急性脑梗死患者血浆纤维蛋白原，抗凝血酶Ⅲ及D—二聚体的研究

目的 研究急性脑梗死后凝血与纤溶活性的变化规律。方法 检测40例脑梗死患者发病时、病后4－5天、病后2周血浆纤维蛋白（Fg)、抗凝血酶Ⅲ（AT-Ⅲ）及D－二聚体（D-dimer）的水平。结果 急性脑梗死后2周内Fg持续升高;AT－Ⅲ在发病时及病后4－5天明显降低;D－dimer在病时及病后4－5天明显升高;AT－Ⅲ与D－dimer在发病后2周末均恢复至正常。结论 较高水平的Fg促使脑梗死发生;急性脑梗死后有凝血及继发纤溶活性的增强,抗凝血活性降低,但病后2周末多恢复正常。     

急性脑梗塞患者血浆D—二聚体在溶栓治疗前后的检测及意义

本文测定了４６例急性脑梗塞患者的血浆Ｄ－二聚体含量及抗凝血酶Ⅲ（ＡＴ－Ⅲ）、纤溶酶原（Ｐｇ）水平，并对其中１６例患者尿激酶溶栓后６ｈ的血浆Ｄ－二聚体再次检测。结果：脑梗塞患者组Ｄ－二聚体含量明显高于对照组（Ｐ＜０．０１），同时伴有ＡＴ－Ⅲ降低、Ｐｇ升高，溶栓前后结果经检验有显著性差异（Ｐ＜０．０５），表明急性脑梗塞患者存在血液高凝状态和继发纤溶激活。     

进展性缺血性脑卒中的形成因素

目的了解进展性缺血性脑卒中的形成因素。方法136例缺血性脑卒中患者筛选出进展性脑卒中38例，与98例卒中及60例健康者作对照，比较血液中血管性血友病因子抗原（vWF：Ag）、a颗粒膜蛋白-140（GMP-140）、凝血酶抗凝血酶Ⅲ复合物（TAT）、抗凝血酶Ⅲ（ATⅢ）、组织型纤溶酶原激活物（t—PA）、D二聚体（D—D）、纤溶酶原激活物抑制物-1（PA11）、同型半胱氨酸（HCY）、空腹血糖（FBG）的浓度及收缩压（SBP）、舒张压（DBP）。结果缺血性脑卒中的发生者vWF、GMP-140、TAT、PAI、DD、HCY、FBG明显增加，ATⅢ、t—PA减少（P〈0．05）；而进展性缺血性卒中vWF、TAT、PAI、DD、HCY、FBG进一步增加，ATⅢ、t-PA进一步减少，SBP、DBP明显下降（（P〈0．05），GMP-140上升无显著差异（P〉0．05）。结论进展性缺血性卒中与vWF：Ag、TAT、DD、PAI、HCY、FBG进一步增加，ATⅢ、t—PA进一步减少，SBP、DBP下降（P〈0．05）有关。     

脑梗死患者血浆纤溶活性的动态检测及其临床意义

对55例脑梗死患者分别于发病后1天、3天、1周、2周、1月时检测血浆D-二聚体（D-D）水平及纤溶酶原（PLG）活性，同时检查记录神经功能缺损评分。结果显示:与43例正常对照组比较，患者组纤溶活性显著增强，D-D水平于3天时达高峰（P＜0.001），与同期明显降低的PLG活性（P＜0.001）呈负相关（r—-0.446，P＜0.001）。D-D水平于1月时仍高于正常（P＜0.01）。脑梗死早期纤溶活性与神经功能缺损评分呈显著性正相关（P＜0.01）。腔隙性梗死组纤溶活性亦有显著性增强，其变化规律与皮层梗死组一致，但程度较低（P＜0.05）。     

高血压脑出血患者急性期凝血,抗凝及纤溶状态的观察

本研究测定了５６例ＨＣＨ 患者发病４８小时内血中凝血功能、抗凝及纤溶状态的９项相关指标。结果表明，ＨＣＨ患者无凝血功能障碍，抗凝血酶消耗性降低，纤溶活性代偿性轻度升高。据此认为抗纤溶药不宜用于治疗ＨＣＨ。     

