脊髓血供及其监测研究

本文主要对脊髓的血供及目前的用于监测脊髓血供的方法和未来可能应用的新技术做一个综述,旨在协助临床脊柱外科医生能更好地对脊髓血供进行监测,预防脊髓缺血的发生,减少脊髓缺血所引起的损伤。     

自血光量子疗法治疗兔脊髓损伤的血气变化

36只家兔所做的动物实验,其中24只家免造成脊髓损伤.通过血气分析,发现伤后家兔的动、静脉血都出现了氧分压(PO_2)、氧饱和度(O_2sat)及氧含量(O_2ct)的明显降低.经自血光量子疗法治疗后,PO_2、O_2sat及O_2ct有明显提高.而PH及五项代谢性指标无明显变化.提示自血光量子疗法能改善组织缺氧状态、加强缺血组织的血液供应,提高脊髓的血流量,促进其功能恢复.     

New Minimally Invasive Model of Spinal Cord Ischemia in Rats

We developed a new minimally invasive model of spinal cord ischemia in rats: intravascular occlusion of the abdominal aorta and its branches. This model can be used on small laboratory animals and allows qualitatively and quantitatively evaluating the morphofunctional state of the nervous system during spinal cord ischemia by clinical manifestations and histological changes. Selective intravascular occlusion determines minimal invasiveness and adequacy of the proposed model to in vivo pathological processes. This model of spinal cord ischemia can be used in experimental pharmacology for evaluation of neuroprotective activity of various drugs and bioactive substances.     

实验性脊髓损伤模型的研究进展

脊髓损伤是一种致残率很高的疾病,建立理想的脊髓损伤模型对于实验研究尤为重要。挫伤型脊髓损伤模型接近人类脊髓损伤的病理生理特点及变化规律,但忽略了持续性的挤压作用;压迫型脊髓损伤模型为非瞬间损伤,便于进行神经功能和代谢改变的检测;锐性脊髓损伤模型适于进行再生性实验研究,但与临床之间相关性差;脊髓缺血及再灌注损伤模型尚不能满足临床治疗的需要。本综述对常用的脊髓损伤动物模型进行总结对比,为进一步研究和完善脊髓损伤模型提供参考。     

有限元分析法在脊髓损伤生物力学中的研究进展

脊髓损伤时的变化非常复杂,动物模型很难精确模拟损伤环境以及测量局部组织的生物力学属性,而有限元模型则可以通过分析脊髓组织的应力和应变分布,从生物力学角度为脊髓损伤的病理研究和治疗提供一个更为高效的方法。目前,有限元模型已被广泛应用,并与动物实验模型相辅相成。本文回顾了有限元法在脊髓损伤中的研究进展,对有限元法在脊髓本体建模、脊髓损伤的生物力学行为及其临床应用等方面的研究现况进行归纳及总结,以期为临床脊髓损伤问题提供更为全面的理论参考。     

Effect of Epidural Injection of Prosidol with Clonidine on the State of Spinal Cord and Spinal Ganglion

Morphological and histoenzymatic changes in cells of the spinal cord and spinal ganglia after epidural injection of a combination of prosidol with clonidine were studied on dogs. No pathological structural and metabolic changes in the nervous tissue were found after combined treatment with the test drugs. Higher activity of nucleic acids and alkaline phosphatase in spinal neurons and spinal ganglion in experimental animals in comparison with those in controls indicates intensification of protein synthesis and active transport in the endothelium of nerve tissue capillaries, which is a favorable factor.     

Morphofunctional Changes in Spinal Cord Neurons After Epidural Lidocaine

Morphofunctional and histoenzymological changes in spinal cord neurons of mongrel dogs were studied after epidural administration of isobaric 2% lidocaine solution. Control animals received epidural 0.9% sodium chloride. The results obtained from these studies provide evidence for the absence of pathological structural-metabolic changes in nerve tissue after treatment with lidocaine. The occurrence of certain morphofunctional rearrangements in spinal cord neurons were typical of animals of both the experimental and control groups. The changes recorded varied within the limits of physiological variation and provided evidence predominantly of the functional response of these nerve tissue structures to epidural injections of both sodium chloride and lidocaine.     

紫外线照射充氧自血回输对家兔脊髓损伤后血液循环的影响

家兔用改良Allen 氏系统造成不完全性脊髓损伤,随机分为对照组、损伤组和治疗组。分别测定血液和脊髓组织TXB 2、 6-keto-PGF 1 a 和ET-1 含量;以及脊髓组织灰质、白质和总血流量,研究紫外线照射和充氧自血回输疗法（UBIO）治疗脊髓损伤的作用机制。实验发现：损伤组血液和脊髓组织TXB 2 含量升高、6-keto-PGF 1 a 含量下降、ET-1 含量升高。脊髓组织灰质和白质血流量以及脊髓组织总血流量均下降。治疗组用UBIO 治疗后,血液和脊髓组织TXB 2 含量下降、6-keto-PGF 1 a 含量升高、ET-1 含量下降。脊髓组织灰质和白质血流量以及脊髓组织总血流量均上升。实验说明：UBIO 可以改善全身和脊髓组织的血液循环。     

