亲体肝移植患者围手术期止血与凝血指标的变化

背景：亲体供肝移植后由于止血和凝血指标的异常可出现出血及血栓等严重并发症,但其具体变化规律如何尚未见报道。 目的：探讨亲体肝移植受体围手术期止血与凝血指标的变化。 方法：抽取44例亲体肝移植受者移植前、移植后1~7 d静脉血,检测患者血浆中活化部分凝血活酶时间、凝血酶原时间、凝血酶时间、纤维蛋白原含量、血小板、抗凝血酶活性、纤溶酶原活性、 纤溶酶原激活物抑制剂1活性、D-二聚体、纤维蛋白降解产物的动态变化。以32名体检中心健康体检者为对照。 结果与结论：移植前活化部分凝血活酶时间、凝血酶原时间、凝血酶时间延长(P < 0.01),纤维蛋白原含量、血小板、抗凝血酶活性、纤溶酶原活性降低(P < 0.01),纤溶酶原激活物抑制剂1升高(P < 0.01);移植后1周凝血酶原时间、活化部分凝血活酶时间、凝血酶时间、血小板、纤维蛋白原含量、抗凝血酶活性逐渐恢复正常,纤溶酶原活性、纤溶酶原激活物抑制剂1、D-二聚体、纤维蛋白降解产物仍异常于正常值(P < 0.01)。结果提示亲体肝移植后凝血因子、抗凝因子的恢复是相对较快的,而纤溶因子的恢复则较为迟缓,纤溶功能亢进,是肝脏移植严重出血的主要原因,因此在移植后凝血与止血功能的监测,是预防出血和血栓形成的有效措施。 关键词：亲体肝移植;止血;凝血;肝移植;器官移植;围手术期     

组织型纤溶酶原激活物及其抑制物与脑血管疾病

组织型纤溶酶原激活物 (ｔｉｓｓｕｅｐｌａｓ ｍｉｎｏｇｅｎａｃｔｉｖａｔｏｒ ,ｔ -ＰＡ)及其抑制物(ｔｉｓｓｕｅｐｌａｓｍｉｎｏｇｅｎａｃｔｉｖａｔｏｒｉｎｈｉｂｉｔｏｒ -1,ＰＡＩ - 1)是纤溶系统的二个重要组成部分。目前对二者的结构、特性以及与脑血管疾病的关系尚未完全阐明。缺血性脑血管病患者血浆中二者的活性、抗原含量测定甚至出现了矛盾的结果。1　ｔ -ＰＡ、ＰＡＩ- 1在纤溶系统中的作用　　纤溶酶原激活物 (ＰＡ)即组织型纤溶酶原激活物 (ｔ -ＰＡ)和尿激酶型纤溶酶原激活物 (ｕ -ＰＡ)以及它们的抑制物在纤维蛋白…     

急性脑梗塞患者血浆t—PA,PAI及vWF：Ag的检测及其与血脂的关系

本文同时检测了22例急性期脑梗塞患者血浆组织纤溶酶原激活物(t-PA)抑制物(PAI)活性及因子Ⅷ相关抗原(vWF:Ag)含量,结果示三指标与对照组比较,均有显著的增高;并对患者组上述指标与血脂间进行了相关性分析,认为血脂与纤溶系统间的相互联系对动脉粥样硬化、脑血栓形成具有重要意义。     

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。     

血管介入与保守方案治疗急性脑梗死的疗效及对纤溶活性水平的影响

目的对比血管介入与保守方案治疗急性脑梗死的临床效果,分析其对纤溶活性水平的影响。方法研究对象来源于我院2014-01—2014-12收治的66例急性脑梗死患者,按随机数字表法分为对照组与观察组。对照组接受保守治疗;观察组接受血管介入溶栓治疗。检测2组治疗前后血浆血管性假血友病因子(vWF)、组织型纤溶酶原激活物(tPA)、血浆纤溶酶原激活物抑制剂-1(PAI-1)水平,观察2组治疗效果。结果观察组总有效率93.9%显著高于对照组的69.7%,差异有统计学意义(P0.05);治疗前2组vWF、tPA及PAI-1对比差异无统计学意义(P0.05);2组治疗后上述指标对比差异均有统计学意义(P0.05)。结论血管介入溶栓治疗急性脑梗死效果更为理想,能有效促进纤溶活性水平升高,适于临床推广应用。     

组织型纤溶酶原激活物与缺血性脑卒中

缺血性脑卒中是一种多因素作用的疾病,其发生机制至今尚无一致看法,高纤维蛋白原血症已被认为是缺血性脑卒中的独立危险因素.血管内纤维蛋白的清除主要靠纤溶酶来调节,组织型纤溶酶原激活物(t-PA)通过激活与纤维蛋白结合的纤溶酶原,来促进纤维蛋白的溶解,保持血管通畅和正常血流,组织纤溶酶原激活物抑制物(PAI)作为抑制剂,能迅速与之作用使之失去活性,对t-PA的活性起调节作用.近年来的研究表明,t-PA,PAI与缺血性卒中的发病密切相关.     

