Effects of methylprednisolone and dextromethorphan on lipid peroxidation in an experimental model of spinal cord injury

Objective. This study examines the effects of agents purported to improve recovery following spinal cord trauma, methylprednisolone sodium succinate, dextromethorphan, and the combination of both, on the post-traumatic alterations of membrane lipid metabolism. Methods. After sparing ten rats for a control group (G1) and performing T3–T6 laminectomies in 150 rats, spinal cord injuries were accomplished in 120 of 150 Wistar rats with an aneurysmal clip compression at the level of T4-5 for 30 sec. Hence the G2 group (n 30) included the "only laminectomy/sham" group. The 120 injured animals were subdivided into four equal groups (n 30 each). Group G3 underwent no therapy, G4 methylprednisolone (MP), G5 dextromethorphan (DM), and G6 MP+DM therapies. Groups G2–G6 were killed ten by ten at 10 min, 30 min, and 120 min after the operation. We measured tissue (MDA) and blood malonyldialdehyde (MDAb), (a product of lipid peroxidation) levels as an indicator of oxidative damage by thiobarbituric acid method and activity levels of antioxidant enzymes superoxide dismutase and glutathione peroxidase in erythrocytes. Intergroup and intragroup results were compared statistically. Results. Methylprednisolone was able to keep the levels for all parameters close to baseline except for 30-min MDA, MDA_b, and SOD values. But their results were all different from those of G3. Dextromethorphan was successful in this respect at 30-min GSH-Px and 120-min SOD and GSH-Px, and all values were also different from G3 values except for 10-min MDA, SOD, and GSH-Px. Combined therapy was not able to keep levels close to baseline for all parameters, but they were different from G3's except for the GSH-Px values. Methylprednisolone values displayed minimal alterations according to baseline at 120 min. Dextromethorphan was relatively unsuccessful at 10 min. Combined therapy did not show benefit superior to MP/DM single therapies. Electronic Publication     

Changes of free iron contents and its correlation with lipid peroxidation after experimental spinal cord injury

Objective: To observe the dynamic changes of free iron contents and its relationship to the changes of lipid peroxidation after experimental spinal cord injury (SCI). Methods: Sprague Dawley rats were randomly divided into three groups: Group A (n=6) received no operation; Group B (n=48) received only laminectomy (sham) ; and Group C (n=48) received both laminectomy and traumatic injury ( SCI model). The SCI animal models were made by using an modified Alien‘s weight-drop device (50 g. cm) on T12. Rats were sacrificed at 0.5, 1, 3, 6, 12, 24 hours after injury. The levels of free iron involved in spinal cord segments at different time points were measured by blcomycin assay. The malondialdehyde (MDA) was also measured by the thiobarbituric acid (TBA). Results: After SCI in Group C, the level of free iron showed a significant increase at 0.5 hour compared to Groups B and A, restored to the control level at 6 h; the level of MDA was increased at 0.5 hour, peaked at 3 hours, returned to the control level at 12 hours; the concentrations of free iron and lipid peroxidation in injured rats were significantly and positively correlated at 0.5-3 hours. Conclusions: After SCI the levels of free iron are increased quickly and might be a major contributor to lipid peroxidation in injured spinal cord.     

Acute phase effects of ATP-MgCl<Subscript>2</Subscript> on experimental spinal cord injury

