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。     

去除外膜的外周神经移植对大鼠脊髓损伤的影响

目的检测大鼠脊髓损伤经显微外科技术处理的自体外周神经移植后神经纤维的再通及后肢功能恢复情况。方法利用改良Allen撞击方法建立脊髓打击损伤模型，12周后，将大鼠分为2组，实验组切取后肢腓肠神经，利用显微外科技术去除神经外膜，将其修剪成小段，游离移植于脊髓损伤处，对照组仅显露脊髓损伤段，不作神经移植。分三个时相点（1、2、3个月）进行辣根过氧化物酶（HRP）逆行示踪，并观察损伤移植处的形态学变化及大鼠后肢运动功能恢复情况。结果损伤移植处脊髓的形态学明显好转；损伤移植处上段脊髓中，移植1个月组有HRP阳性标记物，以后逐渐增多；移植组大鼠后肢运动功能明显恢复。结论经显微外科技术预处理外周神经组织移植后可促进大鼠脊髓结构和功能的恢复。     

利用一级神经元重建完全性脊髓损伤大鼠后肢运动功能的实验研究

目的探讨利用一级神经元重建完全性脊髓损伤大鼠后肢运动功能的效果。方法取40只成年雌性SD大鼠,体质量300~350 g,制备L1椎体水平横断型完全性脊髓损伤模型;模型制备后2周,将大鼠随机分为对照组和实验组(n=20);其中实验组行右后肢一级神经元直接重建手术,对照组除不缝合胫神经远端与股神经近端外,其余处理同实验组。术后观察大鼠一般情况,并于7、30、50、70 d对双侧后肢行BBB评分,观察后肢运动功能恢复情况;于70 d取材行HE染色、神经丝蛋白200(neurofilament 200,NF-200)免疫组织化学染色及辣根过氧化物酶(horseradish peroxidase,HRP)示踪标记染色观察脊髓重建区变化。结果饲养期间6只大鼠死亡。两组右后肢运动功能无明显恢复,各时间点BBB评分均为0分;左后肢运动功能均有不同程度恢复,但各时间点两组BBB评分比较,差异均无统计学意义(P0.05)。实验组HE染色可见脊髓重建部位坐骨神经嵌入脊髓中,坐骨神经束膜显示清楚,连接部位脊髓无明显萎缩;NF-200免疫组织化学染色可见脊髓重建部位周围神经内神经元轴突呈阳性染色,且周围神经与脊髓形成联系。HRP逆行示踪标记染色示,实验组脊髓重建部位头端见HRP显色,对照组无着色。结论一级神经元直接重建手术可使大鼠周围神经与中枢神经通过残留神经元轴突残端再生,重建相应的神经通路,但未见到周围神经支配靶肌肉运动功能的恢复。     

神经营养素-3基因修饰嗅鞘细胞移植对急性脊髓损伤作用的实验研究

目的：观察神经营养素-3（NT-3）基因转染嗅鞘细胞（OEG）移植对急性大鼠脊髓损伤的作用。方法：将自行构建的质粒DEGFP-NT3应用脂质体介导的方法导人体外培养的嗅鞘细胞，并移植入急性脊髓损伤大鼠体内．连续观察12周．与接受单纯OEG、空白质粒转染OEG移植的脊髓损伤大鼠进行比较。结果：移植转染DEGFP-NT3后的OEG能在体内长期存活，表达NT-3基因，与对照组比较能更好地促进脊髓损伤区轴突的再生和后肢功能的恢复。结论：OEG是脊髓损伤基因治疗较好的受体细胞。转染NT-3基因的OEG移植后可以在体内较长时间存活．能明显促进急性脊髓损伤神经纤维的再生和功能恢复，为基因修饰嗅鞘细胞在脊髓损伤治疗中的应用提供了实验和理论依据。     

