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1.
大鼠脊髓损伤后谷氨酸和天冬氨酸含量的变化及其意义   总被引:6,自引:0,他引:6  
采用Allen′s打击法,以25gcm致伤大鼠T8脊髓,于伤后10分及2、4、8、24小时取伤段脊髓,用反相高效液相色谱技术测定谷氨酸(Glu)和天冬氨酸(Asp)含量。结果显示:脊髓损伤后10分钟致伤组Glu、Asp较对照组升高74.60%(P〈0.01)和45.99%(P〈0.01)。Glu的含量在伤后8小时升高37.54%(P〈0.01),在2、24小时的含量低于正常对照组;Asp的含量在伤  相似文献   

2.
目的 探讨脑卒中急性期患者血清和脑脊液(CSF)中游离氨基酸(FAA)含量变化戌临床的关系。方法 对28例脑出血和30例脑梗死患者于急性期测定血清十种氨基酸(AA)含量,选择65例正常人作为对照组:对16例脑出血急性期患者和12例正常人测定CSF中十种AA含量。结果 (1)脑梗死组和脑出血组血清中谷氨酸(G1u)、门冬氨酸(Asp)含量显著高于对照组(P〈0.01),牛磺酸(Tau)、甘氨到(G1  相似文献   

3.
应用丹酰氯-聚酰胺薄层层析法,测定34例新生儿缺氧缺血性脑病(HIE)及30例非HIE脑脊液(CSF)和血清中谷氨酸(GLU)、天冬氨酸(ASP)水平,CSF中两种氨基酸水平显著高于对照组(P〈0.001),且其含量与HIE病情严重程度呈正相关,(r=0.72,P〈0.001),但与血清中GLU、ASP均无相关性,CSF中GLU、ASP含量测定可作为HIE诊断的一个指标。  相似文献   

4.
文中报道了观察大鼠脊髓中度损伤(50g/cm)后脊髓蛛网膜下腔注射兴奋性氨基酸(EAA)受体激动剂N-甲基-D-天冬氨酸(NMDA)对脊髓损伤后脊髓灰质血流量(SCBF)、脊髓诱发电位(SPEP)和运动诱发电位(CMEP)的影响。结果发现NMDA明显加剧脊髓损伤(SCI)后脊髓缺血和脊髓上、下行传导功能障碍。表明在脊髓损伤基础上增加EAA可加剧脊髓组织的损害,进一步证实了EAA通过激活NMDA受体  相似文献   

5.
二种牛神经肽的氨基酸分析   总被引:7,自引:5,他引:2  
用日立835-50型自动氨基酸分析仪对分离的牛神经肽1和2进行了氨基酸分析。结果表明:牛神经肽1主要含有酸性氨基酸Glu和少量的Asp;牛神经肽2主要含有酸性氨基酸Glu,Asp,少量的中性氨基酸Thr,Ser,Gly和一种未知氨基酸。提示:牛神经肽1为一种酸性牛神经肽(ABNP),暂定名为ABNP-1;牛神经肽2也是一种酸性牛神经肽(ABNP),暂定名为ABNP-2。  相似文献   

6.
胆红素脑病模型豚鼠EAA神经递质的检测   总被引:1,自引:0,他引:1  
目的 探讨胆红素神经毒性脑组织兴奋性氨基酸(EAA)神经递质变化。方法 制作胆红素脑病动物模型基础上在体脑内微透析,提取神经突触间细胞外液,HPCL检测分析天门冬氨酸(Asp),谷氨酸(Glu),甘氨酸(Gly)。结果 胆红素毒性脑组织细胞外Gly较对照组明显升高,而Asp,Glu与对照组差异不显著。结论胆红素神经毒性NMDA受体活性变化机制涉及Gly细胞外堆积,提高NMDA 体对NAA神经递质A  相似文献   

7.
测定了17例化脓性脑膜炎(化脑)和22例对照患儿脑脊液(CSF)中谷氨酸(Glu)和γ-氨基丁酸(GABA)含量的变化。结果发现:化脑患儿CSF中Glu,GABA含量及Glu/GABA值均增高,且化脑重组Glu/GABA值高于化脑轻型组。提示化脑时CSF中Clu和Glu/GABA值的增高程度与中枢神经系统功能障碍的程度有关。  相似文献   