急性脑梗死患者血浆纤溶酶原激活物及其抑制剂-1水平的动态变化及其与梗死面积的关系

目的 探讨急性脑梗死患者血浆组织型纤溶酶原激活物(t-PA)及其抑制剂-1(PAI-1)水平的动态变化及其与梗死面积的关系.方法 急性脑梗死患者100例,其中大面积脑梗死22例、小面积脑梗死36例、腔隙性脑梗死42例,采用发色底物显色法检测脑梗死患者病后24 h、2 d、14 d、21 d的血浆t-PA、PAI-1水平,与正常对照组比较;并比较不同面积脑梗死患者血桨t-PA、PAI-1水平.结果 与正常对照组比较,急性脑梗死患者病后24 h、2 d、14 d血浆t-PA水平显著降低,血浆PAI-1水平明显升高(均P＜0.01);病后21 d两者与正常对照组差异无统计学意义(均P＞0.05);大面积脑梗死患者t-PA水平明显低于小面积和腔隙性脑梗死患者,小面积脑梗死患者又明显低于腔隙性脑梗死患者(均P＜0.01);不同面积脑梗死组之间PAI-1水平未见明显差异(均P＞0.05).结论 脑梗死患者急性期血浆t-PA水平降低及PAI水平升高;脑梗死面积越大的患者血浆t-PA水平降低程度越明显,而血浆PAI-1水平与梗死面积无关.     

急性脑梗死及其高危人群血栓前状态指标的测定

目的 探讨血栓前状态(PTS)指标在脑梗死及其高危人群防治中的作用和意义.方法 使用酶联免疫吸附法和凝固法检测33例急性脑梗死,35例脑梗死高危和25例正常对照组患者外周血小板a颗粒膜蛋白(GMP-140)、组织型纤溶酶原激活物(t-PA)、组织型纤溶酶原激活物的抑制物(PAI-1)和纤维蛋白原(Fg) 的水平变化.结果 与对照组相比,脑梗死组、高危组血浆GMP-140、PAI-1水平显著升高、t-PA显著降低(P＜0.01),Fg升高(P＜0.05),脑梗死组与高危组之间无显著性差异.结论 脑梗死及其高危患者存在PTS,在控制原发病的同时给予抗凝、降低血液黏稠度治疗可能会降低血栓的发生率.     

糖尿病性和非糖尿病性脑梗死患者血浆中纤溶酶原激活物及其抑制剂活性的动态观察

目的 :观察糖尿病性脑梗死 (diabeticischemicstroke ,DIS)和非糖尿病性脑梗死 (non diabeticischemicstroke ,NDIS)患者血浆中纤溶酶原激活物 (plasminogenactivator ,PA)及纤溶酶原激活物抑制剂 (plasminogenactivatorinhibitor ,PAI)的动态变化情况。方法 :应用底物发色法测定血浆中PA和PAI活性 ,以观察DIS和NDIS患者血浆PA和PAI活性的动态变化。结果 :NDIS患者血浆中PA活性在4～ 2 1d较非脑梗死患者升高 ;DIS患者的PA活性在 7h～ 2 1d较NDIS患者为低 ,但PAI活性在各组间无明显差异。结论 :DIS患者血浆中PA活性较NDIS患者降低 ,提示其存在纤溶系统激活的紊乱 ,并可能与DIS症状加重有关。     

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）。     

Endothelial cell and hemostatic activation in relation to cytokines in patients with sepsis

Sepsis is commonly associated with disturbances of the hemostatic balance. Most of the pathophysiological changes in sepsis are caused by endotoxin acting directly through endothelial injury or indirectly through release of cytokines with procoagulant effects. The relation between cytokines and hemostatic parameters was assessed in 32 patients with sepsis. Prothrombin fragment 1+2 (F1+2), thrombin-antithrombin III complexes (TAT), tissue type plasminogen activator (t-PA) functional and antigen, plasminogen activator inhibitor-1 (PAI-1), plasminalpha2-antiplasmin complexes (PAP), D-Dimer, thrombomodulin (TM) and von Willebrand factor (vWF) were measured in patients and in 30 healthy subjects. The levels of cytokines TNF-alpha and interleukin-6 (IL-6) also were determined. A significant increase of F1+2, TAT, PAI-1, PAP, and D-Dimer was observed in septic patients as compared with controls (p<0.0001), whereas t-PA activity was significantly reduced (p<0.01). The markers of endothelial cell activation TM, vWF, and t-PA antigen also were elevated significantly as compared with the control group (p<0.01). Finally, we found a marked increase of TNF-alpha and IL-6 (p<0.0001). Whereas the increase of cytokine levels could be partially responsible for the hemostatic activation, it did not correlate with markers of endothelial activation in patients with sepsis.     