The purpose of this study was to study the acute phase effects of adenosine triphosphate (ATP)-MgCl₂ on experimental spinal cord clip compression injury. Spinal cord clip compression injury was performed on 36 albino Wistar rats. The rats were divided into five groups. T4–T8 total laminectomy was performed on all rats. Group 1: sham-operated group. Group 2: clip compression group. In group 3, ATP-MgCl₂ (100 μmol/kg) was given 2 min before the "clip compression injury." In group 4, ATP-MgCl₂ (100 μmol/kg) was given 5 min after the clip compression injury. In group 5, ATP MgC1₂ (100 μmol/kg) was administered 8 h after the injury. The spinal cords were excised for a length of 2 cm and deep frozen at –76°C. Tissue malondialdehyde (MDA) levels were used to determine the effects of ATP-MgCl₂ on spinal cord lipid peroxidation. In the groups in which ATP MgCl₂ was administered after the clip compression injury (groups 4 and 5), the decrease in spinal cord MDA levels was statistically significant when compared with those of the injury group (group 2). Although MDA levels of group 4 were lower than those of group 5, this difference was not statistically significant. Administration of the ATP-MgCl₂ before the clip compression injury (in group 3) did not have a statistically significant effect on lipid peroxidation when compared with the injury group (group 2). In this study, we found that ATP-MgCl₂ has decreased lipid peroxidation in spinal cord injury and protected the spinal cord from secondary injury after the trauma. We concluded that ATP-MgCl₂ may be used in the treatment of spinal cord injuries in conjunction with the other treatment modalities, but further investigations are mandatory. Electronic Publication     

Antioxidation of quercetin against spinal cord injury in rats

Objective : To observe the effect of quercetin on experimental spinal cord injury (SCI) in rats. Methods: Sixty Sprague-Dawley rats were randomly divided into four groups : Group A only for laminectomy, Group B for laminectomy with SCI, Group C for SCI and intraperitoneal injection with a bolus of 200 mg/kg quercetin and Group D for SCI and intraperitoneal injection of saline. SCI model was made by using modified Aliens method on T12. Six rats of each group were killed at 4 h after injury and the levels of free iron and malondialdehyde ( MDA) of the involved spinal cord segments were measured by bleomycin and thiobarbituric acid (TBA) assays separately. The recovery of hind limb function was assessed by Modified Tarlov 's scale and inclined plane method at 7 d,14 d and 21 d after SCI. The histological changes of the damaged spinal cord were also examined at 7 d after SCI. Results: After SCI, the levels of free iron and MDA were significantly increased in Groups B and D, while not in Group C. The Modified Tarlov 's score and the inclined plane angles were significantly decreased in Groups B, C and D. The histological findings were not improved. Conclusions: After SCI, quercetin can reduce the level of lipid peroxidation, but not improve recovery of function.     

Effect of combined treatment with melatonin and methylprednisolone on neurological recovery after experimental spinal cord injury

Spinal cord injury (SCI) results in the loss of function below the lesion. Secondary injury following the primary impact includes a number of biochemical and cellular alterations leading to tissue necrosis and cell death. Methylprednisolone (MP), by reducing edema and protecting the cell membrane against peroxidation, is the only pharmacological agent with a proven clinically beneficial effect on SCI. Melatonin, known as a free radical scavenger, has been shown to have an effect on lipid peroxidation following experimental SCI. The purpose of this study was to examine the effect of MP and melatonin on neurological, ultrastructural, and electrophysiological recovery. Female albino rats weighing 200–250 g were randomized into five groups of 18 rats each and six rats for the control group. Weight-drop trauma was performed for each group and a 30-mg/kg single dose of MP for rats in group 1, a 10-mg/kg single dose of melatonin for rats in group 2, and MP and melatonin in the same doses for rats in group 3 were administered immediately after trauma. The rats in group 4 were the vehicle group (treated with ethanol) and group 5 was the trauma group. The motor and somatosensory evoked potentials were recorded at the 4th hour, the 24th hour, and on the 10th day of the study for six rats in each group. Posttraumatic neurological recovery was recorded for 10 days using motor function score and inclined plane test. After electrophysiological study the rats were terminated for an analysis of lipid peroxidation level of the injured site of the spinal cord. Electron microscopic studies were performed to determine the effects of melatonin, MP, and the combined treatment with MP and melatonin on axons, neurons, myelin, nucleus, and intracytoplasmic edema. The groups treated with MP, melatonin, and a combination of both had significantly enhanced electrophysiological, biochemical, and neurological recovery and also showed better ultrastructural findings than the trauma and vehicle groups. Although combined treatment was significantly more effective on lipid peroxidation than melatonin or MP treatments alone, at the 10th day, neurobehavioral, electrophysiological, and ultrastructural recovery were at the same level. In conclusion, MP, melatonin, and MP and melatonin combined treatment modalities improved functional recovery at the same level. Future studies involving different doses of melatonin and different dose combinations with MP could promise better results since each drug has a different anti-oxidative mechanism of action.Electronic Supplementary Material Supplementary material is available in the online version of this article at The number of references, figures of waveforms obtained from CSEP and MEP tests, and electron micrographs of the samples obtained from trauma and all treatment groups at the 10th day postinjury have been reduced in the printed version. The complete version of the article will be published in the web version of the Journal     