8.
用日立83550型自动氨基酸分析仪对分离的牛神经肽1和2进行了氨基酸分析。结果表明:牛神经肽1主要含有酸性氨基酸Glu和少量的Asp;牛神经肽2主要含有酸性氨基酸Glu,Asp,少量的中性氨基酸Thr,Ser,Gly和一种未知氨基酸。提示:牛神经肽1为一种酸性牛神经肽(Acidbovineneuropeptide,ABNP),暂定名为ABNP1;牛神经肽2也是一种酸性牛神经肽(ABNP),暂定名为ABNP2。  相似文献   

9.
测定了17例化脓性脑膜炎(化脑)和22例对照患儿脑脊液(CSF)中谷氨酸(Glu)和γ-氨基丁酸(GABA)含量的变化,结果发现:化脑患儿CSF中Glu,GABA含量及Glu/GABA值均增高,且化脑重组Glu/GABA值高于化脑轻型组,提示化脑时CSF中Glu/GABA值的增高程度与中枢神经系统功能障碍的程度有关。  相似文献   

10.
兴奋性氨基酸与缺血性神经元损伤   总被引:1,自引:0,他引:1  
缺血性脑血管病是临床上的常见病、多发病。随着其发病率的逐年增加,探讨缺血性神经元损伤的发生机制,成为学者们研究的热点。有报道表明:兴奋性氨基酸(Excitatotyaminoacids,EAA)的神经毒性作用是缺血性神经元损伤的主要原因。1 EAA的正常分布和代谢EAA广泛存在于哺乳动物中枢神经系统中,起着传递兴奋性信息的作用。以谷氨酸(Glutamate,Glu)和天门冬氨酸(Asparticacid,Asp)为代表。Glu是中枢神经系统中含量最多的氨基酸,以大脑皮层和海马中含量最高[1,2]…  相似文献   

11.
Theprimarylossofneuronsresultingdirectlyfromtraumaatthetissuedamagesiteisfollowedbyasecondaryneuronalnecrosisextendingtoaconsiderabledistancefromthelesionepicenter.ThissecondaryInjurycausedmoreneuronallossthaninitialtraumaLIJ.Butthemechanismofsecondaryinjuryhasbeenelusive.Manyfactorsmaybeinvolved.Recently,theneurotoxicltyofexcitatoryamlnoacids(EAA)onneuronshasbeenrecognizedandmayplayanimportantroleinsecondaryinjury.Increasedextracellularlevelsofexcitatoryaminoacidswerefoundfollowingexperim…  相似文献   

12.
目的观察流体冲击致大鼠脑损伤后不同时相点脑组织兴奋性氨基酸(excitatory amino acids,EAA)和局部血流量(regional cerebral blood flow,rCBF)的变化,及它们在脑损伤和继发性脑损伤中的作用.方法用流体冲击装置制作中度脑损伤,氨基酸微量分析系统检测谷氨酸(glutamate,Glu)和天门冬氨酸(aspate,Asp)含量,氢清除法检测大脑局部血流量.结果中度脑损伤后rCBF明显低于伤前和正常对照组;脑组织Glu、Asp的含量在伤后30min即可见明显增加,1h有所回落,2h又有所升高,4h至6h趋于稳定.结论结果显示脑损伤后脑血流量的下降可能与氨基酸释放有着一定的关系,氨基酸大量释放可能在脑损伤和继发性脑损伤中起着主要作用.  相似文献   

13.
IntroductionWeevaluatedtheefectofNGFfolowingspinalcordinjury(SCI)bydetectingthecontentofexcitatoryaminoacids(EAA),andtoexplor...  相似文献   

14.
在大鼠脑缺血再灌注损伤实验模型上.观察、测定在脑缺血后对海马组织的兴奋性氨基酸及氧自由基的影响、结果显才缺血后GM1显著减少,诱发其细胞外谷氨酸和天门冬氨酸增高。表明脑缺血再灌注损伤与EAA的过度释放和氧自由基的产生密切相关,而GM1对大鼠脑缺血具有保护作用(P<0.01)。  相似文献   

15.
目的 研究大鼠脊髓缺血40min和再灌注4h脊髓组织兴奋性氨基酸(EAA)和细胞内Ca^2 ([Ca^2 ]i)的含量变化,及应用地卓西平马来酸盐(MK-801)对上述指标的影响。方法 SD大鼠40只,随机分为假手术组、缺血40min组、再灌注4h组、MK-801治疗组(n=10)。测定各组脊髓组织中谷氨酸(Glu)和[Ca^2 ]i含量,同时观察MK-801对上述指标的影响.结果 缺血40min组Glu含量明显降低,再灌注4h组Glu含量降低更明显;[Ca^2 ]i的含量在缺血40min组时有所升高,再灌注4h组则明显升高,MK-801组能显著升高Glu含量和降低[Ca^2 ]i的含量.结论 EAA的兴奋性神经毒性在脊髓缺血再灌注中发挥着重要的作用,MK-801对该神经毒性有明显的抑制作用。  相似文献   