干细胞移植治疗脊髓损伤的实验研究进展

目的:探讨脊髓损伤后干细胞移植对神经功能恢复的作用机制及临床疗效.方法:检索国内外报道的实验大鼠脊髓损伤造模后干细胞移植的相关文献,对实验结果进行综合分析,评估大鼠神经功能恢复效果.结果:胚胎干细胞、神经干细胞、骨髓间充质干细胞、许旺细胞、嗅鞘细胞移植到受损脊髓实验大鼠后可分化成不同功能类型的神经细胞,能释放促进宿主神经元再生的营养因子,重建轴突的连续性.结论:脊髓损伤后干细胞移植可重建脊髓神经传导的连续性,预示着干细胞在脊髓损伤的治疗中具有良好的应用前景.     

大鼠脊髓压迫损伤后COX-2基因和蛋白的表达

目的观察大鼠脊髓压迫损伤后COX-2mRNA和蛋白在脊髓组织内表达的时间特征,以及COX-2的空间分布特点。方法以压迫装置致脊髓损伤后,在伤后不同时间点(30min、3h、6h、24h、72h、1w)分别应用RT-PCR、Western blotting、免疫组化技术检测COX-2mRNA和蛋白表达和分布。结果RT-PCR和Western blotting显示,COX-2mRNA和蛋白伤后30min表达开始增加,于伤后6h达到峰值,伤后1w表达接近基础水平。免疫组化提示,COX-2蛋白在假手术组表达仅见于脊髓血管内皮细胞,伤后COX-2蛋白表达见于损伤区附近脊髓灰质内的神经元和血管内皮细胞,损伤中心部位COX-2免疫阳性细胞少见。结论脊髓压迫损伤早期可快速诱导COX-2基因的表达上调和蛋白的合成,伤后COX-2蛋白分布发生变化,主要位于脊髓神经元和血管内皮细胞。     

Effects of Spinal Cord Electrical Stimulation in Patients with Vertebrospinal Pathology

Until now, no scientific neurophysiologic methods of diagnostics and treatment of vertebrospinal pathologies were developed. Previous study showed that electrical stimulation of lumbar segments of the spinal cord in animals with complete spinal cord transection induced a well-coordinated weight-bearing locomotion. The present comparative study of motor activity triggered by electrical epidural stimulation of one or two segments of the spinal cord in spinal patients showed that stimulation of lumbar (L2-L4) or sacral (S2) segments facilitated generation of motor patterns of muscle activity. Combination of electrical stimulation with locomotor training resulted in the appearance of stepping patterns characteristic of normal walking and tonic activity of the muscles needed for body balance maintenance.     

人胎脊髓内源性物质对脊髓中GABA神经元的营养作用

目的:从人胎脊髓提取液中寻找对脊髓GABA神经元有神经营养作用的成分。方法:用四月龄人胎制备脊髓提取液,加人体外培养的胎鼠脊髓细胞中,观察提取液对神经元活性、突起生长和分化的影响。结果:人胎脊髓中有提高GABA神经元活性的营养成分,并且小于10kD组分还可以诱导GABA神经元的分化,但是提取液对GABA神经元的突起生长没有影响。结论:实验结果揭示人胎脊髓中可能存在不止一种神经营养活性成分,对GABA神经元的活性和分化起营养作用。     

脊髓半横断损伤后trkB基因表达的变化

脊髓损伤后期trkB的变化及作用仍不清楚,本实验建立脊髓半横断损伤模型（hSCI）,术后14天取损伤脊髓用定量PCR测定trkB表达水平。结果显示,与假手术组比较,损伤脊髓trkB mRNA水平明显下调。推测trkB减少可能是不利于修复的因素之一,值得重视。     

丹参对脊髓损伤后伤区血流量及血液流变学指标的影响

目的 :比较应用丹参对兔脊髓损伤 (SCI)后伤区血流量及血液流变学指标的影响 ,探讨丹参对脊髓损伤的保护机制。方法 :5 8只成年日本大耳白兔 ,随机分成四组 ,A组 10只 ,作为正常组 ;B、C、D组各 16只 ,分别作对照组、地塞米松 (Dex)治疗组和丹参治疗组。比较脊髓损伤前后及应用Dex、丹参治疗后伤区血流量 (SCBF)及血液流变学指标的变化。结果 :脊髓损伤后 ,SCBF下降 ,血液粘度(ηb)、纤维蛋白原 (Fib)、细胞聚集指数 (RAI)增高。Dex对脊髓SCBF和血液流变学指标异常的改善不明显 ,而使用丹参治疗后 ,脊髓SCBF增高 ,血液流变学指标明显改善。结论 :丹参对脊髓损伤具有保护作用 ,且疗效较Dex明显 ,为临床治疗提供依据。     