缺血后处理对兔脊髓缺血-再灌注损伤的保护作用

目的研究缺血后处理是否可以减轻兔脊髓缺血再灌注的损伤。方法雄性新西兰大白兔30只,随机分为五组,每组6只。假手术组(N1组)仅行单纯手术操作但不阻闭腹主动脉;对照组(N2组)行单纯缺血再灌注;缺血后处理15s/30s/60s(PA/PB/PC组)分别于阻闭腹主动脉15min后,再灌注15s/30s/60s,缺血15s/30s/60s,反复3次。再灌注48h时对所有动物的后肢运动功能进行评分并行脊髓前角正常神经元计数。结果PB组再灌注48h后肢运动功能评分[3.5(2～4)分],明显高于N2组[2(1～3)分](P<0.05),其他各组与N2组相比差异无显著意义。脊髓前角正常神经元计数PB组为36.7±7.0,明显多于N2组25.7±4.3(P<0.01),而PA组18.2±2.2和PC组8.0±4.1则明显少于N2组(P<0.05)。结论缺血后处理对兔脊髓缺血再灌注损伤的作用取决于后处理时间,缺血后处理30s/30s对脊髓缺血再灌注损伤具有保护作用,而缺血后处理15s/15s和60s/60s会加重脊髓损伤。     

Dantrolene can reduce secondary damage after spinal cord injury

The aim of this experimental study was to investigate the possible protective effects of dantrolene on traumatic spinal cord injury (SCI). Twenty-four New Zealand rabbits were divided into three groups: Sham (no drug or operation, n = 8), Control (SCI + 1 mL saline intraperitoneally (i.p.), n = 8), and DNT (SCI + 10 mg/kg dantrolene in 1 mL, i.p., n = 8). Laminectomy was performed at T10 and balloon catheter was applied extradurally. Four and 24 h after surgery, rabbits were evaluated according to the Tarlov scoring system. Blood, cerebrospinal fluid and tissue sample from spinal cord were taken for measurements of antioxidant status or detection of apoptosis. After 4 h SCI, all animals in control or DNT-treated groups became paraparesic. Significant improvement was observed in DNT-treated group, 24 h after SCI, with respect to control. Traumatic SCI led to an increase in the lipid peroxidation and a decrease in enzymic or non-enzymic endogenous antioxidative defense systems, and increase in apoptotic cell numbers. DNT treatment prevented lipid peroxidation and augmented endogenous enzymic or non-enzymic antioxidative defense systems. Again, DNT treatment significantly decreased the apoptotic cell number induced by SCI. In conclusion, experimental results observed in this study suggest that treatment with dantrolene possess potential benefits for traumatic SCI.     

The effect of duration of compression on lipid peroxidation after experimental spinal cord injury

The present study was performed to evaluate the effect of duration of acute spinal cord compression on tissue lipid peroxidation in rats. A clip compression method (1) was used to produce acute spinal cord injury. Rats were divided into 3 groups, each consisting of 10. At 1 hour after trauma all rats were sacrificed, and MDA content of the injured spinal cord segment was measured. The tissue MDA contents were 3.922 μmolMDA/gww in group 1 (control), 10.192 μmol MDA/gww in group 2 (30 seconds compression), and 12.147 μmolMDA/gww in group 3 (60 seconds compression). These results demonstrate that the length of duration of compression significantly enhances lipid peroxidation. Our study supported the view that persisting compression may cause progression of secondary mechanisms which may irreversibly eliminate any potential for recovery.     