16.
目的:观察腺苷对脊髓损伤后细胞外液兴奋性氨基酸(EAA)的影响,研究腺苷脊髓损伤后的神经保护机制。方法:腹侧压迫损伤法造成大鼠脊髓T13中度损伤,用微透析法收集伤前15min和伤后即刻,15,30,45min脊髓T13的细胞外液。治疗组伤后立即灌注非特异笥腺苷受体激动剂2-氯腺苷(2-CADO,0.1mmol/L)。采用高效液相色谱仪荧光检测法检测透析液中谷氨酸和天门冬氨酸含量。  相似文献   

17.
Objective To detect the effect of excitatory ammo add (EAA) in the secondary damage following spinal cord injury (SCI). Methods Glutamate (Glu) and Aspartate (Asp) on the injury site (T8) were studied using a rat SCI model induced by Allen's weight drop method (10g×2. 5cm). The result suggested that Asp and Glu were significantly increased in 10 mm. Results Glu was significantly decreased from 2 h to 24 h,while Asp was a tittle reduced in 2 h,and slightly rose in 4 h as compared with Control Group. Though elevated in 8 h,it dropped again in 24h as compared with Control Group. Conclusion The result indicates that the rise of EAA following SCI could be the cause of the secondary spinal cord damage.  相似文献   

18.
目的 探讨急性脊髓损伤后脑脊液中兴奋性氨基酸含量变化与脊髓功能恢复的关系及其对预后的影响。方法 采用氨基酸自动分析仪检测32例急性脊髓损伤患者脑脊液(CSF)中天门冬氨基酸(Asp)和谷氨酸(Glu)在损伤后不同时段的含量变化。结果 天门冬氨基酸(Asp)和谷氨酸(Glu)在损伤后16h达到高峰,24h后开始逐渐下降;兴奋性氨基酸在损伤后高峰越早,升高得越多,脊髓损伤越严重;CSF中兴奋性氨基酸含量升高越高、持续的时间越长,脊髓功能恢复越差。结论 CSF中兴奋性氨基酸含量是脊髓损伤的敏感指标,可以作为早期预测脊髓损伤程度和判断其预后的指标之一。  相似文献   

19.
Excitatoryaminoacidonsecondaryspinalcordinjury:effectanmechanism¥(叶晓健)(李家顺)(王家林),(李明)YeXiaojian,LiJiashun,WangJialinLiMing(De...  相似文献   

20.
Excitatory amino acids (glutamate, aspartate) play an important role in the ischemic cascade leading to cell death. The N-methyl-D-aspartate (NMDA) receptor is an excitatory amino acid (EAA) receptor, and NMDA receptor antagonists have been shown to exert a neuroprotective effect in central nervous system ischemia. The purpose of this study was to investigate the effects of noncompetitive NMDA receptor antagonists MK-801 and to observe the changes in EAAs after spinal cord ischemia in a rabbit model. Spinal cord ischemia was induced by clamping the infrarenal abdominal aorta for 24 min. Group 1 (n = 6) received no pharmacologic infusion. Group 2 (n = 5) was administered an intra-aortic hypothermic MK-801 (1 mg/kg) solution and group 3 (n = 6) was administered an intra-aortic normothermic MK-801 (2 mg/kg) solution immediately after clamping of the abdominal aorta. We evaluated the neurological function at 12, 24 and 48 hrs after spinal cord ischemia. A histopathologic study was carried out 72 hrs after spinal cord ischemia, and the results for groups 1 and 3 were compared. The glutamate and aspartate levels in the blood plasma were compared at pre-ischemia and at 12, 24, and 48 hrs among the groups. The perfusion of a normothermic MK-801 (2 mg/kg) solution significantly reduced the neurological dysfunction and the neuronal damage. There was a significant increase in aspartate at 24 and 48 hrs in group 1, but no such increase in glutamate occurred in groups 1 and 3. In conclusion, these data provide the evidence that therapeutic intervention with MK-801 (2 mg/kg) in the early period of spinal cord ischemia is beneficial in reducing neurological dysfunction and neuronal damage.  相似文献   

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