急性脑梗死患者血浆内神经元特异性烯醇酶的变化：病例对照

BACKGROUND： The plasma level of neuron specific enolase （NSE） can be used to diagnose and evaluate neuronal injury and predict early prognosis.
OBJECTIVE： To observe the dynamic changes in plasma levels of NSE in patients with acute cerebral infarction, and to investigate its correlations with disease severity and prognosis.
DESIGN, TIME AND SETTING： This non-randomized, concurrent case-control experiment was performed at the Department of Neurology, First Hospital Affiliated to Heilongjiang University of Traditional Chinese Medicine between May and July 2007. PARTICIPANTS： Eighteen patients with acute cerebral infarction, who received treatment at the Department of Neurology, First Hospital Affiliated to Heilongjiang University of Traditional Chinese Medicine between May and July 2007, were recruited into the patient group. An additional 10 healthy individuals, who received health examinations simultaneously, were included as controls.
METHODS： Following admission （within 3 days） and at days 6, 12, and 30 subsequent to acute cerebral infarction attack, 3 mL venous blood was taken from each patient before the morning meal to determine the plasma level of NSE by enzyme-labeled immunosorbent assay. One-time blood extraction was performed in each healthy subject during the health examination for the same purpose as in patients. At 6 and 30 days following acute cerebral infarction attack, CT examination was performed for calculation of cerebral infarction volume according to the Tada formula. Following admission and at 30 days of disease invasion, all patients were scored by the National Institutes of Health Stroke Scale （NIHSS, 13 items）.
MAIN OUTCOME MEASURES： Comparison of NSE plasma level between acute cerebral infarction patients and healthy individuals; correlations of NSE plasma level in acute cerebral infarction patients with cerebral infarction volume, NIHSS score, and prognosis.
RESULTS： Following admission and at days 6 and 12 of disease invasion, the plasma level of NSE was significantly higher in the patient group than in the control group （P 〈 0.05）. Following admission and at day 30 of disease invasion, the NIHSS scores of the patient group were 17.706 and 11.222, respectively. Following admission and at day 6 of disease invasion, the plasma level of NSE was positively correlated with cerebral infarction volume （r = 0.503, 0.435, P 〈 0.05）, but it was negatively correlated with NIHSS score （r = -0.571, 0.368, P 〈 0.05）. The plasma level of NSE was mostly correlated with cerebral infarction volume, followed by NIHSS score, and lastly prognosis, with regression coefficients of 0.386, 0.343, and 0.340, respectively.
CONCLUSION： The plasma level of NSE is higher in patients with acute cerebral infarction than in the healthy population. It can reflect infarct severity and predict early prognosis of acute cerebral infarction.     

Neuronal apoptosis in cerebral ischemia/reperfusion area following electrical stimulation of fastigial nucleus

Previous studies have indicated that electrical stimulation of the cerebellar fastigial nucleus in rats may reduce brain infarct size, increase the expression of Ku70 in cerebral ischemia/ reperfusion area, and decrease the number of apoptotic neurons. However, the anti-apoptotic mechanism of Ku70 remains unclear. In this study, fastigial nucleus stimulation was given to rats 24, 48, and 72 hours before cerebral ischemia/reperfusion injury. Results from the electrical stim- ulation group revealed that rats exhibited a reduction in brain infarct size, a significant increase in the expression of KuT0 in cerebral ischemia/reperfusion regions, and a decreased number of terminal deoxynucleotidyl transferase dUTP nick end labeling （TUNEL）-positive cells. Double immunofluorescence staining revealed no co-localization of Ku70 with TUNEL-positive cells. However, Ku70 partly co-localized with Bax protein in the cytoplasm of rats with cerebral ischemia/reperfusion injury. These findings suggest an involvement of Ku70 with Bax in the cy- toplasm of rats exposed to electrical stimulation of the cerebellar fastigial nucleus, and may thus provide an understanding into the anti-apoptotic activity of KuT0 in cerebral ischemia/reperfu- sion injury.     