高氧液预处理对兔脊髓缺血-再灌注损伤的保护作用

目的　探讨高氧液预处理对兔脊髓缺血 再灌注损伤的作用。方法　 2 0只成年雄性新西兰大白兔随机分成对照组 (n =1 0 )及预处理组 (n =1 0 )。预处理组每天静脉给予 1 0ml/kg高氧液 ,2 0分钟匀速泵完 ,连续 5天 ;对照组用同样方法给予等容量生理盐水。最后一次预处理结束后2 4小时 ,夹闭腹主动脉肾下段 2 0分钟 ,制作兔脊髓缺血模型 ;再灌注后 4、8、1 2、2 4和 48小时分别对动物神经功能评分 ;再灌注 48小时后 ,处死动物取脊髓 (L5～ 7) ,制作标本行组织病理学观察。结果　预处理组神经功能评分在各时间点均明显高于对照组 (P <0 0 5) ;与对照组相比 ,预处理组脊髓前角正常神经细胞数明显增多 (P <0 0 5) ,而且神经功能评分与其对应脊髓前角正常神经细胞计数之间有显著相关性 (r=0 894,P <0 0 1 )。结论　高氧液预处理对兔脊髓缺血 再灌注损伤有显著的保护作用。     

蝮蛇抗栓酶对脊髓损伤影响的实验研究

就蝮蛇抗栓酶对大鼠脊髓损伤时脂质过氧化物、超氧化物歧化酶及组织形态学的影响作了研究。结果表明：蝮蛇抗栓酶治疗组脊髓组织和血浆中脂质过氧化物（ＬＰＯ）含量较对照组低，其脊髓组织和红细胞的超氧化物歧化酶（ＳＯＤ）活性较对照组高，光镜和电镜检查均显示治疗组大鼠的脊髓损伤比对照组轻，脊髓神经功能恢复情况亦优于对照组。表明蝮蛇抗栓酶对大鼠脊髓损伤的影响与其抗氧自由基作用有关。     

Effect of norepinephrine on spinal cord blood flow and parenchymal hemorrhage size in acute-phase experimental spinal cord injury

Purpose

In the acute phase of spinal cord injury (SCI), ischemia and parenchymal hemorrhage are believed to worsen the primary lesions induced by mechanical trauma. To minimize ischemia, keeping the mean arterial blood pressure above 85 mmHg for at least 1 week is recommended, and norepinephrine is frequently administered to achieve this goal. However, no experimental study has assessed the effect of norepinephrine on spinal cord blood flow (SCBF) and parenchymal hemorrhage size. We have assessed the effect of norepinephrine on SCBF and parenchymal hemorrhage size within the first hour after experimental SCI.

Methods

A total of 38 animals were included in four groups according to whether SCI was induced and norepinephrine injected. SCI was induced at level Th10 by dropping a 10-g weight from a height of 10 cm. Each experiment lasted 60 min. Norepinephrine was started 15 min after the trauma. SCBF was measured in the ischemic penumbra zone surrounding the trauma epicenter using contrast-enhanced ultrasonography. Hemorrhage size was measured repeatedly on parasagittal B-mode ultrasonography slices.

Results

SCI was associated with significant decreases in SCBF (P = 0.0002). Norepinephrine infusion did not significantly modify SCBF. Parenchymal hemorrhage size was significantly greater in the animals given norepinephrine (P = 0.0002).

Conclusion

In the rat, after a severe SCI at the Th10 level, injection of norepinephrine 15 min after SCI does not modify SCBF and increases the size of the parenchymal hemorrhage.     