带与不带血管周围神经移植的比较

目的：比较带与不带血管周围神经移植的再生情况及探讨其再生机理。方法：用ＳＤ雄性大鼠５０只，随机分组，６只为正常对照组，其余等分为Ａ组（带血管神经移植组）和Ｂ组（不带血管神经移植组）。两组均在移植后不同时间取材，进行光镜、电镜对比观察。结果：在移植后的前４周，Ａ、Ｂ两组组织形态学变化基本相似。从第６周开始，移植段神经纤维再生率、有髓神经纤维再生率、有髓神经纤维直径恢复率、神经纤维变性率，Ａ组均明显优于Ｂ组，并进行了差异程度比较。Ａ组结缔组织增生少，神经纤维再生好。发现Ｂ组神经束内有结缔组织包裹２～３条神经纤维呈小束，再生而又变性的神经纤维多。结论：带血管周围神经移植优于不带血管的周围神经移植。     

高压氧与带血供周围神经移植对成鼠损伤脊髓诱发电位的影响

目的：研究高压氧对带血供周围神经移植修复成鼠损伤脊髓功能恢复的作用。方法：将40只成年Wistar大鼠作成脊髓半切损伤模型,随机分为A、B两组,A组单纯带血供周围神经移植修复脊髓损伤,B组为带血供周围神经移植后给予高压氧治疗。手术后1、2、4、8、10周进行感觉诱发电位（SEP）和运动诱发电位（MEP）检查。结果：SEP和MEP潜峰时的恢复B组优于A组。结论：高压氧与带血供周围神经移植对成鼠损伤脊髓功能恢复有较好的促进作用。     

乙交酯-丙交酯共聚物支架-细胞复合体移植对大鼠损伤脊髓的修复作用

目的 观察神经干细胞、雪旺细胞和组织工程材料乙交酯-丙交酯共聚物共移植后对大鼠损伤脊髓形态和功能的修复作用.方法 36只Wistar大鼠,随机数字法分为乙交酯-丙交酯共聚物移植组、神经干细胞/乙交酯-丙交酯共聚物绀和神经干细胞+雪旺细胞/乙交酯-丙交酯共聚物组.体外培养、鉴定胚胎脊髓源神经干细胞和雪旺细胞,制备和构建乙交酯-丙交酯共聚物支架细胞复合体并移植到大鼠脊髓T9半横断损伤部位,应用BBB行为评分和电生理技术在术后4、12周评价大鼠脊髓功能的恢复情况;应用透射电镜、HE染色和免疫组织化学染色方法在形态结构上观察轴突和髓鞘再生情况,以及神经干细胞在脊髓内的存活、迁移和分化情况.结果术后4、12周,细胞移植组的BBB评分较对照组明显提高(P＜0.05);细胞移植组的体感诱发电位和运动诱发电位波幅较对照组都有所好转.术后12周移植材料正中横断面透射电镜可见新生的无髓及有髓神经纤维;脊髓标本免疫组织化学染色显示移植的神经十细胞呵以在宿主脊髓内存活、迁移并分化成神经元和少枝胶质细胞,未分化成星形胶质细胞.结论 神经干细胞、雪旺细胞和组织工程材料乙交酯-丙交酯共聚物共移植可以促进半横断损伤的大鼠脊髓轴突再生,改善肢体的运动功能.     

活性巨噬细胞与周围神经联合移植治疗

目的脊髓损伤后轴突再生是脊髓功能恢复的基础，但再生轴突受神经自身条件及损伤微环境的限制。研究表明脊髓损伤后损伤区早期、大量的巨噬细胞聚积可改善局部微环境，减轻脊髓继发性损伤并促进其再生；而周围神经移植可为随后发生的再生轴突提供通道和营养物质，两者联合应用则为脊髓损伤的治疗提供一条有效的途径。方法将72只S—D大鼠采用随机的方法分为4组，A组大鼠在T。脊髓半切加洞性损伤；B组在上述基础上行肋间神经移植；C组行巨噬细胞移植；D组行巨噬细胞和肋间神经联合移植。术后1、3天和1、2、4、8周收集脊髓标本并冰冻切片、免疫组化染色，显微镜下巨噬细胞及神经纤维计数。结果D组大鼠术后4周以上时BBB运动功能评分平均提高1分，镜下观察见C、D组大鼠在伤后4周内巨噬细胞及再生轴突数目均高于A、B组。结论该方法可减轻脊髓损伤并促进其再生，可能是治疗脊髓损伤的一条有效途径。     