Studies on the pathogenesis of coagulopathy in patients with arterial thromboembolism and malignancy

Plasma levels of thrombin-antithrombin III complex(TAT), plasmin-₂-plasmin inhibitor complex(PAP), von Willebrand factor antigen (vWF:Ag) plasminogen activator antigen(PA) and plasminogen activator inhibitor-1 antigen(PAI-1), were determined in 110 patients with arterial thromboembolic diseases within 4 weeks after attack (Th; 41 cases with myocardial infarction and 69 with cerebral infarction), 67 patients with various types of carcinoma(Ca; 31 cases without metastasis and 36 with metastasis)and 50 age-matched healthy individuals(Co). The following results were obtained: 1) Mean plasma levels of TAT, PAP, vWF:Ag, PA and PAI-1 were significantly higher in Th than Co. 2) Mean plasma levels of TAT, PA and PAI-1 were significantly higher in Ca than Co regardless of metastasis but those of PAP and vWF:Ag were significantly higher only in Ca with metastasis than Co. 3) Significant relationship was observed between plasma levels of TAT and PAP both in Th and Ca. 4) Significant relationship was also observed between plasma levels of TAT and vWF:Ag, PA or PAI-1 in Th, but not in Ca. It is suggested from these results that the coagulopathies observed in these patients result from the activation of intravascular blood coagulation and fibrinolysis, and that vascular endothelial cell damage may play an important role in the activation in Th.     

Endothelial dysfunction and systemic inflammation in persons with echolucent carotid plaques

Echolucent carotid plaques are associated with high risk for future ischemic cerebrovascular events independent of the degree of stenosis. Elevated levels of markers of systemic inflammation and endothelial dysfunction are predictors for future myocardial infarction and stroke. The present study was undertaken to investigate the relations between plaque morphology, endothelial dysfunction assessed by tissue-plasminogen activator antigen (t-PA ag) and vonWillebrand factor (vWF), and systemic inflammation in persons with carotid stenosis. We conducted a crosssectional study including 133 persons with carotid stenosis and 138 controls without stenosis recruited from the populationbased Troms? Study. High-resolution B-mode and colour Doppler/pulsed-wave Doppler ultrasonography of both carotid arteries was performed, and plaque morphology in terms of echogenicity was assessed. Persons with carotid stenosis had significantly higher plasma t-PA and vWF concentrations than controls. There was a significant inverse relationship between t-PA ag and plaque echogenicity (p = 0.034). The increased plasma t-PA ag in persons with carotid stenosis was not associated with increased plasminogen activator inhibitor-I (PAI-1). Persons with echolucent carotid plaques had higher degree of systemic inflammation, and plasma t-PA and vWF concentration increased significantly across quartiles of WBC, fibrinogen, and hs-CRP. Our findings may suggest that plasma t-PA may be superior to vWF as a marker for endothelial dysfunction due to its ability to discriminate between various plaque echogenicity, and that the predictive role of t-PA ag in cardiovascular disease is independent of inhibited fibrinolysis.     

Endothelial Cell Markers in Chronic Uremia: Relationship with Hemostatic Defects and Severity of Renal Failure

Plasma von Willebrand factor antigen, soluble thrombomodulin, and tissue factor were increased in 31 patients with severe chronic renal failure (creatinine clearance <20 ml/min) under conservative treatment, whereas plasminogen activator inhibitor antigen did not differ significantly from healthy controls. No correlation among plasma levels of these proteins was found. Three patterns of relationship between endothelial cell markers and hemostatic defects were identified: 1) Plasma thrombomodulin, a marker of endothelium damage, was found an independent predictor of bleeding time and platelet aggregation, and secretion defects, and was also related to the severity of renal failure; 2) von Willebrand factor antigen, an index of endothelial cell activation and secretion, was significantly correlated with intravascular markers of thombin and plasmin generation and with platelet adenosine triphosphate content, but not with plasma creatinine levels; and 3) tissue factor and plasminogen activator inhibitor antigen levels were not statistically correlated with the diverse hemostatic defects. Activation of coagulation and fibrinolysis, secondary to endothelial cell activation, appearing early during the evolution of chronic renal failure, is pathogenically related to the platelet dysfunction, and probably to development of atherosclerosis and thrombotic events in this disease. The progression of chronic renal failure, through endothelial cell damage, would lead to aggravation of the platelet functional defect potentiating the hemorrhagic risk.     

