脊柱脊髓损伤患者低钠血症的临床研究

目的：探讨脊柱脊髓损伤患者低钠血症的临床发病情况、发生机制及治疗措施。方法：回顾性分析543例急性脊柱脊髓损伤患者的临床资料。结果：543例患者中发生低钠者202例，占全部病例的37．2％。脊柱脊髓损伤患者低钠血症的发生率与患者脊髓损伤平面和程度有关。202例低钠者中13例出现神经精神症状。结论：脊柱脊髓损伤患者低钠血症的发生与钠盐摄入量减少、过量水负荷、脊髓损伤后肾脏排水保钠能力下降等原因有关。ASIA运动评分与脊柱脊髓损伤患者低钠血症的发生有相关性。     

Erythropoietin exerts neuroprotection after acute spinal cord injury in rats: effect on lipid peroxidation and early ultrastructural findings

Lipid peroxidation has been reported to play an important role in spinal cord injury (SCI). Erythropoietin (EPO) is a hematopoietic growth factor that stimulates proliferation and differentiation of erythroid precursor cells and is also known to exert neurotrophic activity in the central nervous system. The purpose of this study was to investigate the effectiveness of recombinant human EPO in attenuating the severity of experimental SCI. Rats were divided into seven groups. Controls (1) received only laminectomy. The trauma-only group (2) underwent 50-g/cm contusion injury and had no medication. In group 3, 30 mg/kg of methylprednisolone was introduced. The vehicle group (4) received vehicle solution containing human serum albumin, which is a solvent of EPO. Groups 5, 6, and 7 received 100 IU/kg, 1,000 IU/kg, and 5,000 IU/kg of EPO, respectively. All treatments were given as single doses, intraperitoneally, immediately after injury. Thiobarbituric acid-reactive substances were estimated to demonstrate lipid peroxidation, and ultrastructure was evaluated by electron microscopy. The results showed that lipid peroxidation by-products increased after injury. Administration of EPO and methylprednisolone sodium succinate (MPSS) reduced thiobarbituric acid-reactive substances after trauma. The best biochemical results were obtained with 5,000 IU/kg of EPO. Electron microscopic findings showed that EPO protected the spinal cord from injury. Although 1,000 IU/kg and 5,000 IU/kg of EPO inhibited lipid peroxidation better than MPSS, ultrastructural neuroprotection was similar.     

川芎嗪对预防犬急性脊髓损伤神经保护作用的实验研究

目的研究川芎嗪对犬急性脊髓损伤模型的神经保护作用。方法Allen’s法打击犬胸13节段脊髓制成急性脊髓损伤模型，所有动物均行介入下选择性动脉插管至伤椎水平肋下动脉，留置导管作为局部给药途径。实验动物随机分为正常对照组、脊髓损伤组、川芎嗪治疗组。术后采用胥少汀脊髓功能评分标准对脊髓神经功能进行评分、MRI检查、血清和脑脊液中髓鞘碱性蛋白(MBP)和S-100B蛋白的测定来衡量脊髓损伤程度和药物治疗效果。结果川芎嗪治疗组在各时间点的神经功能评分高于脊髓损伤组并且在1W有统计学意义。核磁共振检查发现川芎嗪治疗组的相对信号值低于脊髓损伤组，在72h、1W有统计学意义。川芎嗪治疗组血清和脑脊液中MBP低于脊髓损伤组，并且MBP在72h时差异有显著性。结论川芎嗪对于急性脊髓损伤具有神经保护作用。     

颈髓急性损伤后的磁共振波谱评价

目的:探讨颈髓急性损伤后磁共振波谱(1H-MRS)的诊断价值。方法:对19例急性颈髓损伤患者根据神经功能分为完全性损伤及不全性损伤两组,选取创区与创区头侧远端颈髓行1H-MRS,半定量分析氮-乙酰门冬氨酸(NAA)、胆碱(Cho)、肌酸(Cr)和乳酸(Lac)含量的比值。结果:颈髓完全性损伤组中NAA/Cho、NAA/Cr显著减低,Lac/Cho显著增高,其创区头侧远端Lac/Cho含量也增高(P<0.05);不完全损伤组中仅Lac/Cho含量增加,头侧远端乳酸含量亦增高(P<0.05)。颈髓损伤不同程度组间NAA/Cho、NAA/Cr有显著性差异(P<0.05)。结论:1H-MRS所测NAA/Cho、NAA/Cr从代谢水平反映颈髓损伤的不同程度,创区头侧远端Lac/Cho比值增高提示颈髓隐匿损伤的存在。     