急性脑梗死患者凝血、抗凝及纤溶功能的临床研究

目的研究急性脑梗死患者凝血、抗凝和纤溶系统功能指标的变化,探讨急性脑梗死的发病机制,为其临床早期诊断和治疗提供依据。方法对比检测了209例急性脑梗死患者与100例健康成人的血浆血管性血友病因子抗原(vW F:A g)、P-选择素(GM P-140)、纤维蛋白原(Fg)的含量,抗凝血酶(AT)、蛋白S(PS)、蛋白C(PC)、组织型纤溶酶原激活物(t-PA)、纤溶酶原激活物抑制物-1(PA I-1)的活性,并进行了分析与评价。结果血浆中vW F:A g、GM P-140、Fg的含量、PA I-1活性较对照组均明显升高,而AT、PS、PC、t-PA活性较对照组均明显下降,差异非常显著(P<0.01~0.001)。结论急性脑梗死患者存在着明显的高凝状态和较低的抗凝和纤溶活性,这与其发生及病情进展密切相关。     

急性脑血管病抗凝血酶Ⅲ及纤溶酶原初步测定分析

笔者对75例急性脑血管病人，病后1周内血抗凝血酶Ⅲ及纤溶酶原进行了测定。结果：抗凝血酶Ⅲ值，出血性脑血管病组与对照组比较偏低，但统计学上无明显差异。纤溶酶原值，缺血性脑血管病组与对照组比较明显低下，统计学上有显著差异。固纤溶酶原可以考虑做为缺血性脑血管一项非特性检验指标。     

老年脑血栓患者血浆中t－PA、PAI的变化

本文采用发色底物显色法对３９例脑血栓患者血浆中组织型纤溶酶原激活物（ｔ－ＰＡ）和纤溶酶原激活物抑制物（ＰＡＩ）进行检测。结果ｔ－ＰＡ活性下降，ＰＡＩ活性升高，与健康对照组相比有显著差异性（Ｐ＜０．０１），表明脑血栓患者纤溶活性降低，是产生血栓的因素之一。本栓测结果提示，测定ｔ－ＰＡ、ＰＡＩ有助于脑血栓的诊断。     

自发性蛛网膜下腔出血后血液及脑脊液纤溶活性的研究

目的探讨自发性蛛网膜下腔出血(SAH)后血及脑脊液(CSF)中纤溶活性的变化规律及正常CSF中的纤溶状态。方法组织型纤溶酶原激活物的活性(tPA:A)及纤溶酶原抑制物的活性 (PAI:A)测定采用发色底物法,纤溶酶原抑制物-1(PAI-1)及D-二聚体(D-D)定量测定采用酶联免疫吸附试验(ELISA)双抗体夹心法,血及CSF标本在SAH后0-3 d(急性期),4-9 d(再出血高峰期),及 14-21 d(吸收期)留取三次;正常对照组留取一次。结果 SAH患者血液中,急性期tPA:A显著低于对照组,并随病程延长显著升高,至14-21 d达正常水平,与对照组差异无显著意义;急性期PAI:A 及D-D水平显著高于对照组,并随病程延长而显著降低,至14-21 d降至正常水平,与对照组差异无显著意义;各期PAI-1含量与对照组差异无显著意义。对照绀CSF中,测不到tPA:A及PAI:A及 PAI-1,D-D测得值很小,为(0．28±0．36)mg/L。 SAH患者CSF中,各期测不到tPA:A及PAI:A,但 PAI-1含量急性期显著升高并随病程延长而显著降低,D-D急性期显著升高并随病程延长而显著降低,至14-21 d 与对照组无显著性差异。结论 SAH后血中不存在纤深活性亢进。对照组CSF中不含有纤溶酶系。SAH患者CSF中纤溶活性急性期升高而后降低,于14-21 d恢复到正常水平。再出血高峰期血及CSF中反映纤溶活性的指标变化均显著低于急性期,提示再出血与血及CSF中纤溶活性无关。故SAH后不宜长期大剂量应用抗纤溶药物来预防再出血。     