Immunohistochemical Study of Netrin-1 in the Spinal Cord with Rat Experimental Autoimmune Encephalomyelitis

To investigate whether netrin-1 is involved in autoimmune injury of the central nervous system, the expression of netrin-1 protein was analyzed in the spinal cord of Lewis rats with experimental autoimmune encephalomyelitis (EAE). Western blot analysis revealed significantly increased content of netrin-1 in the spinal cords of rats at the peak stage of EAE, as compared with the levels in normal control animals (p < 0.01). Immunohistochemistry detected the netrin-1 protein in neurons, oligodendrocytes, astrocytes and vascular endothelial cells in the spinal cords of normal controls. In EAE-affected spinal cords, netrin-1 immunoreactivity was detected in infiltrating inflammatory cells at the peak stage as well as in neurons, oligodendrocytes and astrocytes. These results suggest that netrin-1 is transiently increased in rat EAE lesions, where it contributes to the modulation of rat acute EAE.     

BDNF及其受体TrkB在成年恒河猴脊髓的表达

目的观察脑源性神经营养因子BDNF及其高亲合力受体TrkB在成年恒河猴胸髓的表达分布,为成年恒河猴脊髓BDNF、TrkB的功能研究提供形态学依据。方法灌注固定成年雄性恒河猴,取其胸段脊髓制作冰冻切片,用BDNF、TrkB特异性抗体行免疫组织化学SP法染色,观察BDNF、TrkB免疫阳性物质在胸段脊髓的分布。结果成年恒河猴胸髓内均可见BDNF、TrkB免疫反应阳性神经元,反应产物呈棕黄色颗粒。BDNF和TrkB免疫反应阳性细胞遍及胸髓灰质各板层,在腹角、侧角以及中央管邻近区域均可见阳性神经元,它们的阳性产物主要定位于神经元胞浆中,胞浆着色深,胞浆与胞核的界线清楚。BDNF免疫反应细胞的胞核未见染色,而不同的TrkB阳性细胞其胞核染色不一。结论成年恒河猴胸髓存在BDNF、TrkB的表达,其作用可能与猴脊髓的正常生理功能和损伤后的修复有关。     

Alteration of Glial Fibrillary Acidic Proteins Immunoreactivity in Astrocytes of the Spinal Cord Diabetic Rats

Diabetes affects retinal and nervous glial cells, especially the astrocytes. A key indicator of this response is the alteration in the level of intermediate filament glial fibrillary acidic protein (GFAP) and number of GFAP‐immunoreactive astrocytes. To date, no study has investigated the effect of diabetes on the distribution of GFAP‐immunoreactive astrocytes in the spinal cord. Therefore, the present study investigated the effect of diabetes on the number of GFAP‐immunoreactive astrocytes in the gray matter of the spinal cord of streptozotocin‐induced diabetic Wistar rats. Animals were divided into six groups (n = 7); 6 weeks and 12 weeks diabetic duration groups and their respective age‐matched normal control and sham control groups. Our results demonstrated a significant (P < 0.001) decrease in the number of GFAP‐immunoreactive astrocytes in different areas of the spinal cord sections of the 6 weeks and 12 weeks long diabetic rats when compared with the spinal cord of normal and sham control groups of comparable age. The mean percentage in total number of GFAP‐immunoreactive astrocytes in the whole gray matter areas of the spinal cord of the 6 and 12 weeks diabetic groups were approximately 28% and 41% less than control groups. Furthermore, the 12 weeks diabetic group showed a significant (P < 0.001) reduction in the number of GFAP‐immunoreactive astrocytes when compared with the 6 weeks diabetic animals. These results suggest that the induction of diabetes is associated with a reduction in GFAP‐positive astrocytes in the spinal cord, which may affect the functional support and role of astrocytic cells in the nervous tissue. This in turn may contribute to the pathological changes associated with diabetic state in the central nervous system. Anat Rec, 291:390–399, 2008. © 2008 Wiley‐Liss, Inc.     

Calpain Activity in Spinal Cord Cells from Rats with Experimental Allergic Encephalomyelitis of Different Grades

The Ca²⁺-dependent calpain system of intracellular proteases is involved in regulating a multitude of physiological body functions. However, hyperactivation of calpains in cells is observed during the development of a number of responses, and this leads to impairment to the functioning of vitally important physiological systems. We report here our use of a model of experimental allergic encephalomyelitis (EAE) to demonstrate that cell homogenates from different parts of spinal cord show hyperactivation of calpains and that calpain proteolytic activity increases with the severity of EAE; this occurred not only in the lower, but also in the upper parts of the spinal cord. As CNS cells from animals with EAE showed increases in the levels of mRNA for m- but not for μ-calpain, this hyperactivation would appear to be mediated more by m-calpain. The relationship between the distribution of m-calpain hyperactivation in different parts of the spinal cord with the severity of EAE is consistent with data on the volume of neurological destruction of the CNS, suggesting that m-calpain is involved in the processes initiating neuron and cell death during the development of this disease.