional resection of two laminae at 6 h after shortening showed the best effect in alleviating SCI. Timely and adequately extended laminectomy could be a potential therapeutic strategy for SCI attributable to spinal shortening.

Asunto(s)

RESUMEN

OBJECTIVE: In cervical spondylotic myelopathy (CSM), compromise of blood flow to the compressed spinal cord has been postulated to contribute to the development of myelopathy. Although decompressive surgery has been considered to improve spinal cord blood flow, evidence to support this notion is scarce. To determine whether blood flow improves after decompressive surgery for CSM, regional blood flow was measured in a model of chronic cervical compression in rats by using a fluorescent microsphere technique. METHODS: Thin polyurethane sheets, measuring precisely 3 × 5 × 0.7 mm, were implanted under the C5-6 laminae in 24 rats to induce continuous compression on the cervical spinal cord. These sheets expand gradually by absorbing tissue fluid. This animal model has been demonstrated to reproduce the clinical features and histological changes of CSM, including progressive motor weakness with delayed onset and insidious tissue damage prior to symptom onset. Twenty-four rats that underwent sham operation were allocated to a control group. To confirm the development of cervical myelopathy, motor functions were measured weekly over the study period. Nine weeks after implantation of the sublaminar expanding sheets, histological studies and C5-6 decompressive surgery were conducted. Regional blood flow in the brainstem and cervical spinal cord was measured sequentially until 120 minutes after decompression. RESULTS: In the CSM group, bilateral forepaw grip strength deteriorated progressively from 5 weeks after implantation. In the compressed C5-6 segment of the spinal cord, significant flattening of the cord, a decreased number of motor neurons, and vacuolations of gray matter were demonstrated. In the control group, blood flow in the brainstem and cervical spinal cord was unchanged by the decompressive surgery. In the CSM group, however, diminished blood flow and continuous blood flow increments for 120 minutes after decompression were demonstrated in the compressed C5-6 spinal cord segment. CONCLUSIONS: Chronic mechanical compression induced regional spinal cord blood flow insufficiency concomitant with progressive neuronal loss and motor dysfunction in a chronic compression model in rats. Decompressive surgery increased spinal cord blood flow. These findings suggest that blood flow recovery may contribute to postoperative neurological improvement.

RESUMEN

In the traumatically injured spinal cord, decreased perfusion is believed to contribute to secondary tissue damage beyond the primary mechanical impact, and restoration of perfusion is believed to be a promising therapeutic target. However, methods to monitor spinal cord perfusion non-invasively are limited. Perfusion magnetic resonance imaging (MRI) techniques established for the brain have not been routinely adopted to the spinal cord. The purpose of this study was to examine the relationship between spinal cord blood flow (SCBF) and injury severity in a rat thoracic spinal cord contusion injury (SCI) model using flow-sensitive alternating inversion recovery (FAIR) with two variants of the label position. SCBF as a marker of severity was compared to T1 mapping and to spinal cord-optimized diffusion weighted imaging (DWI) with filtered parallel apparent diffusion coefficient. Thirty-eight rats underwent a T10 contusion injury with varying severities (8 sham; 10 mild; 10 moderate; 10 severe) with MRI performed at 1 day post injury at the lesion site and follow-up neurological assessments using the Basso, Beattie, Bresnahan (BBB) locomotor scoring up to 28 days post injury. Using whole-cord regions of interest at the lesion epicenter, SCBF was decreased with injury severity and had a significant correlation with BBB scores at 28 days post injury. Importantly, estimates of arterial transit times (ATT) in the injured spinal cord were not altered after injury, which suggests that FAIR protocols optimized to measure SCBF provide more value in the context of acute traumatic injury to the cord. T1-relaxation time constants were strongly related to injury severity and had a larger extent of changes than either SCBF or DWI measures. These findings suggest that perfusion decreases in the spinal cord can be monitored non-invasively after injury, and multi-parametric MRI assessments of perfusion, diffusion, and relaxation capture unique features of the pathophysiology of preclinical injury.