Electrical stimulation of the vagus nerve protects against cerebral ischemic injury through an anti-inflammatory mechanism

Vagus nerve stimulation exerts protective effects against ischemic brain injury; however, the underlying mechanisms remain unclear. In this study, a rat model of focal cerebral ischemia was established using the occlusion method, and the right vagus nerve was given electrical stimulation(constant current of 0.5 m A; pulse width, 0.5 ms; frequency, 20 Hz; duration, 30 seconds; every 5 minutes for a total of 60 minutes) 30 minutes, 12 hours, and 1, 2, 3, 7 and 14 days after surgery. Electrical stimulation of the vagus nerve substantially reduced infarct volume, improved neurological function, and decreased the expression levels of tumor necrosis factor-α and interleukin-6 in rats with focal cerebral ischemia. The experimental findings indicate that the neuroprotective effect of vagus nerve stimulation following cerebral ischemia may be associated with the inhibition of tumor necrosis factor-α and interleukin-6 expression.     

Antileukocyte therapy of cerebral ischemic stroke in MCAO model in rats

OBJECTIVE To Study protecting effect of antileukocytic drugs on cerebrol ischemic injury. BACKGROUND The purposes of prcsent study aimed at comparing the protecting effect of some antileukocytic drugs: chloroquine, Colchieine, Cyclophosphamid (CTX) ,Cyclosporin A, Multiglycoside tripteygil against cerebral ischemic injury in MCAO models in the rats. METHODS 130 SD rats with MCAO model randomly divided into one control group and 10 treatment groups. The observation items were as follows: (1) The infarction volume. (2) Brain edema. (3) Histopathoiogical evaluation. (4) The count of neurons and microglia cells in the infarction area. (5) Neurological dysfunction score. (6) The determination of serum lL-1 β and TNF- α levels. RESULTS Antileukocytic drugs can decrease the volume of infarction, brain edema, inflammatory reaction and neuron death of ischemic injury, the low dose of chloroquine plus colchicine plus CTX had better effects, and prolonged therapeutic time windows. DISCUSSION The accumulation of infiammatory cell and cytoking release from them can promote and increase neuron death in infarction area. CONCLUSION Antileukocytic drugs are of protecting effect on ischemic neuron in MCAO model in rats.     

Effect of extracranial electric stimulation at cerebellar fastiglal nucleus on serum C-reactive protein of patients with acute cerebral infarction

BACKGROUND: Some reports indicate that electric and/or chemical stimulation at various brain sites of experimental animals can raise regional cerebral blood flow and improve cerebral circulation; however, its mechanism is still unclear. OBJECTIVE: To observe the effects of electric stimulation at cerebellar fastigial nucleus on serum C-reactive protein of patients with acute cerebral infarction. DESIGN: Non-randomized synchronized contrast study. SETTING: The Second People's Hospital of Xinxiang City. PARTICIPANTS: A total of 54 patients with acute cerebral infarction were selected from the Department of Neurology, the Second People's Hospital of Xinxiang from December 2005 to December 2006. There were 31 males and 23 females, and their ages ranged from 56 to 80 years. All patients met the diagnostic criteria of the Fourth National Cerebrovascular Academic Meeting, were finally diagnosed by using CT examination, and provided the confirmed consent. Based on therapeutic demands, patients were divided into electric stimulation group and routine treatment group with 27 cases in each group. In addition, 21 healthy subjects, including 11 males and 10 females and aging 53–78 years, were selected as the control group. All the subjects in the control group did not have any histories of cerebrovascular diseases and severe body diseases. METHODS: Based on routine drug therapy, patients in the electric stimulation group were also treated by using CVFT-010M cerebral circulation function therapeutic device (made in Shanghai). Electrode was fixed at bilateral mastoid in the first group and at extensible sides of upper limbs in the second group. Electric stimulation was given twice a day and lasted for 30 minutes each time. Ten days were regarded as a course. Parameters of device: mode Ⅲ, frequency 198%, and intensity 90%–110% (bionic current). Patients in the routine treatment group received the routine drug treatment. Content of serum C-reactive protein was measured in both electric stimulation group and routine treatment group before treatment and at 20 days after treatment, while in the control group on the exact day of health examination by using immunization. MAIN OUTCOME MEASURES: Level of serum C-reactive protein in the three groups. RESULTS: All 54 patients with acute cerebral infarction and 21 healthy subjects were involved in the final analysis. Level of serum C-reactive protein was higher in both electric stimulation group and routine treatment group than that in the control group before treatment (P < 0.01). While, level of serum C-reactive protein was lower in the electric stimulation group than that in the routine treatment group after electric stimulation at cerebellar fastigial nucleus (P < 0.01). CONCLUSION: Electric stimulation at cerebellar fastigial nucleus can decrease level of serum C-reactive protein in patients with acute cerebral infarction, and this may be one of the therapeutic mechanisms for curing acute cerebral infarction.     