血纤溶活性变化对颈动脉粥样硬化和急性脑梗死患者的影响和分析

目的：研究血纤溶活性变化对颈动脉粥样硬化患者和急性脑梗死患者的影响。方法：67例急性脑梗死患者（ACI组）和62名健康体检老年人（对照组），均行彩色多普勒超声诊断仪超声观察颈动脉有无斑块；同时测定血浆组织型纤溶酶原激活物（t-PA）和纤溶酶原激活物抑制物-1（PAI-1）的活性。结果：对照组中有颈动脉斑块者与无颈动脉斑块者相比，血浆t-PA降低，PAI-1升高，P／t值升高（P〈0．05）；观察组颈动脉斑块发生率明显高于对照组（P〈0．05）；观察组患者急性期血浆t-PA、PAI-1升高，P／t值减少（P〈0．05）。结论：颈动脉硬化时，机体纤溶活性处于减低状态；急性脑梗死发生时，纤溶活性处于相对亢进状态。     

Progression of hypertensive intracerebral hemorrhage

Hypertensive intracerebral hemorrhage (HICH) is generally considered to be a monophasic event. Enlargement of the initial hematoma after several hours or days has rarely been documented. We describe the clinical and CT findings in 8 patients (5 men, 3 women, aged 39 to 68 years) with continued bleeding or rebleeding during the acute phase of HICH. The thalamus was the most frequent site of hemorrhage (6/8). The neurologic status deteriorated in all: 6 within 24 hours, and 2 after 5 and 7 days. Persistent hypertension was common (6/8) prior to extension of the hemorrhage. The 2nd CT revealed an obvious increase in hematoma size in all cases. Four patients died and 4 survived with severe neurologic disability. These serial studies indicate that active bleeding or rebleeding can occur in HICH and suggests that the risk is particularly high with thalamic hemorrhage. We conclude that meticulous control of hypertension after HICH may be justified in selected patients.     

高血压脑出血早期血肿周围脑组织细胞凋亡与凝血酶表达相关性的研究

目的探讨高血压脑出血(HICH)早期血肿周围脑组织细胞凋亡与凝血酶表达的关系。方法取36例高血压脑出血患者血肿周围脑组织作为实验组,按发病至手术的时间分为5组:<6h(7例)、6~12h(11例)、12~24h(8例)、24~48h(6例)、48~72h(4例)。另将侧脑室肿瘤患者经皮层入路取得的正常脑组织作为对照组。采用脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)检测神经细胞凋亡率,免疫组织化学方法检测凝血酶表达。结果对照组脑组织基本无TUNEL阳性细胞(0.32±0.037);<6h组有轻微表达(7.19±2.53,P<0.05),发病6h后逐渐增高(15.11±3.69,P<0.01),12~24h增高显著(28.26±7.83,P<0.01),并于24~48h达高峰(53.79±6.35,P<0.01),48~72h组有所回落,但仍维持较高水平(38.23±3.29,P<0.01)。凝血酶表达变化与此一致。相关分析显示:细胞凋亡与凝血酶表达呈显著正相关(r=0.7451,P<0.05或P<0.01)。结论H ICH患者血肿周围脑组织中存在细胞凋亡,凝血酶表达是细胞凋亡过程中的一个关键事件     

脑出血急性期凝血机制变化规律研究

目的研究脑出血患者急性期凝血机制的变化规律,并对其相关机制进行探讨。方法将经头部CT检查证实的脑出血80例患者作为观察组,按不同出血量、出血部位分组;正常对照组35例。所有患者发病后1、3、7、14、21d行凝血酶原时间(PT)、活化部分凝血酶原时间(APTT)、凝血酶时间(TT)、纤维蛋白原(FIB)、D-二聚体(D-D)5项指标检测;24h内血小板计数(PLT)、血小板压积(PCT)、平均血小板体积(MPV)、血小板分布宽度(PDW)测定。结果脑出血组1、3、7d FIB与D-D均明显高于对照组(P<0.01),14、21d恢复至正常水平;FIB、D-D水平升高与出血量呈正相关,与出血部位无关;两组比较PT、APTT、TT均无统计学意义(P>0.05);脑出血组24h内血小板分布宽度(PDW)、平均血小板体积(MPV)明显高于对照组,两组间比较差异有统计学意义(P<0.01);而脑出血组PLT、PCT与对照组比较,无统计学意义(P>0.05)。结论脑出血急性期血浆FIB、D-D含量增加,血小板MPV、PDW增大,提示脑出血后凝血活性代偿性升高并继发纤溶活性增强,同时血小板体积增大、新生血小板增多,促进止血。     