Asunto(s)

RESUMEN

BACKGROUND: Fibrocartilaginous embolism (FCE) is a rare cause of ischemic myelopathy that occurs when the material of the nucleus pulposus migrates into vessels supplying the spinal cord. The authors presented a case of pediatric FCE that was successfully managed by adapting evidence-based recommendations used for spinal cord neuroprotection in aortic surgery. OBSERVATIONS: A 7-year-old boy presented to the emergency department with acute quadriplegia and hemodynamic instability that quickly progressed to cardiac arrest. After stabilization, the patient regained consciousness but remained in a locked-in state with no spontaneous breathing. The patient presented a diagnostic challenge. Traumatic, inflammatory, infectious, and ischemic etiologies were considered. Eventually, the clinical and radiological findings led to the presumed diagnosis of FCE. Treatment with continuous cerebrospinal fluid drainage (CSFD), pulse steroids, and mean arterial pressure augmentation was applied, with subsequent considerable and consistent neurological improvement. LESSONS: The authors proposed consideration of the adaptation of spinal cord neuroprotection principles used routinely in aortic surgery for the management of traumatic spinal cord ischemia (FCE-related in particular), namely, permissive arterial hypertension and CSFD. This is hypothesized to allow for the maintenance of sufficient spinal cord perfusion until adequate physiological blood perfusion is reestablished (remodeling of the collateral arterial network and/or clearing/absorption of the emboli).

RESUMEN

INTRODUCTION: Spinal cord ischemia after cardiovascular interventions continues to be a devastating problem in modern surgery. The role of intraspinal vascular networks and anterior radiculomedullary arteries (ARMA) in preventing spinal cord ischemia is poorly understood. MATERIALS AND METHODS: Landrace pigs (n = 30, 35.1 ± 3.9 kg) underwent a lateral thoracotomy. Fluorescent microspheres were injected into the left atrium and a reference sample was aspirated from the descending aorta. Repeated measurements of spinal cord and renal cortical blood flow from the left and right kidneys with three different microsphere colors in five pigs were taken to validate reproducibility. Spinal cord blood flow to the upper thoracic (T1-T4), mid-thoracic (T5-T8), lower thoracic (T9-T13), and lumbar (L1-L3) levels were determined. After euthanasia, we carried out selective vascular corrosion cast and counted the left and right ARMAs from levels T1-T13. RESULTS: Blood flow analysis of the left and right kidneys revealed a strong correlation (r = .94, p < .001). We detected more left than right ARMAs, with the highest prevalence at T4 (p < .05). The mean number of ARMAs was 8 ± 2. Their number in the upper thoracic region ranged from 2 to 7 (mean of 5 ± 1), while in the lower thoracic region they ranged from 0 to 5 (mean of 3 ± 1 [p < .001]). CONCLUSIONS: This study shows that combining fluorescence microsphere technique and vascular corrosion cast is well suited for assessing the blood flow and visualizing the arteries at the same time.

Asunto(s)

RESUMEN

PURPOSE: To determine the safe range of shortening the spinal column at middle thoracic spine and to observe the changes in blood-spinal cord barrier (BSCB), microglia/macrophage activation and inducible nitric oxide synthase (iNOS) activity after shortening-induced spinal cord injury. METHODS: Dogs were allocated to four groups. Group A (control) underwent laminectomy of T7 without shortening the spinal column. Groups B, C and D had 1/3, 1/2, and 2/3 of T7 resected, respectively, followed by spinal shortening. Somatosensory evoked potential (SSEP) and hind-limb function were recorded periodically for 14 days after operation. Spinal cord blood flow (SCBF) and BSCB were detected at the acute phase of shortening. Microglia/macrophage reactions and iNOS activity were observed by immunohistochemistry. RESULTS: Shortening of 1/3 of a vertebral height caused no significant changes in SSEP and hind-limb function after operation, whereas shortening of 1/2 of the height caused SSEP abnormality and paraparesis, and severe neurologic deficit of hind-limb was observed when the shortening reached 2/3 of the height. SCBF increased temporarily and showed a trend of recovery when the shortening was within 1/2 of a vertebral segment height. When it reached 1/2 or 2/3 of the height, SCBF at 6 h post-operation was 86.33% or 74.95% of the baseline, and an increasing BSCB permeability was observed. In the subsequent 7 days, obvious activation of macrophage and increased number of iNOS-positive cells were observed. CONCLUSION: It is safe to shorten the spinal cord within 1/3 of a vertebral height in middle thoracic spine under two-segment laminectomy in canine. The BSCB disruption, macrophage activation, and increased iNOS activity were observed in the acute phase of the injury. These slides can be retrieved under Electronic Supplementary Material.

