高同型半胱氨酸血症与缺血性脑血管病相关性探讨

目的 研究血浆同型半胱氨酸(Hcy)与缺血性脑血管病的关系.方法 采用循环酶法技术测定95例动脉硬化性脑梗死、40例腔隙性脑梗死、41例短暂性脑缺血发作和90例对照组的血浆Hcy水平.两样本均数的比较采用t检验.结果 脑梗死组、脑腔梗组与TIA组患者血浆Hcy水平明显高于对照组,有显著性差异(P＜0.001、0.01、0.05);脑梗死组患者血浆Hcy水平也明显高于脑腔梗组与TIA组,显著性差异(P＜0.01、0.001).结论 高Hcy血症是缺血性脑血管病的独立危险因素,并且与脑缺血性病变的严重程度呈正相关.     

基于CISS分型的急性脑梗死患者临床与影像学研究

目的使用中国缺血性卒中亚型(Chinese ischemic stroke subclassification,CISS)对急性脑梗死(acute cerebralinfarction,ACI)患者进行分型,分析急性脑梗死的临床与影像学特点。方法回顾性分析123例缺血性脑卒中患者的影像学资料,依据CISS对其进行分型,包括对LAA亚型发病机制的分析。观察有无脑供血动脉的狭窄,狭窄的位置、程度,并对比分析进展性卒中和非进展性卒中的影像学特点。结果 123例缺血性脑卒中患者中59例(47.97%)存在LAA,其中颈内动脉狭窄14例(11.38%),大脑中动脉狭窄29例(23.58%),基底动脉狭窄9例(7.32%);55例(44.72%)出现卒中进展。进展性卒中与非进展性卒中相比,大脑中动脉狭窄、基底动脉狭窄的差异有统计学意义(P<0.01)。进展性卒中组人群的分水岭脑梗死、大动脉狭窄或闭塞发生率显著高于非进展卒中组人群(P<0.001)。结论大动脉狭窄是急性脑梗死的原因之一,分水岭脑梗死或许可以成为进展性卒中的预测指标之一。     

进展性脑梗死血浆Hcy及hs-CRP水平测定及其临床意义

目的 观察进展性脑梗死与血浆同型半胱氨酸(Hcy)及超敏C反应蛋白(hs-CRP)的关系.方法 测定神经内科住院的32例进展性脑梗死患者(观察组)及37例非进展性脑梗死患者(对照组)的血浆Hcy及hs-CRP水平,收集患者的人口学、血管性危险因素资料,评估患者的卒中类型和病情程度.结果 与对照组相比,观察组的低密度脂蛋白胆固醇水平显著高、完全前循环梗死比例高、美国国立卫生院神经功能缺损评分(NIHSS)显著高、血浆Hcy及hs-CRP水平亦显著升高(P<0.05)且在观察组中两者呈正相关(r=0.414, P=0.019).结论 进展性脑梗死患者的血浆Hcy及hs-CRP的水平高.     

急性缺血性脑卒中患者血浆sICAM-1水平的研究

目的 :通过对急性缺血性脑卒中患者血浆中的主要粘附分子之一 ,s ICAM- 1水平的测定 ,以明确细胞粘附分子与急性缺血性脑卒中的关系。方法 :选取 2 4小时内发病的卒中组病人 36例 ,18例年龄相匹配的同期其他住院病人作为对照组。卒中组的危险因素与对照组无显著差异。采用 EL ISA法测定两组研究对象血浆的 s ICAM- 1水平。结果 :血浆 s ICAM- 1水平卒中组明显高于对照组 (P<0 .0 1) ,所有卒中患者发病 7天后的 s ICAM- 1水平显著低于起病时 (P<0 .0 1) ,与对照组相比无显著差别 (P>0 .0 5 )。结论 :研究表明在急性脑缺血性卒中的过程中确实存在着细胞粘附分子的合成上调。     

进展性缺血性卒中567例临床分析

目的 通过分析进展性缺血性卒中患者的临床资料,研究卒中进展的相关因素.方法 回顾性分析1573例缺血性脑卒中患者的临床资料,其中进展性缺血性卒中567例.依据其卒中进展形式分为5型,分别研究不同类型梗死部位比例及血管受累情况.并比较不同类型卒中患者空腹及餐后2h血糖水平.结果 从梗死部位分析,大面积脑梗死、脑叶及分水岭区脑梗死易于出现进展性卒中.从血管受累情况分析,进展性卒中患者血管狭窄比例更高,前后循环同时受累或单纯后循环受累多见.从血糖水平分析,进展性卒中患者空腹血糖及餐后2h血糖水平均高于非进展性卒中.结论 不同病灶部位及脑动脉受累部位、程度均能预测脑梗死的进展,血糖是进展性卒中的危险因素.     