大鼠牵张性脊髓损伤后细胞凋亡及相关基因表达的实验研究

目的观察大鼠牵张性脊髓损伤后细胞凋亡现象,检测脊髓损伤后凋亡相关基因的表达。方法大鼠脊髓T13～L2经牵张损伤,皮层体感诱发电位(CSEP)监测P1N1波幅下降至术前波幅70%后,分别于术后30min、6h、1、4、7、14、21d处死大鼠,取材(n=4)。应用流式细胞仪、原位末端脱氧核糖核苷酸转移酶介导dUTP标记(TUNEL)技术观察脊髓细胞凋亡情况,用免疫组化检测p53、bax和bcl2的表达。结果流式细胞仪及TUNEL法检测显示,损伤组术后6h凋亡细胞开始增多,术后7d细胞凋亡率达高峰,随后开始回落,持续21d,与空白对照组及椎板切除组比较,差异有显著性意义(P<005,001)。TUNEL法染色显示,白质中出现大量胶质细胞凋亡。免疫组化染色显示损伤组术后6h开始,p53、bax和bcl2阳性表达开始增多,p53阳性细胞数术后4d达高峰,bax和bcl2术后7d达高峰,损伤组各时相点的阳性表达与空白对照组与椎板切除组比较差异有显著性意义(P<005,001)。结论牵张性脊髓损伤后存在细胞凋亡现象,从形态上看包括神经元和胶质细胞凋亡,细胞凋亡是牵张性脊髓损伤继发损害中细胞死亡的一种重要形式,也是继发损伤期的重要病理变化。凋亡相关基因p53、bax大量表达,可能在脊髓细胞凋亡过程中起重要作用。     

The comparison of recovery patterns between ischemic spinal cord injury and traumatic spinal cord injury from acute to chronic phase

Objective: To investigate the neurological and functional recovery patterns of ischemic spinal cord injury (ISCI) compared with traumatic spinal cord injury (TSCI) in the acute to chronic phase.Design: Retrospective cohort study.Settings: Department of Neurology, Neurosurgery, Rehabilitation Medicine at a tertiary hospital.Participants: Fifty-four patients with ISCI and 86 patients with TSCI.Interventions: Not applicable.Outcome measures: MRI findings, American Spinal Injury Association Impairment Scale (AIS), modified Rankin Scale (mRS), Korean Spinal Cord Independence Measure (KSCIM), ambulatory status, and bladder status were reviewed. The functional outcomes were measured at admission, discharge, and >6 months after discharge.Results: AIS classification did not significantly change after 6 months in both ISCI and TSCI groups. Between admission and discharge, the proportion of patients needing a wheelchair or assistive device to ambulate decreased more in the ISCI group compared with the TSCI group [odds ratio (OR) 0.40, P = 0.04]. In addition, the proportion of catheterized voiding in the ISCI group was significantly higher than in the TSCI group at all time points (OR 5.12, P < 0.001). Lastly, both groups showed that functional improvement was the greatest between admission and discharge. In addition, the proportion of catheterized voiding decreased (Diff = −0.12, P = 0.019) and mRS score decreased (Diff=−0.48, P < 0.001) significantly in the ISCI group at >6 months post discharge.Conclusion: The ISCI group showed better recovery of mobility during inpatient rehabilitation period and worse recovery of bladder function as demonstrated by higher number of patients requiring bladder catheterization at all time points when compared with the TSCI group.     

甲基强的松龙与神经节苷脂治疗大鼠急性脊髓损伤

目的探讨早期联合应用大剂量甲基强的松龙(MP)及神经节苷脂(GM1)对大鼠急性脊髓损伤的治疗效果.方法改良Allen's打击法致伤36只大鼠T10～T12脊髓建立急性脊髓损伤模型,随机分为对照组、MP治疗组(应用大剂量MP)及MP+GM1治疗组(早期联合应用大剂量MP及GM1),观察大鼠肢体功能恢复、运动神经元数目及截面积以及胆碱脂酶活性变化,TUNEL标记检测凋亡神经元细胞,比较各组间差别.结果治疗组大鼠神经元细胞结构退变较对照组轻,BBB评分、运动神经元数目及截面积以及胆碱脂酶(CHE)活性较对照组明显提高,尤以MP+GM1组更明显,脊髓凋亡神经元数对照组较实验组明显增多(P＜0.05).结论甲基强的松龙及神经节苷脂对急性脊髓损伤大鼠的脊髓功能具有保护作用,二者联合应用具有协同作用.     

