Further studies of nimodipine in experimental spinal cord injury in the rat.

Previously in our laboratory, nimodipine was effective in reversing posttraumatic ischemia and promoting electrophysiologic recovery in a rat spinal cord injury (SCI) model. However, these beneficial effects were achieved when nimodipine was combined with adjuvant therapy to reverse posttraumatic hypotension, by either volume expansion or vasopressor therapy. The present experiments determined if nimodipine alone can increase spinal cord blood flow (SCBF) and improve function after SCI. The hydrogen clearance technique was used to measure SCBF, and motor and somatosensory evoked potentials (MEP and SSEP) were used to quantitate electrophysiologic function. SCBF, MEP, and SSEP were recorded before and after a 52 g clip compression injury at the T1 segment and then repeated after a 35 minute infusion of nimodipine. Twenty-five rats were allocated randomly to five equal groups, each of which received 35 minute infusions of one of the following doses of nimodipine: (1) 0 mg/kg, (2) 0.005 mg/kg, (3) 0.01 mg/kg, (4) 0.025 mg/kg, or (5) 0.05 mg/kg. SCBF decreased after injury in all groups, and there was no increase in SCBF after nimodipine infusion in any group. MEP and SSEP were abolished by the injury in all rats, and there was no recovery of the evoked potentials in any group. It is concluded that adjuvant therapy for posttraumatic hypotension may be necessary for nimodipine to improve SCBF and promote recovery of function in the injured spinal cord.     

Neuroprotective effect of magnesium on lipid peroxidation and axonal function after experimental spinal cord injury.

STUDY DESIGN: An experimental study examining the neuroprotective effect of magnesium on axonal function and lipid peroxidation in a rat model of acute traumatic spinal cord injury. OBJECTIVE: To determine the effectiveness of postinjury treatment with magnesium on evoked potentials and lipid peroxidation after spinal cord injury (SCI). SETTING: Pamukkale University, Denizli, Turkey. METHODS: Spinal cord injury occurred in 30 rats with an aneurysm clip at T9 and the rats were randomly assigned to undergo subcutaneous administration of one of the following at 1 h after injury: (1) Physiological saline (n = 10); (2) MgSO4, 300 mg/kg (n = 10) and (3) MgSO4, 600 mg/kg (n = 10). Spinal somatosensory evoked potentials (SSEPs) were recorded before injury, 30 min after injury and 3 h after injections. Rats were killed 24 h after the injury, and malondialdehyde (MDA) levels were measured. RESULTS: Following SCI, there were significant decreases in the amplitudes of P1 and N1 (P<0.001) and only high-dose magnesium improved the SSEPs (P<0.01). On the other hand, there was significant difference in lipid peroxide content between high-dose magnesium treated group and both of saline treated and low-dose magnesium treated groups (P<0.01). CONCLUSION: These results suggest that magnesium has a dose-dependent neuroprotective effect on SSEPs and lipid peroxidation after experimental spinal cord injury.     

The effect of nimodipine and dextran on axonal function and blood flow following experimental spinal cord injury