急性动脉粥样硬化性脑梗死患者血清脑红蛋白水平的意义

This study sought to examine neuroglobin (NGB) in the serum of acute cerebral infarction patients with double-antibody sandwich enzyme-linked immunosorbent assay to identify all risk factors, calculate infarct size, assess neurological impairment, and analyze the relation between NGB and each of these factors. The double-antibody sandwich assay indicated that levels of NGB in serum were unaltered within 6 hours following acute cerebral infarction compared with normal levels. NGB levels then underwent a distinct change, peaking at 24 hours then returning to normal levels in 72 hours. The results suggest that the level of NGB might be related to infarct size and low-density lipoprotein at 24 hours after acute cerebral infarction. There were no significant differences in neurological impairment scores and infarct size at different periods following infarction. The findings indicated that the level of NGB in serum of acute cerebral infarction patients was correlated with infarct time.     

不同波形强度低频电刺激局灶性脑缺血大鼠颈部同体质量、肝肾功能及死亡率的变化

Low-frequency electrical stimulation has resulted in favorable effects in the treatment of post-stroke dysphagia.However,the safety of cervical low-frequency electrical stimulation remains unclear because of numerous nerves and blood vessels in the neck.In the present study,rats with ischemic stroke underwent low-frequency electrical stimulation,and systemic and local effects of electrical stimulation at different densities and waveforms were investigated.Electrical stimulation resulted in no significant effects on body mass,liver or kidney function,or mortality rate.In addition,no significant adverse reaction was observed,despite overly high intensity of low-frequency electrical stimulation,which induced laryngismus,results from the present study suggested that it is safe to stimulate the neck with a low-frequency electricity under certain intensities.     

Is longer sevoflurane preconditioning neuroprotective in permanent focal cerebral ischemia?

Sevoflurane preconditioning has neuroprotective effects in the cerebral ischemia/reperfusion model. However, its influence on permanent cerebral ischemia remains unclear. In the present study, the rats were exposed to sevoflurane for 15, 30, 60, and 120 minutes, followed by induction of perma-nent cerebral ischemia. Results demonstrated that 30-and 60-minute sevoflurane preconditioning significantly reduced the infarct volume at 24 hours after cerebral ischemia, and 60-minute se-voflurane preconditioning additionally reduced the number of TUNEL-and caspase-3-positive cells in the ischemic penumbra. However, 120-minute sevoflurane preconditioning did not show evident neuroprotective effects. Moreover, 60-minute sevoflurane preconditioning significantly attenuated neurological deficits and infarct volume in rats at 4 days after cerebral ischemia. These findings in-dicated that 60-minute sevoflurane preconditioning can induce the best neuroprotective effects in rats with permanent cerebral ischemia through the inhibition of apoptosis.     

丁基苯酞加强造血干细胞移植及内源性干细胞动员治疗脑梗死的效应

Exogenous stem cell transplantation and endogenous stem cell mobilization are both effective for the treatment of acute cerebral infarction. The compound dl-3-butylphthalide is known to improve microcirculation and help brain cells at the infarct loci. This experiment aimed to investigate the effects of dl-3-butylphthalide intervention based on the transplantation of hematopoietic stem cells and mobilization of endogenous stem cells in a rat model of cerebral infarction, following middle cerebral artery occlusion. Results showed that neurological function was greatly improved and infarct volume was reduced in rats with cerebral infarction. Data also showed that dl-3-butylphthalide can promote hematopoietic stem cells to transform into vascular endothelial cells and neuronal-like cells, and also enhance the therapeutic effect on cerebral infarction by hematopoietic stem cell transplantation and endogenous stem cell mobilization.     

