Binswanger病血脂异常及纤溶活性改变

<正> 资料及方法 1.一般资料 本组34例Binswanger病(BD)为本院1998.1～2003.2住院病人,其中男29例,女5例,年龄63～85岁,平均68岁。有明确血压记录的26例中24例有高血压病史,最长32年,最短8年,平均16年。隐匿起病,呈渐进性缓慢进展。主要的临床表现如下,头昏34例、偏瘫18例、共济运动失调6例、震颤3例、言语含糊不清11例,精神行为障碍9例、智力减退21例,假性延髓麻痹3例,主要的体征有不同程度的偏瘫、腱反射活跃及肌张力增高、巴彬斯基征、掌颏反射阳性等。全部病人行脑CT检查,均有累及侧脑室前角周围白质、后角周围白质、放射冠区、三角区及半卵圆中心白质的弥漫性、大致对称的边界欠清的侧脑室周围片状和月晕状低密度区,CT值17～26Hu,病灶多发且有明显的融合现象。21例合并脑梗塞,位于基底节、丘脑、放射冠     

动脉粥样硬化与纤溶系统及血管内皮功能关系的研究

目的通过对动脉粥样硬化(AS)动物模型纤溶酶原激活物抑制物-1(PAI-1)及一氧化氮(NO)表达的研究,探讨AS与纤溶系统及血管内皮功能的关系。方法雄性大耳白兔随机分成正常饮食组和高脂饮食组,每组8只。两组动物均于0、8、16周分别取耳缘静脉血,检测血清中PAI-1和NO的水平。16周后处死动物,取主动脉行病理学检查。应用免疫组化方法检测PAI-1在主动脉粥样硬化斑块中的表达。结果正常饮食组和高脂饮食组 0周血清中PAI-1和NO水平无显著差异(P>0．01)。高脂饮食组8周后血清中PAI-1水平较0周明显增加(P< 0．01),16周后PAI-1水平较8周增加更为明显(P<0．01);NO水平在8周时无显著变化(P>0．01),16周时较8周明显下降(P<0．05)。主动脉病理学检查证实动脉粥样斑块形成。免疫组化结果显示高脂饮食组主动脉壁PAI-1的表达明显高于对照组(P<0．01)。结论动脉粥样硬化的发生伴有纤溶系统及血管内皮功能的失调,PAI—1和NO 的异常表达可能是AS发生机制之一。     

陈旧性脑梗塞患者凝血及纤溶活性的临床研究

材料与方法研究对象：脑梗塞患者64例,其中陈旧性脑梗塞OCI18例。脑梗塞急性期（CIAP）46例,男48例．女16例．平均年龄59岁。全部病例符合第二届全国脑血管病会议制定的诊断标准、正常对照28例．男18例．女Ic例．平均年龄58岁．均系正常健康体检者。所有受试者检测前一周均未服用抗凝血和纤溶药物．部分应用钙离子桔抗剂的脑梗塞患者,均于抽血前3天停药。标本留取：住院患者在人院的第2天凌晨、门诊患者于就诊的第二天凌晨空腹抽取静脉血．以38g／I。阿椽酸或O．54mmol／I,EDTA－Na。按1：9（V／V）抗凝,抗凝血以3（）0（斤／mi…     

脑出血继续出血患者血液纤溶活性的研究

目的探讨脑出血（ICH）继续出血与血液纤溶活性的关系。方法将107例ICH患者根据病情分为继续出血组（21例）和非继续出血组（86例）,利用发色底物法及酶联免疫吸附试验双抗体夹心法分别测定两组患者在发病后0-3d、4-9d、14-21d时血浆中组织型纤溶酶原激活物活性（tPAA）、纤溶酶原抑制物活性（PAIA）、纤溶酶原抑制物-1（PAI-1）及D-二聚体（D-D）的水平,并与同期健康体检者进行比较。结果ICH患者发病后0-3d及4-9d血中tPAA显著低于正常对照组（P〈0.05-0.01）,至14-21d与正常对照组差异无统计学意义;ICH后0-3d及4-9d血中PAIA及D-D显著高于正常对照组（P〈0.05-0.01）,至14-21d与正常对照组差异无统计学意义;ICH各期血中PAI-1水平与正常对照组差异无统计学意义;未继续出血组与继续出血组各期各纤溶指标间差异无统计学意义。结论ICH后血中不存在原发性纤溶活性亢进,ICH继续出血与血液纤溶活性无关。     