青年缺血性脑卒中患者血清瘦素和胰岛素水平的测定

目的 研究青年缺血性卒中患者的血清胰岛素和瘦素水平.方法 选取89例健康查体者(对照组)及112例青年缺血性卒中患者(病例组),应用放射免疫技术检测其空腹胰岛素和瘦素水平并进行比较.结果 脑梗死组血清胰岛素水平高于对照组,尤其是女性患者(P<0.05).脑梗死组血清瘦素水平高于对照组(P<0.01).脑梗死组和对照组男性患者瘦素水平均低于女性患者(P<0.05).结论 青年卒中患者存在高瘦素、高胰岛素水平,这两者可能是导致青年缺血性卒中的危险因素之一.     

血浆溶血磷脂酸在进展性脑梗死诊断中的应用研究

目的 探讨溶血磷脂酸（LPA）在进展性脑梗死发病过程中的变化及临床意义.方法 动态检测35例进展性脑梗死患者血浆溶血磷脂酸浓度,分析其与梗死部位、大小、病程、病情的相关性,并分别与稳定性脑梗死、健康体检者对照.结果 进展性脑梗死患者血浆溶血磷脂酸急性期升高,发病3 d达高峰,以后逐渐下降,7 d下降明显,21 d接近正常对照,与稳定性脑梗死组和对照组相比,有非常显著意义（P＜0.01）.梗死体积大则血浆溶血磷脂酸浓度高（P＜0.01）;重型组血浆溶血磷脂酸浓度高于轻型组（P＜0.01）;皮质组与皮质下组相比无显著意义（P＞0.05）.结论 血浆溶血磷脂酸浓度与梗死大小、病程、明显病情严重程度相关,进展性脑梗死患者血浆溶血磷脂酸高于稳定性脑梗死组和对照组.溶血磷脂酸可作为脑梗死的预警因子,对缺血性脑血管病的防治具有重要的临床应用价值.     

血管性痴呆患者血浆、脑脊液AngⅡ、AVP、NSE含量的变化及其临床意义

目的了解血管性痴呆(VD)患者血浆、脑脊液(CSF)中血管紧张素Ⅱ(AngⅡ)、精氨酸加压素(AVP)、神经元特异性烯醇化酶(NSE)的质量浓度变化及临床意义. 方法运用简易精神状态量表(MMSE)、P300潜伏期(P300PL)、Hachinski缺血量表(HIS)和社会功能活动调查(FAQ)评定患者认知功能,用放射免疫分析法(RIA)测定血浆、CSF 中AngⅡ、AVP质量浓度,用双抗体免疫夹心法(ELASA)测定血浆、CSF 中NSE质量浓度. 结果 VD组血浆、CSF 中 AngⅡ质量浓度显著高于对照组(P＜0.01),CSF中 AngⅡ质量浓度亦显著高于脑梗死(CI)恢复期(P＜0.01), 血浆AVP质量浓度无显著变化(P＞0.05),CSF 中AVP质量浓度显著降低(P＜0.01),血浆、CSF 中NSE质量浓度同对照组比较明显下降(P＜0.05);直线相关分析VD组血浆与CSF中 AngⅡ、AVP质量浓度变化无显著相关(P＞0.05), 血浆与CSF中NSE质量浓度变化呈直线正相关(P＜0.01). 结论脑内AVP、AngⅡ在VD发病中可能起重要作用,CSF中AVP、AngⅡ质量浓度变化与认知功能密切相关;脑内NSE质量浓度变化与缺血性脑损害的严重程度密切相关,但不能作为反映认知功能的生化指标.     

人血浆脂蛋白相关磷脂酶A2与缺血性脑血管病的关系

目的探讨Lp-PLA2与缺血性脑血管病的关系,为预测缺血性脑血管病的发生提供准确简便快捷的方法。方法选择缺血性脑血管病患者98例为病例组和30例健康者为对照组,病例组包括短暂性脑缺血发作组21例,无症状脑梗死组31例,症状性脑梗死组46例。病例组与对照组均采用双抗体酶联免疫吸附测定法(ELISA)检测血浆Lp-PLA2水平,同时检测血浆CHOL、TG、LDL-C、HDL-C水平。结果①病例组患者血浆Lp-PLA2水平明显高于对照组(P<0.01);②有症状脑梗死组患者血浆LP-PLA2水平高于短暂脑缺血发作组和无症状脑梗死组(P<0.01),三组比较差异有统计学意义;③无症状脑梗死组患者血浆Lp-PLA2水平高于短暂性脑缺血发作组(P<0.01)。结论 Lp-PLA2可能与缺血性脑血管病的严重程度有关,Lp-PLA2可以作为预测缺血性脑血管病风险的一个生物学标志物。     