基于神经搭桥的中枢神经-周围神经直接连接技术治疗脊髓损伤的实验研究

目的 研究通过自体周围神经移植桥接中枢神经系统和周围神经系统,观察中枢神经系统轴突能否再生并通过移植的周围神经重建脊髓损伤大鼠的股四头肌神经通路,恢复脊髓损伤大鼠肢体部分运动功能. 方法 取200～220 g SD雌性大鼠33只,随机分成3组.A组(18只):脊髓左侧半横断,周围神经移植加远端吻合股神经;B组(10只):脊髓左侧半横断组,周围神经假移植加远端吻合股神经;C组(5只):假手术组,不做任何处理.通过动物行为学观察、肌肉湿重、组织学检查和生物素葡聚糖胺(BDA)顺行示踪评价中枢神经-周围神经直接连接对脊髓损伤的修复效果.结果 术后14周,A组大鼠左下肢有逐渐恢复的运动,股四头肌肌肉力量评分为2.40±1.12,较第4周(0.80±0.41)和第8周( 1.20±0.67)差异有统计学意义(P＜0.05);B组大鼠左下肢未见任何恢复.第14周时,A组动物左下肢股四头肌肌肉湿重占对侧股四头肌的比值(31.0±8.0)较B组(15.0±4.0)差异有统计学意义(P＜0.05).在移植的周围神经中,出现BDA阳性及NF200阳性的神经纤维. 结论 初步结果显示自体周围神经桥接中枢神经-周围神经能起到修复脊髓损伤的作用.     

环磷酸腺苷在大鼠脊髓背侧半切损伤修复中的作用

目的观察在体内给入环磷酸腺苷(cAMP)对大鼠脊髓损伤修复中的作用。方法采用大鼠脊髓T10背侧半切伤模型,通过在脊髓损伤局部、大脑运动皮层、和蛛网膜下腔内给入cAMP,做组织切片免疫组化染色,观察损伤区局部神经丝(NF)、胶质纤维酸性蛋白(GFAP)、皮质脊髓束(CST)纤维、脊髓神经纤维及后肢运动功能评分(BBB)。结果cAMP在脊髓损伤局部和大脑运动皮层给入时,损伤区可见大量脊髓再生纤维,在蛛网膜下腔内给入时损伤区可见极少量皮质脊髓束纤维存在。cAMP组损伤区NF分布较多,GFAP较少。所有动物后肢运动在5～6周恢复正常行走,BBB评分的时间曲线在对照组和cAMP组之间没有明显区别。结论在体内给入cAMP能诱导大鼠脊髓损伤后神经再生。     

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.     

神经干细胞移植促进脊髓损伤后脑源性神经营养因子的表达

目的：探讨神经干细胞（NSCs）移植对大鼠脊髓损伤后脑源性神经营养因子（BDNF）表达的影响及其意义。方法：NSCs提取自新生Wistar大鼠的海马区，经培养、鉴定。制作大鼠脊髓损伤（SCI）模型，于伤后第7天移植NSCs。实验分为3组：NSCs移植组（A组），DMEM填充组（B组），正常对照组（C组）。应用RT—PCR法和免疫组化法观察细胞移植后BDNF基因表达的变化。结果：RT—PCR结果分析，移植术后第1、3、5天，A组BDNF mRNA的表达量明显高于B组，差异有统计学意义（P〈0．05）。组化结果分析，移植术后第7、14、28天BDNF的表达量A组明显高于B组，差异有统计学意义（P〈0．05）。结论：NSCs在移植后可上调脑源性神经营养因子BDNF基因的表达，是其修复脊髓损伤的机制之一。     