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。     

明胶涂层涤纶片携带组织型纤溶酶原激活因子基因定位转移可能影响兔左房血纤溶的活性吗？

背景：机械瓣膜置换后的抗凝治疗一直是困扰心血管外科医生的难题,因此研制一种不需终生抗凝的机械瓣膜具有重要的现实意义。目的：观察明胶涂层涤纶片(Dacron片)携带组织型纤溶酶源激活因子(tPA)基因左心房局部定位转移对兔左房血纤溶活性的影响,为tPA基因瓣膜的研制奠定基础。方法：48只新西兰大耳白兔随机分为3组：转基因组左心耳植入携带tPAcDNA的明胶涂层的Dacron涤纶片;载体对照组左心耳植入携带载体DNA的明胶涂层的Dacron片,空白对照组左心耳植入不携带任何基因的明胶涂层的Dacron片。术后3,14 d取心肌组织,RT-PCR检测左房局部心肌组织tPAmRNA转录水平,Western-Blot和免疫组化方法检测外源性tPA蛋白表达;术后3,14 d取兔左房血和外周静脉血,底物发色法检测其tPA活性。结果与结论：术后3,14 d,RT-PCR可检测到局部心肌tPAmRNA表达,Western-Blot可检测到tPA蛋白表达,免疫组化见阳性心肌细胞胞浆呈黄褐色,术后3,14 d,转基因组左房血tPA活性明显高于各对照组(P < 0.05)。3组术后外周血tPA活性差异无显著性意义。说明使用明胶蛋白涂层方法能够将tPA基因成功的转移到左心房,使之在局部持续表达、分泌有活性的tPA蛋白,从而使左房血纤溶活性增强。关键词：组织型纤溶酶原激活因子;基因;明胶涂层;左心房;纤溶活性;生物材料doi:10.3969/j.issn.1673-8225.2010.12.013     

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）。     

实验性糖尿病大鼠脑缺血纤溶酶原激活物和纤溶酶原激活物抑制剂活性测定

目的 :了解糖尿病大鼠脑缺血 /再灌注后纤溶系统的变化。方法 :糖尿病和正常大鼠于脑缺血 1h再灌注 1、2、5、11、2 3h后 ,用发色底物法测定脑组织中PA和PAI的活性。结果 :糖尿病大鼠脑梗死体积增大、再灌注时血流恢复显著降低 ;脑缺血后 ,正常组和糖尿病组PAI活性无变化 ,PA活性增高 ;再灌注 5h ,正常大鼠PA活性和PA/PAI比值增高。结论 :大鼠脑缺血 /再灌注后PA活性和PA/PAI增高 ,且呈动态变化 ;糖尿病大鼠实际的应激促纤溶功能降低     

蚓激酶对动脉粥样硬化性脑梗死二级预防作用探讨

目的探讨蚓激酶药物对动脉粥样硬化性脑梗死二级预防的作用。方法在我院住院和急诊观察的动脉粥样硬化性脑梗死和短暂性脑缺血发作患者268例,随即分为对照组134例,治疗组134例,2组均应用阿司匹林100mg qd,并且对其他危险因素均给与干预。治疗组加用蚓激酶40万U tid 4w为1疗程,服用3个疗程。通过到院随诊1年,以脑卒中复发、心血管事件为研究终点。结果治疗组缺血性脑卒中1年复发率7.8%,心血管事件发生率7.0%分别明显低于对照组16.5%和13.8%,P0.05有统计学意义。结论蚓激酶对动脉粥样硬化性脑梗死的二级预防是有效的。     

Effects of long-term erythropoietin therapy on fibrinolytic system in haemodialyzed patients