There is evidence that posttraumatic ischemia is important in the pathogenesis of acute spinal cord injury (SCI). In the present study spinal cord blood flow (SCBF), measured by the hydrogen clearance technique, and motor and somatosensory evoked potentials (MEP and SSEP) were recorded to evaluate whether the administration of nimodipine and dextran 40, alone or in combination, could increase posttraumatic SCBF and improve axonal function in the cord after acute SCI. Thirty rats received a 53-gm clip compression injury on the cord at T-1 and were then randomly and blindly allocated to one of six treatment groups (five rats in each). Each group was given an intravenous infusion of one of the following over 1 hour, commencing 1 hour after SCI: placebo and saline; placebo and dextran 40; nimodipine 0.02 mg/kg and saline; nimodipine 0.02 mg/kg and dextran 40; nimodipine 0.05 mg/kg and saline; and nimodipine 0.05 mg/kg and dextran 40. The preinjury physiological parameters, including the SCBF at T-1 (mean +/- standard error of the mean: 56.84 +/- 4.51 ml/100 gm/min), were not significantly different (p greater than 0.05) among the treatment groups. Following SCI, there was a significant decrease in the SCBF at T-1 (24.55 +/- 2.99 ml/100 gm/min; p less than 0.0001) as well as significant changes in the MEP recorded from the spinal cord (MEP-C) (p less than 0.0001), the MEP recorded from the sciatic nerve (MEP-N) (p less than 0.0001), and the SSEP (p less than 0.002). Only the combination of nimodipine 0.02 mg/kg and dextran 40 increased the SCBF at T-1 (43.69 +/- 6.09 ml/100 gm/min; p less than 0.003) and improved the MEP-C (p less than 0.0001), MEP-N (p less than 0.04), and SSEP (p less than 0.002) following SCI. With this combination, the changes in SCBF were significantly related to improvement in axonal function in the motor tracts (p less than 0.0001) and somatosensory tracts (p less than 0.0001) of the cord. This study provides quantitative evidence that an increase in posttraumatic SCBF can significantly improve the function of injured spinal cord axons, and strongly implicates posttraumatic ischemia in the pathogenesis of acute SCI.     

Failure of naloxone to improve spinal cord blood flow and cardiac output after spinal cord injury

It has been reported that the narcotic antagonist, naloxone, can improve spinal cord blood flow (SCBF) and clinical recovery after experimental spinal cord injury produced by the weight-dropping technique. The purpose of the present study was to determine the effect of naloxone on SCBF, cardiac output (CO) and blood flow to other organs following clip compression injury. Rats were anesthetized, paralyzed and ventilated, with mean systemic arterial pressure (MSAP) recorded continuously. After a C-7-T-1 laminectomy and a 1-minute acute compression injury with a 50-g clip at T-1, rats were given injections of radioactive microspheres for measurement of SCBF, CO, and blood flow to other organs. The first determination was made 15 minutes after injury and a second was made after a 1-hour treatment with naloxone. Treated animals each received an intravenous bolus injection of naloxone (10 mg/kg) followed by a 1-hour intravenous infusion (2 mg/kg/hour). Naloxone failed to improve posttraumatic SCBF in the injured spinal cord. In addition, naloxone did not prevent posttraumatic hypotension or the progressive decline in CO seen between 15 and 75 minutes after injury. Thus, this study does not support the previous claims of a beneficial effect of naloxone on posttraumatic SCBF and MSAP.     

Successful improvement of blood pressure, cardiac output, and spinal cord blood flow after experimental spinal cord injury

Thirty-seven rats were anesthetized and ventilated and had continuous monitoring of mean systemic arterial pressure (MSAP) and central venous pressure (CVP). The animals underwent a 60-g clip compression injury at T-1 for 1 minute. Fifteen minutes after injury, microspheres were used to measure cardiac output (CO) and spinal cord blood flow (SCBF). Each animal was then randomized into one of five groups. Four groups received intravenous infusions for 1 hour each of 5% albumin, autologous packed cells, low molecular weight dextran, or autologous whole blood to maintain the MSAP. The fifth group served as a control group and received an infusion of normal saline. Seventy-five minutes after injury, CO and SCBF were measured. The posttraumatic reduction in CO was significantly improved by all four treatment infusions. However, only autologous whole blood and dextran successfully reversed the posttraumatic hypotension. Dextran significantly elevated the CVP (P less than 0.01) and reduced the hematocrit (P less than 0.01). Whole blood improved SCBF in all segments of the spinal cord by nearly 100% (P less than 0.05), and dextran increased SCBF by 200% (P less than 0.01). Thus, the most marked improvements in MSAP, CO, and SCBF were produced by hypervolemia and hemodilution associated with dextran infusion. The therapeutic implications of this reversal of local and systemic changes in acute spinal cord injury are discussed.     