Role of Rho-associated coiled-coil containing protein kinase in the spinal cord injury induced neuropathic pain

BACKGROUND CONTEXTSpinal cord injury (SCI) can lead to increased phosphorylation of p38 in spinal cord microglia. This is one of the main causes for the development of persistent pain. Recently, we reported our study on the activation of p38 mitogen-activated protein kinases (MAPK) in spinal microglia, which has been considered the key molecule for the onset and maintenance of neuropathic pain after peripheral nerve injury, using a rat model. We also reported that the RhoA/Rho-associated coiled-coil containing protein kinase (ROCK) pathway mediates p38 activation in spinal microglia in peripheral nerve injury. But the precise mechanisms of neuropathic pain induced by SCI are still unclear.PURPOSEThis study aimed to examine the activation of microglia and the p38 MAPK expression in the lumbar spinal cord after thoracic SCI in rats, and the correlation to the therapeutic effect of ROCK inhibitor ripasudil in rats with SCI.STUDY DESIGNMale Sprague–Dawley rats underwent thoracic (T10) spinal cord contusion injury using an Infinite Horizon impactor device. SCI rats received ROCK inhibitor ripasudil (24 nmol/day or 240 nmol/day) from just before SCI to 3 days after SCI.METHODSThe mechanical threshold in the rat's hind paws was measured over four weeks. Morphology of microglia and phosphorylation of p38 (p-p38) in the lumbar spinal cord and were analyzed using immunohistochemistry.RESULTSThe p-p38 positive cell and Iba1 (a maker of microglia) positive area were significantly increased at the lumbar spinal dorsal horn (L4–5) 3 days and 7 days after SCI compared with the sham-control (p<.05), whereas phosphorylated p38 was co-localized with microglia. Three days after SCI, the intensity of phosphorylated p38 and Iba1 immunoreactive cells in the dorsal horn was significantly lower in the ripasudil treated groups than in the saline group. However, administration of ROCK inhibitor did not affect the numbers of microglia. Moreover, the withdrawal threshold of the ripasudil-treated rats was significantly higher than that of the saline-injected rats on 14 days and 28 days after SCI.CONCLUSIONSOur results suggest that activation of ROCK in spinal cord microglia is likely to have an important role in the activation of p38 MAPK, which has been considered as a key molecule that switches on neuropathic pain after SCI. Inhibition of ROCK signaling may offer a means in developing a novel neuropathic pain treatment after SCI. It may help patients with neuropathic pain after SCI.CLINICAL SIGNIFICANCEThe findings in the present study regarding intracellular mechanisms suggest that modulation of ROCK signaling may be a focus for novel treatment for neuropathic pain after SCI.     

Effect of VEGF and CX43 on the promotion of neurological recovery by hyperbaric oxygen treatment in spinal cord–injured rats