氢饱和生理盐水对兔脊髓缺血再灌注损伤的神经保护作用

目的 研究氢气对脊髓缺血再灌注损伤的保护作用及其潜在机制。方法 新西兰兔随机分为3组：对照组、脊髓缺血再灌注损伤组和氢水治疗组。对照组仅接受暴露,无脊髓缺血再灌注损伤;缺血再灌注组动物采用ZIVIN法建立脊髓缺血再灌注损伤模型,造成脊髓腰骶段缺血35 min 后行再灌注;氢水治疗组动物在再灌注前5 min腹腔注射饱和氢盐水（5 mL/kg）,再灌注后8 h重复注射。不同时间点检测后肢运动功能。术后72 h取脊髓进行HE染色、TUNEL染色、氧化-抗氧化指标检测及ELISA检测细胞因子。结果 含氢生理盐水治疗能显著改善动物神经功能、抑制脊髓神经元凋亡、抑制氧化应激、改善抗氧化能力,同时降低炎症相关细胞因子,从而发挥脊髓保护作用。结论 腹腔注射含氢生理盐水通过抗氧化和抗炎对脊髓缺血再灌注损伤发挥保护作用。     

Effect of naloxone on functional recovery after experimental spinal cord injury in the rat

The effect of the opiate antagonist naloxone on the functional recovery of rats injured with a 10 g-cm impact to the spinal cord at the T-3 level is studied. Sixteen rats were treated with 0.8 mg of naloxone in an intraperitoneal bolus 45 and 120 minutes after injury, 16 rats were given 4 mL of saline instead of naloxone, and 16 rats were neither injured nor treated. To asses weekly the motor recovery of the injured animals, the inclined plane method was employed. After the 10-week assessment period, naloxone-treated animals showed a significantly better performance on the inclined plane than saline-treated animals. Naloxone may be useful for the treatment of spinal cord injury although its mechanism of action remains unknown.     

促甲状腺素分泌激素对实验性脊髓损伤的治疗

为研究促甲状腺素分泌激素（TRH）对脊髓损伤的早期及晚期治疗效果，将24只猫分为4组，伤后1h治疗组、伤后24h治疗组、伤后48h治疗组及对照组。用改良Allen’s打击法致伤L1部，治疗组用Zmg/kgTRH冲击剂量及1mg／ks／h持续量（4h）治疗，观察动物神经功能情况，定期检测MEP、SEP和形态学的量化分析。结果显示，虽然四组之间形态学无明显差异，但治疗组神经功能及MEP明显优于对照组。     

钙蛋白酶抑制剂对缺血再灌注损伤脊髓的保护作用

目的 观察大鼠脊髓缺血再灌注损伤后应用钙蛋白酶特异性抑制剂E-64-D,对脊髓神经细胞组织学改变和凋亡的影响及对大鼠后肢运动功能的保护作用.方法 选用纯种雄性成年SD大鼠106只,夹闭右肾动脉分支下腹主动脉30 min,再灌注即刻静脉应用钙蛋白酶特异性抑制剂E-64-D,观察再灌注后3、24、72 h和7 d脊髓损伤节段神经细胞的凋亡及再灌注后24、72h组织病理学改变;对再灌注后72 h的大鼠后肢功能进行评分.结果 脊髓缺血再灌注24 h开始出现神经细胞凋亡现象,脊髓组织出现病理学改变,神经元死亡,胶质细胞增生.应用E-64-D后,凋亡现象和细胞坏死得到抑制,差异有统计学意义(P<0.01).再灌注后72 h后肢功能也得到一定程度的保护.结论 脊髓再灌注损伤后静脉应用E-64-D治疗,可以明显抑制脊髓神经细胞的凋亡,有利于神经元的存活,损伤后3 d大鼠后肢运动功能得到一定程度的改善.     