脑血管病患者CGRP的临床研究

目的：1．观察脑出血（CH）、脑梗死（CI）患者降钙素基因相关肽（CGRP）水平改变及其动态变化;2观察CH、CI病情、病灶大小与CGRP水平变化的关系;3．研究CGRP与脑血管病（CVI））伴发疾病的关系;4．探讨CGRP参与各型CVD及其伴发病中的病理生理机制及其临床意义,并探讨其异常分泌的可能机制;5探讨CVD防治的新途径。方法：选择CVD1I8例,其中CH组46例．CI组62例。用放免法检测血浆CGRP浓度。结果：1．CI组CGRP的变化：显著低于对照组,发病24h内即显著降低,2～3d与4～7d则进一步降低,8～15d开始升高,15d后逐渐升至正常水平。伴发病积分＞6分组显著低于＜6分组,高血糖组显著低于正常血糖组。2．CH组CGRP的变化：显著低于对照组．发病24h内即显著降低,2～3d与4～7d进一步降低,8～15d有所升高,15d后进一步升高,仍低于正常水平。随病情加重,脑出血量增加,CGRP水平明显降低。结论：l．CICH患者存在CBRP分泌异常,CGRP参与了CVD的病理生理过程。2．各组CVD、CGRP动态检测可作为病情严重程度、病灶大小及预后的重要指标。3．本研究结果提示,调整CGRP的分泌将有助于改善各组CVD的预后．并为应用CGRP治疗缺血性脑损伤提供了广阔的前景。     

脑梗死患者血液和脑脊液NSE质量浓度测定及其临床意义的相关性研究

目的　观察急性期和恢复期脑梗死患者血液和脑脊液的神经元特异性烯醇化酶 (neuron-specific enolase,NSE)质量浓度变化 ,探讨其与神经功能缺损程度、脑梗死体积、颅内压以及患者年龄等方面的相关性。方法　该实验采用酶联免疫吸附法 (enzyme-linked immunosorbent assay,ELISA) ,检测观察组 (4 6例 )、对照组 (2 5例 )血液及脑脊液 NSE质量浓度 ,并应用 SPSS1 0 .0统计软件包进行统计学分析。结果　急性脑梗死 (acute cere-bralinfarction,ACI)患者血液和脑脊液 NSE质量浓度显著高于恢复期患者和对照组 (P <0 .0 1 ) ;ACI患者脑脊液 NSE质量浓度显著高于血液 (P <0 .0 1 ) ;血液和脑脊液 NSE质量浓度与梗死体积均呈显著正相关 (P <0 .0 1 ) ,与出院时神经功能缺损程度呈显著正相关 (P <0 .0 1 )。结论　脑脊液或血清中的 NSE质量浓度是脑组织破坏后较合适的生化标记物 ,有助于判断脑梗死患者梗死范围、监测病情变化及疗效观察。     

Caspase-1抑制剂对大鼠局灶脑缺血再灌注后神经元损伤的影响

目的：研究YVAD-FMK(Caspase-1抑制剂)对大鼠局灶脑缺血再灌注后神经元损伤的影响。方法：采用大鼠局灶脑缺血再灌注模型,动态测量脑组织中IL—1β含量、脑含水量及血清NSE含量的变化以及YVAD-FMK对上述指标的影响。结果：YVAD-FMK能够减少脑组织IL-1β的含量,减轻脑水肿及能显著降低血清NSE升高的幅度。结论：YV4D-FMK对局灶脑缺血再灌注后神经元的损伤具有保护的作用。     

神经元特异性烯醇化酶在急性脑梗死治疗中的临床价值

目的　探讨急性脑梗死患者血清神经元烯醇化酶 (NSE)对梗死灶大小和临床预后的评估价值。方法　采用酶联免疫吸附法 (ELISA)检测 62例急性脑梗死患者第 1、 3、 7d血清NSE水平 ,并分析与梗死灶大小及临床预后的关系。结果　急性脑梗死患者血清NSE浓度在起病第 1、 3d显著高于对照组 (P <0 0 1) ,第 3d达峰值 ,且与梗死灶大小及临床预后有显著相关性。结论　血清NSE变化对准确反映脑梗死患者的严重程度及预后的评估有重要价值。     

The effects of acute and chronic lipopolysaccharide infusion in rats on the efferent function of sensory nerves in the isolated mesenteric arterial bed