周围神经移植修复脊髓损伤的实验研究

目的：探讨自体坐骨神经移植修复脊髓损伤的可行性。方法：将58只雌性Wistar大鼠分为二组，实验组：采用显微外科技术，将50只大鼠于T13水平切除左半侧脊髓10mm，再取右侧坐骨神经10mm移植到脊髓缺损处，近端接脊髓，远端接马尾，分别于术后2、4、6、8、12、22周在光镜和电镜下观察移植处坐骨神经、吻合口远端马尾神经、左后肢坐骨神经再生情况，并用摄像机记录患肢功能恢复情况。对照组：8只大鼠，于13水平切除左半侧脊髓10mm，不移植坐骨神经，观察脊髓缺损远端马尾神经和左右肢坐骨神经再生情况。结果：对照组坐骨神经的轴突及髓鞘部分崩解，密度降低，无再生轴突形成。实验组术后4周电镜下偶见移植处坐骨神经髓鞘及轴突形成，术后8周光镜及电镜下可见较多细的有髓神经纤维，22周时接近正常；同时观察到左后肢坐骨神经再生；大鼠后肢功能部分恢复，肌力达3级。结论：大鼠脊髓损伤后有再生能力，周围神经移植修复脊髓损伤是可行的。     

脊髓损伤早期及制动后大鼠股骨远端骨量丢失的实验研究

目的:建立大鼠脊髓损伤及后肢废用模型,观察建模早期两种模型大鼠股骨远端骨密度及远端破骨细胞数量的改变。方法:24只SD大鼠随机分为3组(每组8只),对照组(A组),行T10椎板切除,不损伤硬膜及脊髓;脊髓损伤(SCI)组(B组):切除T10椎板后用Allen′s法(60g.cm势能)造成脊髓损伤;制动组(C组):采用大鼠双侧腿-尾缝合,造成双下肢制动。分别于造模后第1、7天采用BBB(Basso,Beattie and Bresnahan)评分评估脊髓损伤大鼠后肢运动功能,确定模型建立成功。建模第10天后处死,取一侧尺、桡骨及股骨远端,行骨密度检测。取另一侧股骨远端行TRAP染色,观察大鼠股骨远端破骨细胞数量的变化。结果:A、B、C 3组股骨远端骨密度值分别为0.114、0.096、0.108g/cm2,B组骨密度值最低,其次为C组,A组最高(P<0.05)。尺、桡骨骨密度3组比较无差异(P>0.05)。与A组比较,B组大鼠股骨干骺端破骨细胞数量增加显著,其次为C组,A组最少(P<0.01)。结论:脊髓损伤后,股骨远端破骨细胞数量大量增多,活性增强,骨吸收加强,引起脊髓损伤平面以下肢体骨量的迅速丢失,比废用性骨量丢失的程度更重。     

Beneficial effects of local profound hypothermia and the possible mechanism after experimental spinal cord injury in rats

Objective: The primary focus of this study was to investigate the effects of local profound hypothermia and to explore the possible mechanism in adult rats with spinal cord injury.

Study Design and Methods: Spinal cord injury models were established by placing aneurysm clips on T10. An epidural perfusion device was applied to maintain a steady temperature (18?°C) for 120?min with gradual rewarming to 37?°C Total hypothermic duration lasted up to about 170?min. The expression of axon regeneration inhibitors was tested by Western blot and real-time PCR. Luxol Fast Blue (LFB) stain and Bielschowsky silver stain were used to observe spinal cord morphology. Motor function of the hind limbs (BBB score) was monitored for 21 days.

Results: The expressions of RhoA, ROCK-II, NG2, Neurocan, Brevican, and Nogo-A were downregulated by regional hypothermia (RH) after spinal cord injury. Subsequent observation showed that rats that had received RH had an alleviated demyelinating condition and a greater number of nerve fibers. Furthermore, the RH group achieved higher BBB scores than the spinal cord injury (SCI) group.

Conclusions: Recovery of hind limb function in rats can be promoted by local profound hypothermia; this may be caused by the suppression of axon regeneration inhibitors.     

胚胎脊髓移植与甲基强的松龙联合应用治疗脊髓损伤的实验研究

目的 :探讨胚胎脊髓移植 (FST)与大剂量甲基强的松龙 (MP)联合应用治疗脊髓损伤的效果。方法 :选用SD大鼠 5 0只 ,随机分为A、B、C、D、E 5组 ,前 4组行T12脊髓半切损伤后为治疗组。A组行大剂量MP与FST联合应用 ;B组行大剂量MP治疗 ;C组为FST治疗 ;D组为单纯半切损伤 ;E组为空白对照。治疗后 2 4h及 8周时行脊髓体感诱发电位检查 ,观察行为变化 ,并对各组损伤区脊髓横断面神经纤维数进行统计学分析。结果 :A组与B、C、D组之间脊髓体感诱发电位及损伤区神经纤维计数均存在明显差异 (P <0 0 5 ) ,行为学无明显改变。结论 :大剂量甲基强的松龙与胚胎脊髓移植联合应用治疗脊髓损伤可起协同促进损伤脊髓修复的作用。     

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.     