Biochemical studies of the cerebral ischemia in the rat--changes in cerebral free amino acids, catecholamines and uric acid

Changes in cerebral free amino acids, catecholamines and uric acid levels were explored for up to 7 days after cerebral ischemia in the rat. Fifty male Sprague-Dawley rats were subjected to occlusion of the middle cerebral artery on the olfactory tract, under halothane anesthesia. The animals were decapitated at 2, 4, 6, 12, 24 hours and 2, 3, 5, 7 days after the surgery, respectively. The brains were rapidly removed. The cerebral hemispheres were divided into right and left halves, and homogenized in sulfosalicylic acid solution. Free amino acids were analyzed by colormetric method. Cathecholamines and uric acid were analyzed by high-performance liquid chromatography. Each parameters were measured both on the ischemic and contralateral hemispheres. The time course of changes in each parameters were observed by means of the ratio, which is the value of ischemic side divided by that of contralateral side. Free amino acids Dicarboxylic group; Decreases in glutamate and increases in glutamine suggest one aspect of detoxication of ammonia within the ischemia tissue. Monocarboxylic group; GABA, glycine, alanine were increased in early ischemic state, and gradually lowered to the normal values. These suggest the impairment of tricarboxylic acid (TCA) cycle in the ischemic tissues, since these amino acids are closely related to TCA cycle. Essential amino acids, except for tryptophan, were increased until the end of study. These increases suggest the utilization of essential amino acids for protein synthesis might be disturbed in the ischemic tissues. Catecholamines and precursors; Norepinephrine and dopamine were lowered gradually. On the other hand, phenylalanine and tyrosine were increased during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

盐源山蛭注射液治疗脑出血的实验研究

目的 :探索纯化的盐源山蛭注射液促进血肿吸收的作用及其作用机理。方法 :采用定量胶源酶注入大鼠尾状核建立脑出血模型 ,观察盐源山蛭注射液对鼠脑内血肿容积、脑水含量、血浆 F。 a活性、 AT- 活性、 D- D含量及组织病理变化的影响。 BWC采用称重法 ,酶活性测定采用发色底物法 ,D- D含量测定采用 EL IAS测定。结果 :(1)盐源山蛭注射液治疗后 6 d、 10 d的脑内血肿明显缩小 ;使治疗后 3d、 6 d的 BWC明显减轻。 (2 )盐源山蛭注射液能抑制脑出血后 F。 a活性的升高 ,不影响 AT- 活性 ,增加纤溶活性。 (3)盐源山蛭注射液能加快脑出血后的病理组织修复。结论 :(1)盐源山蛭注射对大鼠脑出血后脑内血肿有治疗作用 ;(2 )作用机制可能为 :拮抗凝血形成的稳定因素 ,激活内源性纤溶系统 ,促进胶质细胞增生 ,改善微循环     

亚低温治疗对高血压脑出血后水通道蛋白-4表达的影响

目的探讨亚低温治疗对大鼠高血压脑出血后血肿周围脑组织水通道蛋白-4（AQP-4）表达的影响。方法将制成高血压脑出血模型的大鼠随机分为亚低温治疗组（40只）和常温对照组（10只）,其中治疗组又根据从发病至亚低温治疗的时间间隔分为2、4、8、12h四个亚组,每亚组10只动物。大体观察动物行为学变化,3d后处死动物取脑组织进行脑含水量测定（干湿重法）及AQP-4表达的测定。结果对照组的脑含水量为（89．16±0．48）％,治疗组中出血后2h、4h和8h三个亚组的脑含水量分别为（81．42±0．58）％、（83．86±0．28）％和（86．95±0．29）％,与对照组相比有显著性差异（P〈0．05）,而出血后12h亚组的含水量与对照组相比无显著性差异（P〉0．05）。对照组AQP-4的表达（以吸光度表示）明显高于出血后2h、4h及8h三个亚组（P〈0．05）,与出血后12h亚组相比无显著差别（P〉0．05）。结论本研究提示高血压脑出血后早期应用亚低温治疗可以下调AQP-4的表达,并可有效控制脑水肿的发生。     