Capsaicin-sensitive sensory neurons are stimulated by noxious stimuli, and may be activated in endotoxaemia. The present study investigated the acute and chronic effects of lipopolysaccharide upon the efferent function of these nerves. Conscious rats received infusion (i.v.) of lipopolysaccharide (150 microg kg(-1) h(-1)) or saline for 2 or 24 h. Following infusion, animals were killed and the mesenteric arterial bed isolated and perfused with Krebs' solution. Electrical field stimulation of capsaicin-sensitive sensory nerves was investigated. Postjunctional mechanisms of sensory neurotransmission were examined using calcitonin gene-related peptide, and endothelial and smooth muscle function assessed using acetylcholine and sodium nitroprusside, respectively. All preparations exhibited dose dependency to the agonists, and frequency dependency to electrical field stimulation. No significant differences were observed between the four groups (2-h saline, 24-h saline, 2-h lipopolysaccharide and 24-h lipopolysaccharide) with regard to responses to electrical field stimulation, acetylcholine, sodium nitroprusside or calcitonin gene-related peptide. Thus, the efferent function of capsaicin-sensitive sensory nerves is unaltered in the isolated mesenteric arterial bed prepared ex vivo from rats receiving lipopolysaccharide, either acutely (2 h) or chronically (24 h).     

神经元特异性烯醇酶与急性脑梗死

目的：探讨急性脑梗死患者血清神经元特异性烯醇酶（NSE）的变化及其临床意义。方法：采集69例脑梗死患者起病3天内的血标本,用酶联免疫分析法测定血清NSE含量（其中35例2周时复测）。结果脑梗死3天内血清NSE明显高于对照组及2周时（P＜0．001）,血清NSE含量与梗死灶大小,神经功能缺损程度明显正相关（P＜0．001）,与意义障碍明显负相关（P＜0．001）,临床疗效赵差血清NSE含量越高（P＜0．001）。结论：脑梗死早期血清NSE明显升高,血清NSE含量与临床表现关系密切。     

亚低温对大鼠迟发性脑血管痉挛降钙素基因相关肽mRNA表达变化的影响

目的探讨亚低温防治蛛网膜下腔出血(SAH)脑血管痉挛(CVS)的作用机制。方法将60只Wistar大鼠随机分为对照组和亚低温组,两组分别于注血前及注血后30 min及2、3、71、4 d应用逆转录-聚合酶链反应(RT-PCR)检测各组动物脑基底节区降钙素基因相关肽(CGRP)mRNA的表达。结果对照组SAH后2、3d脑基底节区CGRP mRNA表达较注血前及注血后30 min明显降低(P<0.01),7 d时仍降低(P<0.01),14 d时趋于正常(P>0.05)。亚低温组具有相同的变化趋势,且注血后30 min及2、3、7 d时CGRP mRNA的表达均较对照组增高(P<0.05,P<0.01)。结论亚低温可能通过促进CGRP mRNA表达上调而达到防治SAH后CVS的作用。     

115例脑卒中患者血清神经元特异性烯醇化酶测定及其意义

目的 研究脑卒中时血清神经元特异性烯醇化酶（NSE）的变化及与神经功能缺损的关系。方法 脑出血46例,脑梗死69例,正常对照21例,患者分别在起病3d内及2周时采集血标本。血清NSE测定采用酶联免疫分析方法,神经功能缺损评定按斯堪的纳维亚卒中量表（SSS）标准进行,结果 脑梗死,脑出血组3d内及起病2周时血清NSE明显高于正常对照组（均为P＜0．001）,并与SSS呈明显正相关（P＜0．001）,结论 脑卒中早期血清NSE明显升高,血清NSE与SSS之间有明显相关性。     

不同剂量甘露醇治疗急性大面积脑梗死病人其血清神经元特异性烯醇酶的变化

目的 探讨应用不同剂量甘露醇治疗急性大面积脑梗死病人时对其血清神经元特异性烯醇酶(NSE)的影响。方法 将急性大面积脑梗死病人分成两组,分别给予小剂量和常规剂量甘露醇治疗,均于发病后1、3、7、14d测定其血清NSE的浓度,比较两组病人同天内的测量值有无差别,并与正常健康人相对照。结果 两组病人起病后第1、3、7d血清NSE浓度较对照组显著升高(P<0.05),第3d最高,第14d NSE浓度与对照组比较无统计学意义(P>O.05)。两组间第1、3、7、14d NSE浓度分别比较均无显著性差异(P>0.05)。结论 急性大面积脑梗死病人应用小剂量甘露醇与应用常规剂量甘露醇治疗时,对于血清中NSE的变化具有一致的影响结果。