脊髓损伤后逼尿肌细胞钙通道改变

目的 探讨脊髓损伤(SCI)后逼尿肌细胞钙通道改变及其与逼尿肌反射亢进(DH)的关系.方法 建立SD大鼠骶髓上损伤动物模型,进行逼尿肌条钙通道阻滞实验及逼尿肌细胞钙震荡激光共聚焦线性扫描.结果 相同前负荷下逼尿肌条的收缩频率SCI组(2.51±0.39)明显高于正常对照(C)组(1.95±0.58,P<0.05),滴加高浓度T型钙通道阻滞剂咪拉地尔后两者收缩频率降低至相同水平,滴加高浓度L型钙通道阻滞剂异搏定后两者收缩频率下降相同;逼尿肌细胞钙振荡频率SCI组(2.68±0.42)明显高于C组(1.87±0.48,P<0.05),滴加高浓度咪拉地尔后两者钙振荡频率降低至相同水平,滴加高浓度异搏定后两者振荡频率下降相同.结论 SCI后DH的发生与逼尿肌细胞T型钙通道性状改变密切相关.     

The effects of systemically administered methylprednisolone and recombinant human erythropoietin after acute spinal cord compressive injury in rats

The study design was to decrease the damage of spinal cord on the experimentally induced acute spinal cord injury in rats. The objective of this study was to evaluate whether recombinant human erythropoietin (rHu-EPO) and methylprednisolone (MPSS) improve neurological function and histopathological changes if systemically administered after traumatic spinal cord injury. This study included 48 rats that underwent experimental SCI. Forty-eight animals were randomly divided into six groups. Animals constituted a moderate compression of 0.6 N that was produced by application of an aneurysm clip at level T3 for 1 min. rHu-EPO (1,000 and 3,000 U (Unit) per kg of body weight i.p.) and MPSS (30 mg/kg) were administered 5 min after injury, and control group was saline treated. (1) Control group (n=8), (2) MPSS group (n=8), (3) rHu-EPO 1,000 U group (n=8), (4) MPSS + rHu-EPO 1,000 U group (n=8), (5) rHu-EPO 3,000 U group (n=8), and (6) MPSS + rHu-EPO 3,000 U group (n=8). The neurological function and histopathology were evaluated at 24 and 72 h. According to the neurological functional test scores significant improvements between the control group and the other groups that had taken medical treatment were observed (P<0.001). Histopathologically severe ischemic findings were observed in the control group. A significant decrease in ischemic damage was detected in MPSS + rHu-EPO 3,000 U group (P<0.001). The most significant neurological functional and histopathological improvements were observed after systemical administration of MPSS + rHu-EPO 3,000 U and rHu-EPO 3,000 U. Furthermore, the MPSS + rHu-EPO 3,000 U group provides the most improved neurological functional and histopathological recovery.     

盐酸戊乙奎醚对大鼠急性脊髓损伤修复的作用

目的 观察盐酸戊乙李醚对大鼠急性脊髓损伤后脊髓损伤修复的作用.方法 选用健康成年雄性SD大鼠90只分为3组,A组:盐酸戊乙奎醚治疗组(n=40),从造模后1 h开始,经腹腔注射盐酸戊乙奎醚每天3 mg/kg,卣至取材;B组:单纯损伤组(n=40),单纯损伤组同法给予等量生理盐水;C组:正常对照组(n=10),不作任何处理.A组、B组大鼠采用改良Allen'S重物坠落法在T10段制作急性脊髓损伤模型.各组取材前24 h腹腔注射溴脱氧尿嘧啶核苷(BrdU)溶液,对距离损伤中心5 mm处的脊髓进行BrdU、nestin阳性细胞数检测.结果 C组脊髓中央管周围及外膜可见少量BrdU阳性细胞,几乎看不到nestin阳性细胞.B组造模后24 h即可见大量BrdU阳性细胞,1周达到高峰,2周后开始明显减少,4周时仅见少量BrdU阳性细胞.与B组比较,24 h时A组BrdU阳性细胞差异无统计学意义,1周时BrdU阳性细胞数明显增多(P<0.05),至2周时仍处于较高水平,4周时仍有大量BrdU阳性细胞表达.B组造模后7 d nestin阳性细胞增多,14 d达到高峰,28 d时可见极少量nestin瞄H性细胞.与B组比较,7 d时A组nestin阳性细胞差异无统计学意义,14 d时nestin阳性细胞数明显增多,至28 d时仍处于较高水平(P<0.05).结论 盐酸戊乙奎醚能够促进急性脊髓损伤大鼠损伤区BrdU及nestin的表达,提示有促进神经干细胞增殖的能力,增强脊髓损伤后自体的修复功能.     