Platelet function and coagulation in normal and preeclamptic pregnancy

Platelet function and coagulation activity were followed prospectively throughout normal pregnancy and in puerperium in 17 healthy women. Plasma beta-thromboglobulin reflecting platelet activation increased progressively during pregnancy. This was not accompanied by any changes in platelet count or lifespan nor in serum or plasma thromboxane B2 levels. The levels of both factor VIII:C and factor VIIIR:Ag increased, the former less than the latter resulting in a rise of the FVIIIR:Ag/FVIII:C ratio. Antithrombin III (AT III), however remained unaltered. FVIIIR:Ag/FVIII:C ratio was increased both in mild (n = 7) and severe (n = 9) preeclampsia, whereas beta-thromboglobulin was increased and AT III was decreased only in severe preeclampsia. Platelet count and lifespan, plasma and serum thromboxane B2 as well as FVIII:C were normal in severe preeclampsia.     

Stability of coagulation assays performed in plasma from citrated whole blood transported at ambient temperature

Many preanalytical variables affect the results of coagulation assays. A possible way to control some of them would be to accept blood specimens shipped in the original collection tube. The aim of our study was to investigate the stability of coagulation assays in citrated whole blood transported at ambient temperature for up to two days after specimen collection. Blood samples from 59 patients who attended our haematology outpatient ward for thrombophilia screening were transported at ambient temperature (outdoor during the day, indoor overnight) for following periods of time: <1 hour, 4-6, 8-12, 24-28 and 48-52 hours prior to centrifugation and plasma-freezing. The following coagulation tests were performed: PT, aPTT, fibrinogen, FII:C, FV:C, FVII:C, FVIII:C, FIX:C, FX:C, FXI:C, VWF:RCo, VWF:Ag, AT, PC activity, total and free PS antigen, modified APC-sensitivity-ratio, thrombin-antithrombin-complex and D-dimer. Clinically significant changes, defined as a percentage change of more than 10% from the initial value, were observed for FV:C, FVIII:C and total PS antigen starting at 24-28 hours, and for PT, aPTT and FVII:C at 48-52 hours. No statistically significant differences were seen for fibrinogen, antithrombin, or thrombin-antithrombin complexes (Friedman repeated measures analysis of variance). The present data suggest that the use of whole blood samples transported at ambient temperature may be an acceptable means of delivering specimens for coagulation analysis. With the exception of factor V and VIII coagulant activity, and total PS antigen all investigated parameters can be measured 24-28 hours after specimen collection without observing clinically relevant changes.     

D-二聚体与进展性颅内出血的相关性研究

目的研究急性颅脑损伤病人早期D-二聚体（D-D）的变化,分析D-D与进展性颅内出血（PIH）的相关性,评估D-D对急性颅脑损伤的病情及预后的价值。方法检查292例急性颅脑损伤患者血浆D-D于颅脑损伤后24 h、3 d、7 d、14 d的变化。对其进行前瞻性研究,分析D-D与PIH、颅脑损伤病情及预后的关系。结果 292例患者中伤后24 h D-D异常发生率64.73%,明显高于伤后7 d、14 d（P〈0.01）,且易发生PIH。病情重者及死亡组D-D异常更显著（P〈0.01）。结论急性颅脑损伤中D-D异常发生率高,血液高凝状态与纤溶亢进并存,纤溶指标升高显著时,伤情严重,PIH发生率高,死亡率高。提示D-D可作为PIH发生的预测因素,对急性颅脑损伤病情评估及预后判断有较高价值。