Asunto(s)

RESUMEN

Bradykinin is a mediator of vasogenic brain edema formation. Recent reports suggest that bradykinin interacts with nitric oxide synthase (NOS) system in the central nervous system (CNS). However, role of bradykinin in spinal cord injury (SCI) induced alterations in the blood-spinal cord barrier (BSCB), spinal cord blood flow (SCBF), edema formation and cell changes are still not well known. Our previous reports showed that SCI induces marked upregulation of neuronal NOS (nNOS) in the cord associated with BSCB disruption, edema formation and cell injury. Thus, a possibility exists that bradykinin participates in SCI induced nNOS upregulation and cord pathology. To explore this idea a potent bradykinin B2 receptor antagonist HOE-140 was used in our rat model of SCI and cord pathology. SCI was inflicted in Equithesin anesthetized rats by making a longitudinal incision (2mm deep and 5mm long) into the right dorsal horn of the T10-11 segment. The animals were allowed to survive 5h after injury. A focal SCI significantly disrupted BSCB to Evans blue and [131]I-sodium in the traumatized and adjacent segments. Interestingly, far remote spinal cord segments C4 and T5 segments also affected within 5h. These spinal cord segments also exhibited pronounced reductions in the SCBF (mean-30%), increased edematous swelling and profound neuronal damages. Upregulation of nNOS expression is seen in both the dorsal and ventral horns of the spinal cord exhibiting cord pathology. At the ultrastructural level, exudation of lanthanum is seen within the endothelial cell cytoplasm and occasionally in the basal lamina. Pretreatment with low doses of HOE-140 (0. 1mg to 1mg/kg, i.v.) 30min prior to SCI significantly enhanced the SCBF and reduced the BSCB disruption, edema formation, nNOS upregulation and cell injury. However, HOE-140 in doses ranging from 2mg to 5mg/kg, i.v. did not induce significant neuroprotection. These observations are the first to suggest that bradykinin B2 receptors play an important role in BSCB permeability, SCBF, edema formation, nNOS upregulation and cell injury following acute SCI, not reported earlier.

Asunto(s)

RESUMEN

The main purpose of the present study was to examine the time-dependent alterations in the endothelial cell density that occur in the first 180 days after irradiation of the spinal cord and the functional role of these alterations in the spinal cord blood flow. An irradiated cervical spinal cord rat model (C2-T2 segment) was generated using a (60)Co irradiator to deliver 30 Gy. A significant loss of forelimb motor function was observed 180 days post-irradiation. The number of neurons in the anterior horn of the spinal cord began to decrease significantly 3 days post-irradiation compared with normal controls, reaching the lowest number at 90 days post-irradiation. A significant reduction in the endothelial cell density was observed from 14 days post-irradiation in the white matter and from 3 days post-irradiation in the gray matter. The lowest endothelial cell density was reached at 30 days post-irradiation in the white matter and at 60 days post-irradiation in the gray matter. A significant reduction in the microvessel density was observed from 3 days post-irradiation in both the white matter and the gray matter. The lowest microvessel density was reached at 90 days post-irradiation in both the white matter and the gray matter. A significant reduction in the relative magnitude of spinal cord blood flow was observed from 21 days post-irradiation. The lowest relative magnitude of spinal cord blood flow was reached at 90 days post-irradiation. We did not find any evidence of demyelination. The results revealed that a single 30-Gy irradiation dose resulted in impaired forelimb motor function, a decreased number of neurons, and reduced endothelial cell density, microvessel density and relative magnitude of spinal cord blood flow. However, a 30-Gy single-dose irradiation was not sufficient to induce demyelination in the rat spinal cord.