INTRODUCTION: Recombinant human erythropoietin (rHuEPO) is the cornerstone of anaemia therapy in uraemic patients however the effects of this hormone on fibrinolytic system are difficult to interpret. MATERIALS AND METHODS: Assessment of fibrinolytic parameters: tissue-type plasminogen activator (tPA) antigen, urokinase-type plasminogen activator (uPA) and its soluble receptor (suPAR), plasminogen activator inhibitor 1 (PAI-1) and plasmin/antiplasmin (PAP) complexes were performed in haemodialyzed (HD) patients without rHuEPO therapy: Group I (n=8, Hg<10 g/dl); Group II (n=12, Hg>10 g/dl); and in HD patients treated with rHuEPO for more than 6 months (Group III, n=10) or for more than 12 months (Group IV, n=9) in relation to the healthy controls. RESULTS: Patients of Group I had the significantly lower haematological parameters than those of Groups II, III and IV. All the fibrinolytic parameters studied, except PAI-1, were significantly higher in HD patients without rHuEPO therapy when compared to the controls. There were no significant differences in fibrinolytic system between the Groups I and II. Erythropoietin therapy resulted in progressive decrease in antigenic tPA levels, which reach normal range values after 6 months rHuEPO administration. uPA and PAP concentrations were also decreased and reached normal values after 12 months of rHuEPO therapy. In these patients a significant decrease in uPAR levels was also observed. Therapy with rHuEPO did not alter PAI-1 concentrations in HD patients. CONCLUSIONS: These results suggest that long-term rHuEPO therapy can correct fibrinolytic parameters in patients undergoing regular HD irrespective from haemoglobin levels and in the absence of concomitant iron supplementation.     

Excess soluble urokinase-type plasminogen activator receptor in the plasma of dialysis patients correlates with increased fibrinolytic activity

INTRODUCTION: Elevated levels of soluble urokinase-type plasminogen activator receptor (suPAR) and other fibrinolytic parameters related to the urokinase-type plasminogen activator (uPA) system can be implicated in clot lysis in plasma. In this study, we examined whether the excess suPAR was associated with increased plasma fibrinolytic activity, determined as plasmin/antiplasmin (PAP) complexes in dialysis patients. MATERIALS AND METHODS: Twenty-six patients on maintenance haemodialysis (HD) and 18 on maintenance peritoneal dialysis (CAPD) were examined together with 20 healthy controls. Pre-dialysis blood levels of suPAR, uPA and PAP were determined using commercially ELISA kits. RESULTS: suPAR, uPA, PAP levels and suPAR/uPA ratio were increased in both groups of dialyzed patients compared to the controls. Moreover, increased suPAR levels directly correlated with those of uPA and PAP (r=0.443 and r=0.393, both p<0.01, respectively); the fibrinolytic markers were also positively associated with each other (r=0.506, p<0.001). CONCLUSIONS: The plasma suPAR antigen levels are significantly increased in uraemic patients undergoing maintenance dialysis compared with healthy volunteers and are closely associated both with uPA as well as PAP. These positive associations suggest a link between suPAR and the fibrinolytic activity in these patients.     

叶酸、维生素B_(12)治疗高同型半胱氨酸血症对颈动脉粥样硬化的影响

目的观察叶酸、维生素B12治疗高同型半胱氨酸(Hcy)血症脑梗死患者对颈动脉粥样硬化的影响。方法高同型半胱氨酸脑梗死患者122例,随机分为研究组(65例),对照组(57例),研究组每日给予叶酸5mg,维生素B12500ug干预治疗,对照组不给予叶酸和维生素B12治疗,分别于入院时、治疗12、24及36个月测定血清Hcy、叶酸和维生素B12浓度,并进行颈动脉斑块积分及斑块类型超声检查。结果 (1)研究组第12、24、36个月血清Hcy水平较治疗前显著降低(p<0.01),叶酸及维生素B12浓度较治疗前显著性升高(p<0.01),对照组血清同型半胱氨酸、叶酸、维生素B12浓度无明显变化(p>0.05),两组间同一时期比较有显著性差异(p<0.01);(2)研究组随着疗程延长,颈动脉斑块积分减少且有显著性差异(p<0.05,),对照组颈动脉斑块积分增加且有显著性差异(p<0.05);两组间同期颈动脉斑块积分比较有显著性差异(p<0.01);(3)研究组随着疗程延长,颈动脉不稳定性斑块率呈下降趋势,有显著性差异(p<0.05);对照组颈动脉不稳定性斑块率呈上升趋势,有显著性差异(p<0.05);研究组与对照组第12、24及36个月相比不稳定斑块率差异有显著性(p<0.05、p<0.01)。结论叶酸、维生素B12可降低高同型半胱氨酸脑梗死患者同型半胱氨酸水平,可改善颈动脉粥样硬化程度,有稳定斑块作用。     