羟乙基淀粉行急性等容血液稀释对兔脊髓缺血-再灌注损伤的保护作用

目的 探讨用羟乙基淀粉(HES130/0.4)急性等容血液稀释(ANH)对兔脊髓缺血-再灌注损伤的保护作用.方法 24只新西兰雄性大白兔,随机均分成三组:HES组,生理盐水组(NS组),对照组(C组).HES组和NS组分别用HES130/0.4和生理盐水行ANH,使红细胞压积(Hct)达30%.ANH的方法为:15 min内经股动脉恒速放出计算的血量,同时利用微量输液泵经静脉输注与放血量等量的液体(HES组)或输注3倍于放血量的液体(NS组),放血和输液速度相等,维持术中大白兔的血压和心率恒定.稳定15 min后,行肾下腹主动脉(IRA)阻闭建立脊髓缺血-再灌注损伤模型.分别于稀释前、稀释后和腹主动脉开放后采集动脉血进行血气分析.评估再灌注后4、8、12、24及48 h后肢运动功能,并于48 h处死动物取脊髓(L5)制标本行病理组织学观察.结果 再灌注后48 h.HES组和NS组动物的后肢运动功能比C组明显改善(P＜0.05或P＜0.01);HES组和NS组动物脊髓前角正常运动神经元计数比C组显著增加(P＜0.05或P＜0.01),但两组间差异无统计学意义.结论 HES130/0.4行适度ANH对脊髓缺血-再灌注损伤具有显著地保护作用.     

Blockade of sodium channels by phenytoin protects ultrastructure and attenuates lipid peroxidation in experimental spinal cord injury

Summary Spinal cord injury (SCI) involves a series of pathological events. Abnormal sodium influx has been implicated as one of the key events in the pathophysiology of the SCI. Pharmacological blockade of sodium channels can reduce secondary injury and increase recovery from trauma. The aim of the present study was to show the neuroprotective effect of phenytoin, a sodium channel blocker, after experimental SCI.Control and laminectomy-only groups were not injured. 50g-cm weight drop injury was produced in the trauma group. In the treatment groups, methylprednisolone (30mg/kg) and phenytoin (1mg/kg, 10mg/kg, or 30mg/kg) were given intraperitoneally immediately after injury. Malondialdehyde (MDA) levels in the spinal cord samples were examined for lipid peroxidation. Spinal cord ultrastructure was evaluated and grading system was used for quantitative evaluation.Trauma increased tissue MDA levels. Treatment with methylprednisolone and phenytoin decreased MDA levels compared to trauma in all doses. Significant ultrastructural neuroprotection was observed with 30mg/kg of phenytoin treatment according to general neural score. This ultrastructural neuroprotection of phenytoin was not different from methylprednisolone. Phenytoin appears to protect spinal cord against injury by decreasing lipid peroxidation and lessening neuronal damage associated with SCI in rats.     

淫羊藿苷在大鼠脊髓损伤中的神经保护作用

目的:研究淫羊藿苷在大鼠脊髓损伤中的神经保护作用。方法:108只SPF级雄性3月龄SD大鼠按随机数字表法分为实验组、对照组及假手术组3组,每组36只。对照组和实验组采用改良Allen法制作脊髓损伤模型,假手术组仅切开椎板不损伤脊髓。术后即刻实验组给予淫羊藿苷(100 mg/kg)灌胃,对照组和假手术组给予等量生理盐水灌胃,每日2次。术后1、2、3 d采用BBB评分法评定大鼠运动功能;术后72 h采用分光光度法检测髓过氧化物酶(myeloperoxidase,MPO)的活性,酶联免疫吸附测定(ELISA)法检测肿瘤坏死因子(tumor necrosis factor,TNF)-α、白介素(interleukin,IL)-1β的含量,免疫组化染色检测MPO、TNF-α、IL-1β的表达;采用硫代巴比妥酸法检测丙二醛(malondialdehyde,MDA)含量,黄嘌呤氧化酶法检测超氧化物歧化酶(superoxide dismutase,SOD)活性;采用TUNEL法检测细胞凋亡并计算细胞凋亡指数(apoptosis index,AI);光镜观察脊髓损伤后组织病理学的改变并行组织病理学评分。结果:术后各时间点对照组和实验组大鼠BBB评分均显著低于假手术组(P0.05);术后2、3 d实验组大鼠BBB评分均显著高于对照组(P0.05)。术后72 h,对照组和实验组MPO活性和TNF-α、IL-1β的含量显著高于假手术组(P0.05);实验组显著低于对照组(P0.05)。对照组和实验组MPO、TNF-α、IL-1β的表达显著高于假手术组(P0.05);实验组显著低于对照组(P0.05)。对照组和实验组MDA含量显著高于假手术组,实验组显著低于对照组(P0.05);对照组和实验组SOD活性显著低于假手术组,实验组显著高于对照组(P0.05)。对照组和实验组脊髓组织中AI显著高于假手术组,实验组显著低于对照组(P0.05)。对照组和实验组脊髓组织病理学评分均显著高于假手术组,实验组均显著低于对照组(P0.05)。结论:淫羊藿苷能够抑制脊髓损伤后的炎症、脂质过氧化和细胞凋亡,减轻脊髓组织病理学损伤,改善脊髓损伤大鼠的运动功能,有效保护脊髓组织,具有明显的神经保护作用。     