TRH对大鼠脊髓损伤后SCBF和SEP的影响

脊髓损伤（ＳＣＩ）后内源性阿片肽释放，并参与脊髓的继发损伤机制。ＴＲＨ可阻断阿片肽的自主神经效应，而不影响痛觉。本实验探讨大剂量ＴＲＨ（２ｍｇ／ｋｇ／ｈ）治疗对大鼠脊髓打击伤（Ａｌｌｅｎｓ法１０ｇｘ５ｃｍ）后脊髓血流量（ＳＣＢＦ）和脊髓诱发电位（ＳＥＰ）的影响。脊髓损伤后１ｈ，ＳＣＢＦ开始显著下降，持续至伤后２４ｈ，ＳＥＰ峰潜时呈进行性延长趋势；伤后即刻静脉注射ＴＲＨ（２ｍｇ／ｋｇ／ｈ，共５次），可使伤后即刻和２４ｈ的ＳＣＢＦ显著升高，并使伤后ＳＣＢＦ下降时间延迟３ｈ，同时ＳＥＰ峰潜时有不同程度改善。结果表明，ＴＲＨ对受伤脊髓早期有一定的防治作用，并具有一定的后发效应；同时也可促进脊髓的神经传导功能。本文亦对ＴＲＨ治疗ＳＣＩ的病理生物学机制进行了讨论。     

Effect of a calcium channel blocker on posttraumatic spinal cord blood flow

The normal rat spinal cord blood flow (SCBF) has been shown to increase after administration of nimodipine, a calcium channel blocker. The present study investigates the capability of nimodipine to improve SCBF, as measured by the hydrogen clearance technique, after a 53.0-gm clip compression injury to the T-1 segment of the rat spinal cord. The profound drop in mean systemic arterial blood pressure (MSAP) after cervical cord injury precluded any improvement in posttraumatic SCBF by nimodipine alone. Hence, in a randomized controlled study with five rats per group, pressor agents (whole blood, angiotensin, or adrenaline) were infused to maintain MSAP between 100 and 120 mm Hg after injury. Control animals received only a saline infusion. Nimodipine at the optimal dose found in normal animals (1.5 microgram/kg/min) was added to the pressor agents. The MSAP and other physiological parameters were measured in rats receiving the pressor agents only and in those receiving pressor agents combined with nimodipine. In rats receiving whole blood, angiotensin, or adrenaline the posttraumatic MSAP improved to between 100 and 120 mm Hg, but there was no improvement in SCBF compared to the saline group. The addition of nimodipine decreased MSAP and SCBF in all groups except those animals also receiving adrenaline, where the MSAP was maintained at 109 +/- 5 mm Hg. In these animals a significant increase in posttraumatic SCBF from 16.5 +/- 2.1 to 20.2 +/- 2.3 ml/100 gm/min (mean +/- standard error of the mean) occurred at the site of injury with the addition of nimodipine. The maintenance of an adequate MSAP by a pressor agent was crucial for nimodipine to improve posttraumatic SCBF by its ability to dilate the spinal vascular bed. Adrenaline was the only pressor agent that could fulfill the above criteria, although other pressor agents need to be investigated. Experiments are underway with the combination of adrenaline and nimodipine to further verify these encouraging results demonstrating an improvement in posttraumatic ischemia of the spinal cord.     

钙调素拮抗剂对大鼠脊髓损伤的作用及意义

目的观察钙调素（ＣａＭ）特异性拮抗剂三氟啦嗪（ＴＦＰ）对脊髓损伤（ＳＣＩ）的影响,探讨ＣａＭ在ＳＣＩ病理机制中的作用。方法采用氢清除法、斜板试验和电生理技术,以６４只大鼠为实验对象观察ＴＦＰ对ＳＣＩ后脊髓血流量（ＳＣＢＦ）、运动功能和诱发电位（ＭＥＰ）的影响。结果在肾上腺素维持系统动脉压的条件下,ＴＦＰ可明显改善ＳＣＩ后ＳＣＢＦ、ＭＥＰ和运动功能。结论ＣａＭ拮抗剂对ＳＣＩ具有保护作用,ＣａＭ可能是参与ＳＣＩ病理机制的重要因素     