脑动脉微栓子与颈动脉硬化的关系

目的探讨急性脑梗死患者脑动脉系统微栓子（MES）与颈动脉硬化的关系。方法收集急性脑梗死患者146例,进行脑动脉和颈动脉彩色多普勒超声检测,对有脑动系统微栓子的病例进行监测。结果（1）82例有颈动脉斑声,64例无颈动脉斑块;（2）有颈动脉斑块者MES阳性率（46．34）较无斑块者MEs阳性率（21．88）高（P〈0．05）;（3）颈动脉不稳定斑块MES阳性率（80％）较稳定性斑块MES阳性率（26．92％）高（P〈0．01）;（4）MES与颈动脉的狭窄程度、内膜增厚及斑块的个数无相关性。结论颈动脉粥样硬化斑块的存在及不稳定性是导致脑动脉系统微栓子的重要因素之一,应高度重视,稳定颈动脉斑块是防治动脉栓塞的重要措施。     

行为激活疗法在老年抑郁症患者中的应用研究进展

本文对行为激活（BA）疗法在老年抑郁症患者中的应用现状及疗效进行综述。介绍了BA疗法的内容和研究现状,在老年抑郁症患者中的临床应用情况及特点,并总结了其局限性和未来可能的研究方向,以期为BA疗法在老年抑郁症患者中的本土化应用提供参考。     

急性脑梗死患者脑微栓子与颈动脉硬化的关系

目的 探讨急性脑梗死患者脑动脉系统微栓子(MES)与颈动脉硬化的关系.方法 收集急性脑梗死患者73例,进行脑动脉微栓子监测和颈动脉彩色多普勒超声检测,观察有脑动脉系统微栓子的病例数.结果 (1)41例有颈动脉斑块,32例无颈动脉斑块;(2)有颈动脉斑块者MES阳性率(46.34%)较无斑块者MES阳性率(21.88%)高(P<0.05);(3)颈动脉不稳定斑块MES阳性率(80%)较稳定性斑块MES阳性率(26.92%)高(P<0.01);(4)MES与颈动脉的狭窄程度、内膜增厚及斑块的个数无相关性.结论 颈动脉粥样硬化斑块的存在及不稳定性是导致脑动脉系统微栓子的重要因素之一,应高度重视,稳定颈动脉斑块是防治动脉至动脉栓塞的重要措施.     

瑞舒伐他汀对急性缺血性卒中患者炎性因子及颈动脉粥样硬化斑块的影响

评价瑞舒伐他汀对缺血性卒中患者血清脂质、炎性因子及颈动脉粥样硬化斑块的影响。共98例急性缺血性卒中伴颈动脉粥样硬化患者应用瑞舒伐他汀10 mg,睡前顿服。连续治疗6个月后分别测定血清超敏C.反应蛋白、肿瘤坏死因子.α及血清脂质变化,对比颈动脉内.中膜厚度,计算颈动脉粥样硬化斑块积分。结果显示,瑞舒伐他汀治疗6个月后患者血清超敏C.反应蛋白、肿瘤坏死因子.α及血清脂质水平下降(P<0.01);颈动脉粥样硬化斑块总数减少、稳定性斑块数目有所增加、颈动脉内.中膜厚度及颈动脉粥样硬化斑块积分下降(P<0.05)。提示瑞舒伐他汀具有抗炎及改善颈动脉粥样硬化斑块程度的作用。     

Significant relationship between platelet activation and intra-media thickness of the carotid artery in patients with ischemic cerebrovascular disease

Introduction

We have studied the relationship between the ratio of activated platelets and the thickness of intima and media of the carotid artery in ischemic CVD patients in the chronic stage.

Methods

Platelet activation was assessed by means of flow cytometry of whole blood using activation-dependent monoclonal antibodies (MoAb). Forty-one MRI-proven normative subjects and 55 patients with a history of ischemic CVD were examined. The intima-media thickness of the carotid artery was measured by using B-mode ultrasound in all subjects.