Background contextSpinal cord injury (SCI) is a serious health issue that may result in high health care costs, with additional social and psychological burdens. Hyperbaric oxygen (HBO) treatment has been found to be beneficial for neurological recovery; however, the underlying mechanisms are yet to be characterized.PurposeThe aim of this study was to investigate the mechanisms of HBO treatment in SCI by measuring the expression levels of vascular endothelial growth factor (VEGF) and Connexin43 (CX43) in the injured spinal cord tissue.Study design/settingAn experiment animal study of rats undergoing SCI and HBO treatment.MethodsThe spinal cord injury model was established in rats, which were randomly divided into the following four groups: (1) the sham-operated group (SH), (2) the sham-operated and hyperbaric oxygen treatment group (SH+HBO), (3) the spinal cord injury group (SCI), and (4) the spinal cord injury and hyperbaric oxygen treatment group (SCI+HBO). For groups of SH+HBO and SCI+HBO, the animals received 1 hour of HBO at 2.0 ATA in 100% O2 twice per day for 3 days and then daily for the following days consecutively after surgery. After operation, neurological assessments were performed, the spinal cord tissue samples were harvested for histopathological evaluation, Western blot and real-time polymerase chain reaction analysis.ResultsThe Basso-Bettie-Bresnahan scores were significantly improved in the SCI+HBO group compared with the SCI group on the postoperative 7th and 14th days. The histology scores were significantly decreased by HBO treatment compared with that in the SCI group on the postoperative 3rd, 7th, and 14th days. Western blot analysis and real-time polymerase chain reaction revealed that the expression level of vascular endothelial growth factor (VEGF) in the SCI+HBO group was significantly increased compared with the SCI group. The protein expression level of CX43 and its mRNA level in the SCI+HBO group were significantly decreased on the postoperative 3rd and 7th days, whereas its expression was significantly increased by HBO treatment on the postoperative 14th day compared with the SCI group.ConclusionsHBO treatment improved neurological recovery when applied after SCI. The expression level changes of VEGF and CX43 may contribute to the further understanding on the molecular mechanisms of HBO treatment on SCI.     

大剂量甲基强的松龙对大鼠急性脊髓半切损伤的早期神经保护作用

目的研究大剂量甲基强的松龙（methylprednisolone,MP）对大鼠急性脊髓半切损伤的早期神经保护作用。方法 50只SD大鼠随机取10只仅行椎板切除,作为对照组。其余40只随机分为2组,脊髓半切损伤组及MP治疗组各20只。各组动物再随机平分为2个小组,分别在脊髓半切损伤后1d、7d进行BBB法神经功能评分、脊髓组织形态学观察、神经中丝（neurofilament NF）和胶质纤维酸性蛋白（glial fibrillary acidic protein,GFAP）免疫组化测定。结果脊髓半切损伤后立即使用大剂量MP明显提高了伤后7d时MP治疗组的BBB评分;对损伤脊髓的组织形态学有明显改善;明显提高了NF的表达,抑制了GFAP的表达。结论早期大剂量使用MP对大鼠急性脊髓半切损伤有神经保护作用。     

骨髓间充质干细胞移植对大鼠脊髓损伤后氧化应激的影响

目的研究骨髓间充质干细胞（bone marrow mesenchymal stem cells,BMSCs）移植对大鼠脊髓损伤（spinal cord injury,SCI）后氧化应激的影响。方法取大鼠股骨和胫骨骨髓培养BMSCs并传代。参照Taoka方法制作30只大鼠脊髓压迫损伤模型,随机分为3组,损伤组（SCI）、假移植组（SCI＋生理盐水）、移植组（SCI＋BMSCs）。脊髓损伤30 min时,假移植组和移植组于损伤周围相应注射生理盐水和BMSCs。在损伤后第3天、7天、14天和28天,进行BBB（Basso-Beattie-Bresnahan,BBB）行为学评价。应用MTT方法检测血清中超氧化物岐化酶（SOD）活性和丙二醛（MDA）水平。结果脊髓损伤后,BMSCs移植第14天即可观察到大鼠后肢运动功能明显改善,第28天BBB评分有明显提高。与损伤组和假移植组大鼠相比,第7天、14天和28天移植组血中MDA水平降低（P〈0.05）;血中SOD水平较高（P〈0.05）。结论 BMSCs移植对SCI神经功能恢复有促进作用,其机制可能与其抑制氧化应激有关。     