脊髓纵向压缩过程中脊髓诱发电位,血流量和微循环变化

根据临床上脊往后凸畸形矫正过程中，脊柱截骨缩短后的脊髓受力情况，采用脊柱立体定位仪来调节脊髓的压缩量，设计了大鼠脊髓纵向压缩动物模型，模拟脊往后凸畸形矫正的病理变化．使用末梢循环血流仪（氢清除法）、奥林巴氏生物显微镜及显示系统、 ＳＥＮ３２０１刺激器、 ＡＰＰＬＥⅡ机诱发电位检测系统（硬膜外记录），分别观测了脊髓压缩部位及邻近节段不同压缩量脊髓灰白质血流量、动态微循环、运动诱发电位（ＭＥＰ）、感觉诱发电位（ＳＥＰ），并常规光镜检查．结果表明；大鼠脊髓不可逆性压缩的临界值为６．０ｍｍ，脊髓回缩率为１／２６— ｌ／２３；脊髓监护时ＭＥＰ较ＳＥＰ更敏感地反映脊髓功能，是较理想的监护手段；脊髓压缩过程中主要为瘀血性缺血改变，与目前脊髓牵拉压迫过程中报道的变化有所不同。     

The long-term effects of pre-treatment with activated protein C in a rat model of compression-induced spinal cord injury

OBJECTIVES: Recently, we demonstrated that activated protein C (APC) can lessen the severity of spinal cord injury (SCI) in rats during the acute and subacute phases. The purpose of the present study is to determine the long-term effects of pre-treatment with APC following SCI in rats. METHODS: The motor function of rats was assessed using the inclined-plane test during 8 weeks after SCI, and the grid runway test 7 weeks after the trauma. Somatosensory evoked potentials (SEPs), brainstem-derived motor evoked potentials (B-MEPs) and corticomotor evoked potentials (CMEPs) were used to quantify axonal function 8 weeks after SCI. Morphometric analysis of the spinal cord lesion was carried out to determine lesion size. Twelve male Sprague-Dawley rats were randomly allocated to either APC (25 IU/kg) or saline group and then subjected to 20 g compression injury of the spinal cord for 20 min at T12. The sham group (n=6) received laminectomy alone. RESULTS: APC significantly reduced the motor disturbances and electrophysiological impairments induced by SCI. APC-treated animals also showed a trend towards a reduction in lesion size. However, this change, was not significant. CONCLUSION: Pre-treatment with APC attenuates the harmful effects of SCI not only during the acute and subacute phases but also in the chronic stage.     

胚胎脊髓移植联合应用MK-801促进大鼠脊髓损伤后功能恢复

目的　研究胚胎脊髓移植并应用N 甲基 D 天门冬氨酸 (NMDA)受体拮抗剂MK 80 1能否促进半切洞脊髓损伤后功能恢复。方法　将成年大鼠分为 3组 ,A组 :单纯脊髓半切洞损伤组 ;B组 :脊髓半切洞损伤 胚胎脊髓移植组 ;C组 :脊髓半切洞损伤 胚胎脊髓移植 MK 80 1组。手术后应用联合行为评分 (CBS)、感觉诱发电位 (SEP)、运动诱发电位 (MEP)检查。结果　 3组CBS得分A组>B组 >C组 ,SEP和MEP潜峰时A组 >B组 >C组 ,统计学分析差异有显著性 (P <0 0 5 )。结论　胚胎脊髓移植联合应用NMDA受体拮抗剂MK 80 1能够促进脊髓损伤后功能恢复     

Anti-apoptotic effect of insulin in the control of cell death and neurologic deficit after acute spinal cord injury in rats