高同型半胱氨酸血症与进展型卒中的关系

目的 研究高同型半胱氨酸(Hcy)血症与进展型卒中(SIP)的关系.方法 本研究采用放免荧光法检测法测定47例进展性卒中患者,45例非进展性卒中患者的血浆Hcy水平.结果 血浆Hcy水平在SIP组为(25.49±15.73)μmol/L,在非进展性卒中组为(19.78±9.36)μmol/L.SIP组显著高于非进展性卒中组和对照组.结论 SIP患者的Hcy水平显著高于非进展性卒中患者,其鉴别诊断意义可做进一步研究.     

Body iron stores and early neurologic deterioration in acute cerebral infarction

BACKGROUND: Iron-dependent free radicals formation has been related to greater damage in cerebral ischemia. The authors analyzed whether increased body iron stores were associated with early neurologic worsening and excitatory amino acid release in patients with acute ischemic stroke. METHODS: Ferritin, total iron, and glutamate concentrations in plasma and CSF were measured on admission in 100 consecutive patients with a cerebral infarction of <24 hours' duration. The authors diagnosed progressing stroke when the Canadian Stroke Scale score decreased one or more points between admission and 48 hours. Cranial CT was performed on admission and repeated on days 4 to 7 of hospitalization. RESULTS: Ferritin concentrations in plasma (median 391, range 119 to 500 versus 148, 21 to 399 ng/mL) and in CSF (17.4, 6.8 to 82, versus 4.8, 0.6 to 14 ng/mL) were significantly higher in the 45 patients with subsequent progressing stroke than in those with nonprogressing stroke (p < 0.001). There was a positive correlation between ferritin and glutamate concentrations in plasma (r = 0.81, p < 0.001) and CSF (r = 0.64, p < 0.001). Plasma ferritin concentrations >275 ng/mL in plasma (OR, 33.5; 95% CI, 4.7 to 235) and >11 ng/mL in CSF (OR, 11.4; 95% CI, 3. 1 to 41) were independently and significantly related to early neurologic worsening. The effect was reduced by >60% after controlling for glutamate concentrations, but remained significant. CONCLUSIONS: High plasma and CSF ferritin concentrations within the first 24 hours from the onset of ischemic stroke are associated with early neurologic deterioration. Increased body iron stores may contribute to stroke progression by enhancing the cytotoxic mechanisms in cerebral ischemia.     

Serum amino acid levels after permanent middle cerebral artery occlusion in the rat

BACKGROUND AND PURPOSE: High levels of glutamate in plasma and cerebrospinal fluid (CSF) have been demonstrated in patients with acute ischemic stroke. Whereas this glutamate increase in CSF is only evidenced during the first 6 h in stable ischemic stroke, it is sustained for 24 h in progressing stroke. The aim of this investigation was to study the evolution of serum glutamate levels after stroke in a rat model of permanent cerebral artery occlusion. METHODS: Glutamate, glycine, aspartate, taurine and tryptophan were measured by high-performance liquid chromatography from serum samples taken before and at different times after permanent middle cerebral artery occlusion (MCAO) and from sham-operated rats. RESULTS: After MCAO, a 3-fold increase in glutamate and a 2-fold increase in glycine and aspartate were observed in rat serum. The onset of this amino acid increase began 4-6 h after ischemic induction, reached peak values at 8-24 h and returned to preischemic values by 48-72 h. Serum concentrations of taurine and tryptophan were not modified after MCAO. Sham-operated rats did not exhibit changes of basal amino acid concentrations in serum. CONCLUSIONS: The serum excitatory amino acid profile in this experimental model confirms that the early detection of increased concentrations of glutamate and glycine at systemic circulation observed in patients with acute stroke is a consequence of the cerebral ischemic process.     