辛伐他汀促进脊髓损伤后神经功能修复的实验研究

目的:探讨脊髓损伤后急性期应用辛伐他汀对大鼠脊髓神经功能修复的影响。方法:成年雌性SD大鼠32只,假手术组(A组)8只,只做椎板切除,不损伤脊髓,不给药,重物坠落法制作脊髓损伤模型24只,损伤大鼠随机分为三组:羧甲基纤维素钠溶液组(B组)、5mg/kg辛伐他汀治疗组(C组)和10mg/kg辛伐他汀治疗组(D组)(n=8)。术后1d开始灌胃给予辛伐他汀每天一次,连续治疗5周。术后1d、3d以及1～8周,进行BBB评分、斜板试验评价大鼠脊髓神经功能,在第8周时电生理检测大鼠运动及感觉功能的恢复情况,随后处死取材,病理学检查(Luxol fast blue染色)观察残余髓鞘情况。结果:术后2周时,BBB评分D组高于B组(P<0.05);建模3周～8周,BBB评分D组及C组均高于B组(P<0.05),且D组最高(P<0.05)。建模3周时,斜板试验D组及C组均大于B组(P<0.05),且4周～8周,D组角度均大于C组(P<0.05)。感觉诱发电位检查发现,D组,C组的潜伏期小于B组(P<0.05),且D组波幅高于B组(P<0.05)。病理学检查,D组,C组比B组有更多的髓鞘残余(P<0.05)。结论:辛伐他汀急性期治疗脊髓损伤可以促进大鼠损伤脊髓神经功能修复。     

神经妥乐平对兔脊髓放射性损伤的治疗作用

目的:观察神经妥乐平(NTP)对兔放射性脊髓损伤的治疗效果。方法:新西兰大白兔60只,体重2.5~3kg,随机分成实验组与对照组,每组30只,各组再随机分成5小组接受不同剂量的放射性照射,每组6只,照射剂量分别为20Gy,25Gy,35Gy,40Gy,45Gy。照射部位为T4水平,所有兔在照射前以及照射后均做MRI检查。兔出现临床表现后实验组每天肌肉注射NTP3.6NU一次,共4周;对照组每天肌肉注射生理盐水3ml一次,共4周。观察两组治疗前后兔症状变化和脊髓MRI的表现及病理改变。结果:照射后平均16周时,动物受照射脊髓节段MRI出现明显异常信号,而临床症状的出现约在照射后平均18周。在治疗结束后3周,实验组各项指标(瘫痪、尿潴留和针刺反应)与对照组相比均明显改善(P<0.05);MRI图像上实验组治疗后病灶面积比治疗前明显缩小;神经元肿胀明显减轻,髓鞘结构趋于正常。而对照组变化不明显。结论:神经妥乐平对放射性脊髓损伤有一定的治疗作用。