Recent studies confirmed that the new cell survival signal pathway of Insulin-PI3K-Akt exerted cyto-protective actions involving anti-apoptosis. This study was undertaken to investigate the potential neuroprotective effects of insulin in the pathogenesis of spinal cord injury (SCI) and evaluate its therapeutic effects in adult rats. SCI was produced by extradural compression using modified Allen's stall with damage energy of 40 g-cm force. One group of rats was subjected to SCI in combination with the administration of recombinant human insulin dissolved in 50% glucose solution at the dose of 1 IU/kg day, for 7 days. At the same time, another group of rats was subjected to SCI in combination with the administration of an equal volume of sterile saline solution. Functional recovery was evaluated using open-field walking, inclined plane tests, and motor evoked potentials (MEPs) during the first 14 days post-trauma. Levels of protein for B-cell lymphoma/leukemia-2 gene (Bcl-2), Caspase-3, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) were quantified in the injured spinal cord by Western blot analysis. Neuronal apoptosis was detected by TUNEL, and spinal cord blood flow (SCBF) was measured by laser-Doppler flowmetry (LDF). Ultimately, the data established the effectiveness of insulin treatment in improving neurologic recovery, increasing the expression of anti-apoptotic bcl-2 proteins, inhibiting caspase-3 expression decreasing neuronal apoptosis, reducing the expression of proinflammatory cytokines iNOS and COX-2, and ameliorating microcirculation of injured spinal cord after moderate contusive SCI in rats. In sum, this study reported the beneficial effects of insulin in the treatment of SCI, with the suggestion that insulin should be considered as a potential therapeutic agent.     

Effect of epidural lidocaine on spinal cord blood flow

The effect of epidural lidocaine on spinal cord blood flow (SCBF) was measured in mongrel dogs. Spinal evoked potentials were used to measure spinal cord conduction and enabled us to time the measurement of SCBF associated with maximum reduction in latency and amplitude of spinal evoked potentials produced by instillation of 5 ml of 2% lidocaine in the epidural space. We used the radioactive microsphere technique to quantitate SCBF in the cervical, upper thoracic, lower thoracic, and lumbar regions of the spinal cord. A narcotic/relaxant technique was used to eliminate SCBF changes associated with other anesthetic agents. Other parameters known to affect SCBF were kept constant and within normal physiologic values. As compared with saline solution controls, there were significant decreases in SCBF in all the four areas of spinal cord in animals given epidural lidocaine, most marked in the lumbar area.     

Methylprednisolone in spinal cord compression

In acute nonsurvival studies, eight anesthetized lambs were subjected to cord compression at T13 by means of an epidural balloon distended to a pressure of 200 mm Hg for 40 minutes. Subsequent to withdrawal of the balloon, each animal received 30 mg/kg of methylprednisolone succinate in an intravenous bolus followed by a continuous infusion of 10 mg/kg/hr for the duration of the experiment. Spinal cord blood flow (SCBF) and spinal evoked potential (SEP) determinations were obtained sequentially prior to, during, and at 1/2, 1 1/2, and 2 1/2 hours following compression. In spite of the absence of ischemia following compression, SEPs failed to recover. Methylprednisolone had no apparent effect on blood flow or on the recovery of SEPs when compared with results in ten control animals that received saline alone.     

Sustained spinal cord compression: part II: effect of methylprednisolone on regional blood flow and recovery of somatosensory evoked potentials