Raised plasma oxidised LDL in acute cerebral infarction

BACKGROUND: The association between oxidised low density lipoprotein (OxLDL) and cerebral infarction is suspected but not established. OBJECTIVES: To determine whether plasma OxLDL is a useful marker for monitoring oxidative stress in stroke patients. METHODS: Plasma OxLDL concentrations were determined in 56 stroke patients with cerebral infarction (n = 45) or cerebral haemorrhage (n = 11), and in 19 age matched controls, using a novel sandwich enzyme linked immunosorbent assay. RESULTS: Compared with the controls (0.130 (0.007) ng/ micro g LDL, mean (SEM)), OxLDL was significantly raised in patients with cerebral infarction (0.245 (0.022); p < 0.0001) but not in those with haemorrhage (0.179 (0.023)). Patients with cortical ischaemic infarcts (n = 22) had higher OxLDL levels than either the controls (p < 0.0001) or the patients with non-cortical ischaemic infarcts (n = 23) (p < 0.001). Increased OxLDL concentrations in patients with cortical infarcts persisted until the third day after stroke onset. The National Institutes of Health stroke scales in patients with cortical infarction were higher than in those with non-cortical infarction (p < 0.01). CONCLUSIONS: There is a significant association between raised plasma OxLDL and acute cerebral infarction, especially cortical infarction. Plasma OxLDL may reflect oxidative stress in stroke patients.     

Nitric oxide-related brain damage in acute ischemic stroke

BACKGROUND AND PURPOSE: The neurotoxic and neuroprotective role of nitric oxide (NO) in experimental cerebral ischemia has generated considerable debate. The aim of this study was to analyze the relationship between NO metabolite (NO-m) concentrations in cerebrospinal fluid (CSF) and clinical and neuroimaging parameters of brain injury in patients with acute ischemic stroke. METHODS: We studied 102 patients and 24 control subjects who were included in a larger previous study conducted to analyze risk factors of progressing stroke. NO generation was calculated by quantifying nitrates and nitrites with a colorimetric assay in CSF samples obtained within the first 24 hours from symptoms onset. Early neurological deterioration was defined as a fall of 1 or more points in Canadian Stroke Scale score between admission and 48 hours after inclusion. Infarct volume was measured on days 4 to 7 by cranial CT. RESULTS: Median NO-m concentrations [quartiles] were 2.1 [1.0, 4.5] micromol/mL in patients and 1.0 [1.0, 1.0] micromol/mL in control subjects (P<0.0001). In 45 patients with subsequent early neurological deterioration, NO-m levels in CSF were significantly higher than in those with stable stroke (4.0 [1.7, 7.8] versus in 1. 6 [1.0, 2.5] micromol/mL, P<0.0001). There was a moderate correlation between NO-m and infarct volume (coefficient 0.39, P<0. 001). NO-m concentrations >5.0 micromol/mL were significantly associated with early neurological worsening (OR 5.7, 95% CI 1.2 to 27.4; P=0.030) independent of other important factors related to progressing stroke, such as CSF glutamate levels. CONCLUSIONS: Our clinical findings suggest an important role of NO generation in acute ischemic stroke. Increased NO-m in CSF are associated with a greater brain injury and early neurological deterioration.     

脑梗塞患者血浆抑制性氨基酸变化及兴奋性氨基酸的关系

目的目前对兴奋性氨基酸（EAA）和抑制性氨基酸（IAA）的临床研究较少，从临床方面探讨EAA，IAA在脑梗塞发展过程中的作用可为今后临床深人研究提供一定的参考资料。方法应用高效液相色谱法对44例动脉粥样硬化性血栓性脑梗塞病人急性期和病后2周血浆EAA和IAA的含量进行测定，进行病人自身前后对照并与30例正常人对比。结果脑梗塞病人急性或血浆谷氨酸（Glu）、天门冬氨酸（Asp）、牛磷酸（Tau）含量明显高于正常对照组（P＜0.01）；病后2周其血浆含量有所下降，其中Glu含量与急性期相比有显著性差异（P＜0．01），但三者均未恢复正常，与正常对照组相比仍有显著性差异（P＜0．01）；血浆丙氨酸（Ala）、甘氨酸（Gly）在脑梗塞急性期及病后2周与正常对照组相比均无显著性差异（P＞0．05）。结论Glu、Asp作为损伤因素参与了脑梗塞的发生发展过程，研究EAA在脑梗塞中的作用时应同时观察IAA的相应变化．兴奋性毒性指数的概念值得进一步研究。测定血浆Glu的含量可考虑作为估计脑梗塞病程的一项生化指标。     