急性脊髓损伤模型大鼠血清和脊髓的代谢组学研究

目的:采用~1H NMR核磁共振代谢组学的方法研究急性脊髓损伤模型大鼠的代谢组学特征及生物标志物,探讨核磁共振代谢组学应用于脊髓损伤研究的可行性。方法:取8周龄清洁级雄性SD大鼠20只,体重(200±10)g,按照随机数字法分为假手术组和模型组,每组10只,模型组采用改良的Allens法制作急性脊髓不完全损伤模型,假手术组不损伤脊髓,术后第1、5、7天采用BBB运动功能评分法进行行为学观察,术后第7天收集脊髓组织作病理学观察,核磁共振代谢组学对两组大鼠血清和脊髓样本进行代谢组学分析。结果:BBB评分显示假手术组术后后肢运动无明显改变,各时间点差异无统计学意义,模型组大鼠术后双下肢呈迟缓性瘫痪,BBB运动评分较低,各时间点差异存在统计学意义,两组运动功能评分在各时间点的差异均有统计学意义;病理切片显示假手术脊髓结构正常,神经分布均匀,模型组脊髓组织结构紊乱,神经元数目减少,存在炎性细胞浸润和空腔坏死组织。代谢组学分析表明,血清中极低密度脂蛋白(VLDL)、低密度脂蛋白(LDL)、谷氨酰胺(glutamine)、柠檬酸(citrate)、二甲基甘氨酸(DMG)等物质和脊髓中谷胱甘肽(glutathione)、3-羟基丁酸(3-OH-butyrate)、N-乙酰天冬氨酸(NAA)、磷酸胆碱(GPC)、谷氨酸(glutamate)、抗坏血酸(ascorbate)等物质浓度有明显变化(P0.05)。结论 :通过对假手术组和模型组大鼠血清和脊髓样本进行代谢组学检测和分析得到了两组样本的差异性代谢物质,有助于解释急性脊髓损伤后血清和脊髓组织中的特异性小分子物质的变化规律,为后期针对性地研究这些代谢标记物在急性脊髓损伤中的作用提供研究基础。     

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。     

大剂量甲基强的松龙与东莨菪碱治疗急性脊髓损伤的临床观察

目的比较甲基强的松龙(MP)与东莨菪碱(SCP)治疗急性脊髓损伤(ASCI)的治疗效果.方法将44例ASCI患者随机分为3组,伤后8h以内患者随机分入大剂量MP治疗组及SCP治疗组,受伤时间超过8h的患者分人对照组.分别于入院时、伤后6周和6个月时对脊髓功能进行评分.结果两治疗组的感觉功能在伤后6周和6个月时均有明显好转,运动功能MP治疗组在伤后6周时即有明显好转,而SCP治疗组在伤后6个月时才有明显好转.对照组患者脊髓功能恢复不明显.结论MP与SCP均是治疗ASCI有效的药物,MP能够早期促进运动功能的恢复,对ASCI患者的康复有重要意义.     

人胚神经干细胞移植治疗大鼠脊髓损伤

目的 探讨人胚神经干细胞（hNSC）移植治疗脊髓损伤（SCI）的可行性。方法 分离、培养和鉴定hNSC；用5溴-2脱氧尿苷嘧啶（BrdU）标记hNSC，并将其移植到14只T10半横断的Wistar大鼠损伤脊髓内（另外14只T10半横断损伤的大鼠作为对照组，仅损伤脊髓内注射DMEM／F12培养液），用BrdU的FITC免疫荧光染色检测移植细胞的存活和迁徙，用NF-200、GFAP免疫组织化学鉴定移植细胞的分化，BBB评分评定大鼠功能恢复情况。结果 （1）获得了大量的hNSC；（2）用免疫组织化学可以检测到移植的hNSC能在体内长时间存活（达2个月）并向远处迁徙，并分化为神经元和胶质细胞；（3）检测到实验组大鼠BBB得分明显高于对照组大鼠（P〈0．01），在SCI后第10周时实验组和对照组BBB得分最大差距达到2．1分。结论 hNSC移植能促进SCI大鼠后肢功能恢复，它是SCI移植治疗较有价值的细胞资源。     

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.