BACKGROUND: The efficacy of methylprednisolone in the treatment of traumatic spinal cord injury is controversial. We examined the effect of methylprednisolone on regional spinal cord blood flow and attempted to determine whether recovery of electrophysiological function is dependent on reperfusion, either during sustained spinal cord compression or after decompression. METHODS: The effects of methylprednisolone therapy on recovery of somatosensory evoked potentials and on spinal cord blood flow were examined in a canine model of dynamic spinal cord compression. Methylprednisolone (30 mg/kg intravenous loading dose followed by 5.4 mg/kg/hr intravenous infusion) or saline solution was administered to thirty-six beagles (eighteen in each group) five minutes after cessation of dynamic spinal cord compression and loss of all somatosensory evoked potentials. After ninety minutes of sustained compression, the spinal cords were decompressed. Somatosensory evoked potentials and spinal cord blood flow were evaluated throughout the period of sustained compression and for three hours after decompression. RESULTS: Seven dogs treated with methylprednisolone and none treated with saline solution recovered measurable somatosensory evoked potentials during sustained compression. After decompression, three more dogs treated with methylprednisolone and seven dogs treated with saline solution recovered somatosensory evoked potentials. Four dogs treated with methylprednisolone lost their previously measurable somatosensory evoked potentials. In the methylprednisolone group, spinal cord blood flow was significantly higher (p < 0.05) in the dogs that had recovered somatosensory evoked potentials than it was in the dogs that had not. Reperfusion blood flow was significantly higher (p < 0.05) in the saline-solution group than it was in the methylprednisolone group. Spinal cord blood flow in the saline-solution group returned to baseline levels within five minutes after decompression. It did not return to baseline levels in the dogs treated with methylprednisolone. CONCLUSIONS: The methylprednisolone administered in this study did not provide a large or significant lasting benefit with regard to neurological preservation or restoration. Methylprednisolone may reduce regional spinal cord blood flow through mechanisms affecting normal autoregulatory blood-flow function.     

一氧化氮合成酶抑制剂对大鼠损伤脊髓血流及功能的影响

通过Nystrom脊髓后路压迫模型（35．0g／10min）造成脊髓中度损伤，应用激光多普勒血流仪观测了大鼠伤前30min，蛛网膜下腔注射生理盐水及亚硝基左旋精氨酸甲酯（L－NAME）0．15mg、1．5mg三组动物伤后局部脊髓血流的动态变化，并评定了伤后4周神经功能恢复情况。结果发现，L－NAME0.15mg短时间内抑制了脊髓血流，而L－NAME1．5mg较长时间抑制了脊髓血流。4周后L－NAME0．15mg组脊髓功能优于盐水组，而L－NAME1．5mg组脊髓功能较盐水组差。结果提示，适量的L－NAME由于短时间限制了一氧化氮（NO）的释放，有利于神经功能恢复；大剂量的L－NAME由于持续抑制了NO释放而致脊髓损伤加重。     

Methylprednisolone inhibits production of interleukin-1beta and interleukin-6 in the spinal cord following compression injury in rats

Interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) are major inflammatory cytokines produced after spinal cord injury (SCI). This study sought to evaluate the effects of methylprednisolone (MP) on IL-1beta and IL-6 protein in spinal cord tissue following SCI. Halothane-anesthetized, female Sprague-Dawley rats weighing (280-320 g) underwent laminectomy at T7-T8. No lesions were produced in animals in the saline control and MP control groups. SCI was induced by temporary placement of an aneurysm clip at T7-T8, with a closing pressure of 55 g at the spinal level of T7-T8, resulting in spinal cord compression for one minute. Animals with SCI were treated with MP (30 mg/kg sc) or an equal volume of saline. IL-1beta and IL-6 spinal cord protein were measured by enzyme-linked immunosorbent assays (ELISA). Data were summarized as mean +/- SD and compared by two-way analysis of variance (ANOVA). IL-1beta and IL-6 levels were elevated in the SCI + Saline animals (P < 0.01) compared with saline control, MP control, and SCI + MP-treated animals. The rise in IL-1beta and IL-6 levels after SCI was blunted after administration of MP, suggesting an interaction between glucocorticosteroids and the cytokine cascade after spinal cord trauma. Further evaluation of the effects of MP on the cytokine cascade may be important in assessing whether or not the anti-inflammatory effects of glucocorticosteroids confer neuroprotection after SCI.     