脑梗塞患者血LP(a)、ox-LDL、D-D、Fbg含量的研究

本研究按不同年龄组分别测定了110例正常人和123例脑梗塞患者急性期和恢复期血中LP（a）、ox-LDL、D-D、Fbg的含量，结果显示：脑梗塞患者血中LP（a）、ox-LDL、D-D、Fbg较正常对照组显著升高（P＜0．01），并且LP（a）、ox-LDL、D-D在脑梗塞人血中呈正相关（r=0.876，P＜0．05）。正常人D-D的含量随年龄的增高有增长趋势，低年龄组与高年龄组有显著性差异（q=4．82，P＜0．01）。LP（a）、OX-LDL、Fbg含量各年龄组无差异（P＞0．05）。D-D随年龄增长塔高明显（R=0．596P＜0．01）并且与梗塞面积正相关（r=0．819，P＜0．01），而LP（a）、OX-LDL、Fbg与梗塞面积无关。同时发现D-D在脑梗塞恢复期明显降低（P＜0．05），证实了脑梗塞急性期确实存在高凝状态和内源性纤溶功能活跃。     

CSF cyclic AMP and CSF adenylate kinase in cerebral ischaemic infarction

Summary The severity of neurological deficits, size of hypodense zone on CT, concentration of cAMP and activity of adenylate kinase in cerebrospinal fluid (CSF) were evaluated at predefined intervals in the acute stage of supratentorial cerebral ischaemic infarction in 52 patients. Patients with cerebral infarction had raised activities of adenylate kinase CSF as compared with normal persons. Patients with marked neurological deficits, only slight improvement of neurological signs and large infarction zones on CT had higher average activities of adenylate kinase and lower concentration of cAMP in CSF. Alterations of CSF adenylate kinase and CSF cAMP values were most distinct on the 3rd day after the stroke. Reasons for the changes may be metabolic disorders following brain ischaemia.     

Thrombogenesis in patients with ischemic stroke

The activity of thrombinogenesis process is shown by thrombin restrain reaction by its physiological inhibitor antithrombin III, as a result of which biologically nonactive thrombinantithrombin III complexes (TAT) are created. The aim of the study was to evaluate TAT complexes in the blood of ischaemic stroke patients. 25 persons with ischaemic stroke and 15 controls took part in the examination. Taking into consideration brain CT outcomes 2 groups of patients were selected: with ischaemic stroke of small and great extent. The patients were also divided into a group of patients with less severe and with more severe ischaemic stroke, and into a group of patients with ischaemic stroke with and without accompanying atrial fibrillation. TAT complexes were determined with an enzyme-linked immunosorbent assay method on days 1st, 5th, and 12th after ischaemic stroke onset. TAT complexes were significantly higher in patients with cerebral infarction than in controls, significantly higher in patients with ischaemic stroke of great extent compared to patients with ischaemic stroke of small extent, and significantly higher in patients with more severe cerebral infarction than in patients with less severe cerebral infarction. In patients with cerebral infarction and atrial fibrillation TAT complexes were significantly higher only on the 1st day of the disease compared to patients with cerebral infarction without atrial fibrillation. Our investigations confirm intense activity of thrombinogenesis process in ischaemic stroke patients.     

Concentration of magnesium in serum and cerebrospinal fluid in patients with stroke]

Magnesium concentration in blood serum and cerebrospinal fluid (CSF) was determined in 131 patients aged from 21 to 91 years, with RIND, complete stroke, cerebral haemorrhage and control group. Magnesium was estimated by the use of colorimetry and the method of Mann and Yoe. The results are presented in figures. Statistical evaluations revealed significant decrease of magnesium concentrations in blood serum and CSF in ischaemic stroke compared with control group. In complete stroke significantly lower concentrations of magnesium in blood serum and CSF were found compared with RIND. In ischaemic stroke higher MgSER/MgCSF index was found compared with control group. Magnesium concentration in blood serum was not statistically different within 2 weeks of the disease. No relationships were found between blood serum or CSF Mg concentrations and gender or age.     

CSF neuron-specific enolase as a quantitative marker of neuronal damage in a rat stroke model

A technique for chronic cisternal cerebrospinal fluid (CSF) sampling in conscious rats was used to obtain multiple 50 microliters samples before and up to 7 days after middle cerebral artery occlusion. Neuron-specific enolase (NSE) concentrations were measured by radioimmunoassay using a readily available kit. The volume of infarction was measured by integrating the area of damage on 9 evenly spaced histological sections of the forebrain. This correlated well (r = 0.97, P less than 0.001) with the concentration of CSF neuron-specific enolase integrated over the first 5 days post occlusion, in animals with pure cortical and mixed cortical and striatal lesions. The correlation was maintained in animals given the NMDA antagonist MK-801. There was also a good correlation between the CSF NSE concentration 3 days post-MCAO and the volume of infarction (r = 0.92, P less than 0.01). It is therefore possible that CSF neuron-specific enolase may be useful as a quantitative marker of ischaemic damage in humans and provide a useful adjunct in the assessment of neuroprotective drugs in stroke.