Results

The appearance rates of PAC-1-positive and CD62P-positive platelets (%) were increased in ischemic CVD patients compared with those in controls (p < 0.0001, p < 0.001, respectively) The patients and controls were divided into those with atherosclerosis (Ath+), defined as intima-media thickness 1.1 mm, and those without (Ath−). There was no significant difference of PAC-1-positive platelets between the Ath− and Ath+ subgroups in either group, but there was increase in Ath− ischemic CVD patients versus Ath− control subjects (p < 0.01), and in Ath+ patients versus Ath+ controls (p < 0.05). CD62-positive platelets in the Ath+ subgroup were significantly increased versus the Ath− subgroup in both the controls (p < 0.001) and ischemic CVD patients (p < 0.05), and there was also an increase in Ath− patients versus Ath− controls (p < 0.05).

Conclusion

Platelet activation markers were increased in patients with ischemic CVD compared with controls. A significant relationship was found between increased CD62-P-positive platelets and carotid artery abnormalities in both controls and ischemic CVD patients, suggesting that platelet activation may be a potential marker for atherosclerosis.     

Platelet activation during treadmill exercise in patients with chronic peripheral arterial disease

β-Thromboglobulin (β-TG) and platelet factor 4 (PF-4) were measured in 59 patients with chronic peripheral arterial disease before and within 5 min. after treadmill exercising till occurrence of claudication. Plasma levels of β-TG before treadmill exercise ranged from 24 to 260 ng/ml with a geometric mean of 63.7 ng/ml, PF-4 levels ranged from 2 to 240 ng/ml with a mean of 18.5 ng/ml. These levels were significantly higher than those obtained in 28 normal individuals in which β-TG ranged from 7 to 39 ng/ml with a geometric mean value of 19.4 ng/ml and PF-4 from 1 to 19 ng/ml with a mean value of 4.6 ng/ml. No correlation between plasma β-TG or PF-4 and extent of arterial disease was found. β-TG levels, measured within 5 min. after treadmill exercise, showed a statistically significant increase to a mean value of 74.3 ng/ml but PF-4 did not rise significantly (mean value : 19.8 ng/ml) The supplementary increase of already elevated β-TG levels may be explained by enhanced in vivo platelet activation during treadmill exercising till occurrence of claudication. As the clearance of PF-4 from human plasma has been shown to be much faster than the clearance of β-TG, increases in PF-4 levels may be more difficult to detect during dynamic explorations of the vascular system.     

Association of the fibrinolytic system and hemorheology with symptoms in patients with carotid occlusive disease

BACKGROUND AND OBJECTIVES: The risk of stroke caused by a symptomatic high-grade carotid stenosis (CS) is high. Disturbed balance between the procoagulant and fibrinolytic activity in blood associated with unfavorable hemorheology could render CS symptomatic. We wanted to assess whether hemostatic and fibrinolytic plasma markers as well as basic indicators of hemorheology differentiate asymptomatic and symptomatic patients with a high-grade CS and whether they are associated with the macroscopic appearance of the plaque and the rate of microembolization. METHODS: We recruited 92 consecutive consenting patients referred to the neurological or the surgical department of our university teaching hospital for treatment of their high-grade CS. Blood samples were collected before surgery for determination of prothrombin fragments F1 and 2, thrombin-antithrombin complex, tissue-type plasminogen activator (tPA) activity and antigen, plasminogen activator inhibitor-1 (PAI-1) activity and antigen, D-dimer, homocysteine, fibrinogen, in plasma, and hematocrit in blood, and the patients underwent transcranial Doppler ultrasonology for evaluation of microembolic signals (MES). RESULTS: Patients with symptomatic plaques had higher hematocrit levels (p = 0.04), as well as trends for higher tPA antigen and MES rate (p = 0.07). Hematocrit, tPA antigen, and PAI-1 antigen and activity were positively correlated with the degree of stenosis. Ulceration was more common in symptomatic plaques but did not reflect variables of hemostasis or fibrinolysis. In multivariate analysis, tPA antigen and hematocrit were risk factors for a symptomatic high-grade stenosis. CONCLUSION: Mediators of fibrinolysis and unfavorable hemorheology may contribute to the development of a symptomatic disease in patients with a high-grade CS.