Corticomotor and somatosensory evoked potential evaluation of acute spinal cord injury in the rat

Somatosensory evoked potentials (SSEPs) and corticomotor evoked potentials (CMEPs) were utilized to study acute blunt spinal cord trauma. Rats, anesthetized with ketamine hydrochloride, were subjected to a parasagittal craniotomy and a midthoracic laminectomy. SSEPs were cortically recorded and CMEPs were transcortically produced using epidural ball and disc electrodes. SSEPs were elicited and CMEPs were recorded via hindlimb percutaneous needle electrodes. After control records were made, animals were subjected to a 25-, 50-, or 75-g/cm impact to the dorsal cord surface via a modified weight drop procedure. Evaluation of neurological injury was made by SSEP and CMEP analysis as well as by physical testing with noxious stimulation applied to the hindlimb. Neurohistopathological verification of each spinal cord lesion was performed. No significant change in SSEP configuration was identified in animals subjected to a 25-g/cm cord impact; however, a small decrement in CMEP amplitude was consistently observed. Although vocalization to noxious stimulation was present, flexion activity was less than normal. Animals subjected to a 50-g/cm cord impact also showed no change in SSEP wave forms. All components of the CMEP were greatly attenuated with this injury. Either very weak movement or no movement to noxious stimulation was present without vocalization. After a 75-g/cm cord impact, both SSEPs and CMEPs were abolished. There was no movement or vocalization in response to noxious stimulation. Serial sections of the spinal cords revealed incremental destruction with increasing severity of injury. These results support the hypothesis that CMEPs are a more sensitive indicator of residual spinal cord function after injury than are SSEPs.     

内皮素受体拮抗剂对损伤脊髓早期保护作用

目的评价非选择性内皮素(ET)受体拮抗剂PD145065对损伤脊髓的保护作用,证实ET参与脊髓损伤(SCI)后继发损伤的假设并探讨其作用机制。方法压迫法致伤大鼠脊髓(50g,1min)。损伤前10min鞘内注射PD145065或生理盐水,观察脊髓血流(SCBF)、丙二醛(MDA)、细胞内钙(［Ca2+］i)、伊文思兰(EB)及水含量变化。结果伤区SCBF在伤后5min即有明显下降,为基线的(75.23±9.21)%,2h降为(57.06±7.35)%;伤区邻近血流下降较慢,伤后30min降为(79.82±7.98)%。伤区及邻近区伤后4h?SCBF都未恢复。伤段脊髓组织中MDA、［Ca2+］i、EB和水含量均高于假手术组(P＜0.05)。PD145065明显改善了伤区SCBF,消除了伤区邻近段SCBF的下降。PD145065预处理组脊髓中MDA、［Ca2+］i、EB和水含量均低于生理盐水组(P＜0.05)。结论PD145065对损伤脊髓早期有明显保护作用,ET及其受体可能通过多种途径参与SCI后的继发损伤。临床应用ET受体拮抗剂对SCI可能有治疗作用。     

脊髓损伤后早期减压对诱发电位影响的实验研究

[目的]观察脊髓损伤后早期减压对体感诱发电位及经颅磁刺激运动诱发电位的影响，以探讨诱发电位在判断手术时机及预后中的应用价值。[方法]日本大耳兔32只随机分4组。A组为对照组，不造成脊髓损伤。B、C、D组为脊髓损伤组。对每组动物于不同时间分别检测SEP、MEP。分析波形的潜伏期、峰问波幅。用后肢的Tarlov分级法作伤后运动功能评分。取脊髓标本，行组织学观察。[结果]随着脊髓压迫时间的延长，SEP、MEP的潜伏期逐渐延长，波幅逐渐减小．波幅变化较潜伏期更为敏感。在恢复过程中，脊髓受压时间越短，诱发电位恢复越早。潜伏期恢复早于波幅，而且SEP恢复早于MEP，MEP的恢复早于功能评分。[结论]SEP与TMS-MEP对脊髓损伤十分敏感，能较早反映脊髓损伤程度，可用于指导临床手术治疗和判断预后。