带血运的组织移植对损伤脊髓细胞凋亡的影响

目的：探讨带蒂的大网膜和椎旁肌移植覆盖脊髓对脊髓损伤后细胞凋亡的影响。方法：应用改良的Ａｌｌｅｎ‘ｓ法致伤脊髓,将动物分为单纯脊髓损伤组（Ａ组）,损伤＋椎旁肌组（Ｂ组）,损伤＋大网膜组（Ｃ组）。移植后１、３、７、１４、２８天对脊髓损伤区进行细胞凋亡的检测（ＴＵＮＥＬ）以及Ｂｃｌ－２蛋白表达的测定（免疫组化法）。结果：Ａ、Ｂ、Ｃ组中均发现凋亡细胞及ＢＣＬ－２蛋白阳性表达,图象分析发现,细胞凋亡率为Ａ     

绿色荧光蛋白转基因大鼠骨髓间充质干细胞在急性脊髓损伤大鼠中的迁移和分化

目的观察绿色荧光蛋白转基因大鼠来源的骨髓间充质干细胞(bone mesenchymal stem cells,BMSCs)在急性脊髓损伤大鼠脊髓组织中的迁移和分化情况。方法全骨髓贴壁培养法培养BMSCs,Allen法制作脊髓损伤大鼠模型,共30只大鼠。于造模1周后进行干预,随机选取造模成功的24只大鼠并随机分为脊髓损伤组、假移植组(生理盐水注射)和细胞移植组(BMSCs注射),每组8只。于移植前、移植后7 d、14 d、21 d、28 d、35 d及42 d进行BBB(Basso,BeattieBresnahan locomotor rating scale)评分。HE染色、免疫荧光观察脊髓损伤的组织修复和BMSCs的迁移分化情况。结果从第14天始,细胞移植组大鼠的BBB评分较脊髓损伤组和假移植组大鼠高,差异具有统计学意义(P0.05)。HE染色显示细胞移植组大鼠的脊髓结构相对完整,液化和囊泡区缩小,炎性细胞减少。免疫荧光显示BMSCs聚集于脊髓损伤处,且能分化为神经元、神经胶质细胞和神经前体细胞。结论 BMSCs能向脊髓损伤部位迁移和聚集,并分化为相应的神经细胞促进脊髓功能恢复。     

大鼠脊髓损伤松质骨神经SP免疫反应性的变化

目的：探讨脊髓损伤后大鼠松质骨中神经末梢P物质（SubstanceP,SP)免疫反应性的变化及在脊髓损伤（Spin al Cord Injury,SCI)后骨代谢变化中的意义。方法：3月龄SD大鼠60只随机均分为SCI组与对照组，SCI组于T10处完全横断脊髓；对照组仅行椎板切除术，术后1、3、6周处死动物测定血钙，碱性磷酸酶，尿钙、尿机苷；对股骨髁松质骨行SP免疫组化染色，结合计算机图像分析系统对SP免疫阳性神经的染色强度进行定量分析。结果：血尿生化结果SCI组各时间段骨吸收显著增强；分布于小梁骨内的SP阳性神经的免疫反应性在1、3周组显著增高与对照组比较差异显著。结论：SCI后松质骨内SP的增加可能与SCI早期破骨性骨吸收增强有关。     

油红O染色在大鼠脊髓损伤中的应用

目的:探讨油红O染色在评价大鼠脊髓损伤中的应用价值。方法:选取体重220～260 g的SD雄鼠24只,编号后简单随机抽样分为正常对照组与脊髓横断组,正常对照组6只,脊髓横断组18只。脊髓横断组于T₁₀节段横断脊髓。于术后1、2、4周在脊髓横断组分别随机各抽取6只处死,以横断部位为中心取脊髓组织标本。正常组取相同部位脊髓组织标本,行冰冻切片,进行油红O染色观察。结果:正常对照组大鼠脊髓白质均匀着色,与灰质有较明显的区分。脊髓横断组在术后1、2、4周时白质着色不均匀,断端液化坏死灶呈进行性扩大,油红O染色逐渐明显。结论:油红O染色能够较明显的区分白质及灰质,在一定程度上反映了白质的完整程度。断端坏死灶内油红O染色随脊髓损伤时间的延长逐渐明显反映了脂质在脊髓损伤过程中起着重要作用。