上海地区汉族人群组织型纤溶酶原激活物基因多态性与脑梗死的关系

目的：探讨上海地区汉族人群组织型纤溶酶原激活物基因（TPA）多态性与脑梗死的关系。方法：采用PCR及基因测序技术检测157例急性脑梗死患者及169例对照组TPA-7351位点的多态性。应用非条件Logistic回归模型，调整混杂因素后，分析各基因型与急性脑梗死发生的关系。结果：在急性脑梗死组C／C基因型、C／T基因型和T/T基因型者分别为0．42、0．45和0．13。对照组依次分别为0．44、0．47和0．09。经调整混杂因素后，与C／C基因型相比，T/T基因型发生急性脑梗死的危险性显著升高（P〈0．05）；分层分析发现T/T基因型主要与腔隙性脑梗死的发病风险有关（P〈0．05）。结论：在上海地区汉族人群中，TPA-7351C／T基因多态性与腔隙性脑梗死发病有关。     

脑外伤后迟发性脑梗塞患者急性期纤溶状态研究

目的初步探讨脑外伤后迟发性脑梗塞患者急性期血浆及脑脊液凝血纤溶状态变化,为临床脑外伤后迟发性脑梗塞提供诊治依据。方法脑外伤后迟发性脑梗塞患者72例,采集血浆,同时采集脑脊液,测定脑脊液及血浆部分凝血纤溶指标,并与171例脑外伤后无脑梗塞患者对照进行比较。结果脑外伤后迟发性脑梗塞组(实验组)脑脊液及血浆组织型纤溶酶原激活物(t-PA)、D-二聚体(D-D)含量明显高于非脑梗塞组(对照组)(P<0.01)而纤溶酶原(PLG)活性明显下降(P<0.01)。结论脑外伤后迟发性脑梗塞患者急性期存在明显的高凝状态和继发性纤溶活性增高。     

脑梗死患者血纤溶系统活性指标的改变和预后的关系

目的 研究脑梗死患者血浆组织型纤溶酶原激活物（ｔ－ＰＡ）及其抑制物（ＰＡＩ－１）水平的改变和预后的关系。方法 对１１２例脑梗死患者进行了血浆ｔ－ＰＡ、ＰＡＩ－１、血糖、血脂的检测及神经功能缺损程度的评分。分为脑梗死组,再梗死组和正常对照组进行比较;并根据神经功能缺损程度的评分分型、重型３组比较各组间的血浆ｔ－ＰＡ、ＰＡＩ－１水平差异及其和预后的关系。结果 脑梗死组、再梗死组的血浆ｔ－ＰＡ、ＰＡＩ－     

Relationship between maternal and cord blood hemostatic disturbances in preeclamptic pregnancies

Endothelial cell activation or damage is believed to play a key role in preeclampsia (PE) and may underlie the hemostatic changes observed in this syndrome. The aim of this study was to evaluate a relationship between maternal and cord blood hemostatic disturbances in preeclamptic pregnancies. We measured the plasma levels of tissue plasminogen activator (tPA) antigen and of plasminogen activator inhibitor type 1 (PAI-1) antigen, both markers of hemostatic and endothelial function, and fibrin fragment D-dimer. Maternal blood from uncomplicated (n = 42) and PEc pregnancies (n = 44) were collected before delivery, and umbilical cord blood (UCB) immediately after delivery.In preeclamptic cases, UCB presented significantly higher tPA values and significantly lower PAI-1/tPA ratio. Preeclamptic women also presented significantly higher tPA, as well as PAI-1 values, when compared with normal pregnant women; no significant difference was found for D-dimer. In preeclamptic women, proteinuria (a marker of PE severity) correlated positively and significantly with tPA and PAI-1 antigen levels. An inverse relationship between maternal tPA antigen levels and fetal birth weigh in PE was also observed.Our data show that the hemostatic maternal disturbances observed in preeclamptic women have similarities with the UCB circulation, and that endothelial dysfunction is the most plausible underlying cause. Moreover, maternal hemostatic disturbances seem to be associated with the severity of PE. Further studies are needed to strength the values of tPA and PAI-1 as markers of severity in PE.     

缺血性脑卒中患者血浆NO浓度变化的研究

目的 研究不同类型的缺血性脑卒中患者的血浆一氧化氮（NO）浓度变化及其临床意义。方法 采用硝酸还原酶法测定230例脑梗死患者、103例腔隙性脑梗死患者以及169名正常对照者的血浆NO浓度。结果 脑梗死组血浆NO浓度与另两组相比显著增高（均P＜0．01）,而腔隙性脑梗死患者的血浆NO浓度低于对照组（P＜0．05）。结论 脑梗患者急性期血浆NO浓度可作为缺血损害的一个参考指标;而腔隙性脑梗死组NO浓度下降反映患者的高血压等基础病变的存在。