Asunto(s)

RESUMEN

[Objective]To research the influence of spinal cord blood flow(SCBF) and the evoked potential(EP) by the extramarrow impacting and to explore the correlation and regularity between the spinal cord blood flow and evoked potential after spinal cord injury.[Method]Normal 120 SD rats were randomized into 4 groups,with 30 in each.Group A was the control group.In groups B,C,D,impacts of 10,15,20N were given to lamina respectively.The blood flow of impacting position and evoked potential were observed at different time points including 0 min,1 h,6 h,1 d,6 d,12 d,24 d.[Result]The blood flow of spinal cord represents a dimning trend with the impacting load raising.The blood flow of group A,had no marked change,the SEP and MEP also.The blood flow of group B represented a temporaly lowing,then recovered normal,the SEP and MEP also.The blood flow of group C and D represented a continuous lowing,then slowly raising.The group C recovered normal at 24d,the group D still lower than normal.[Conclusion]The impact load to lamina can influence the spinal cord function through altering the spinal cord blood flow.There is evident correlation between the SCBF and EP.

RESUMEN

Objective To study the influences of impact of different loads to lamina on spinal cord with a closed spinal cord injury model and to explore the mechanisms of blood vessels in spinal cord injury. Methods 120 normal male SD rats were randomized into 4 groups, with 30 in each. Group A served as the control group which received no impact. In Groups B, C and D,impacts of 10, 15 and 20 N were given to lamina respectively. The blood flow in the spinal cord central gray matter and the dorsal white matter, the blood pressure and the heart rate were observed at different experimental time points. Results No obvious change was observed in the blood pressure and heart rate in every group at different time points. The spinal cord blood flow (SCBF) in Groups C and D varied in a regular pattern. Conclusions The impact load to lamina can affect the spinal cord mainly by altering the spinal cord microcirculation. The influence is the most obvious on the blood flow of microcirculation of the gray matter.

RESUMEN

A growing body of biochemical, physiological, and pharmacological evidence has suggested that oxygen free radical-induced lipid peroxidation plays a key role in progressive posttraumatic spinal cord ischemia. Recently, it has been reported that the newly developed compound, U74006 F, a non-glucocorticoid 21-aminosteroid, is extremely potent as an inhibitor of lipid peroxidation and effective preventor from the posttraumatic ischemia. In this investigation, the effects of 21-aminosteroid U74389F, analog of U74006F on posttraumatic spinal cord blood flow and somatosensory evoked potential have been studied in cats. The results of this study are summarized as follows:(1) U74389F, given 3 mg/kg, blood flow decreased significantly and somatosensory response returned to none of five cats. (2) U74389F, given 10 mg/kg or 20 mg/kg, the blood flow did not decreased and maintained near the preinjury level. The recovery rate of somatosensory evoked potential ranged from 40 to 60%. (3) There was no statistical difference of blood flow change between the cats treated with 10 mg/kg and those treated with 20 mg/kg of U74389F. It is thought that the adequate dosage of U74389F to prevent posttraumatic spinal cord ischemia is more than 10 mg/kg or 20 mg/kg of U74389F, was statistically significant compared to much more decrease in naloxone-treated cats. The reason is thought to be much longer half life of U74389F in serum. From the above results, it is speculated that U74389Fhas beneficial effect on posttraumatic spinal cord ischemia and functional recovery. The effects last longer than those of naloxone.

Asunto(s)

RESUMEN

The effect of naloxone on blood flow was studied in cats subjected to 400 gm-cm contusion injuries of the thoracic spinal cord. Ten cats were treated with 10 mg/kg naloxone 45 to 60 minutes after injury. Ten cats were given 10 mL of saline instead of naloxone, and 10 cats were neither injured nor treated. Hydrogen clearance was used to measure blood flow in the lateral white column at the contusion site. Naloxone, given intravenously, significantly improved the blood flow rates in the lateral column white matter. At 2 hours after injury, the mean blood flow in the saline-treated cats fell to 6.01+/-0.90 mL/100 gm/min, whereas it increased 8.47+/-1.14 mL/100gm/min in naloxone-treated cats (p<0.05). The authors conclude that naloxone may be useful for spinal cord injury.

Asunto(s)