康复医疗对脑血栓形成患者血液流变学及TXB_2、6-keto-PGF_(1a)的影响

将89例脑血栓形成患者,随机分为康复医疗组(60例)和对照组(29例),观察了两组治疗前后肢体运动功能、血液流变学、血浆TXB_2、6-keto-PGF_(1a)的变化。结果显示:治疗1个月两组对比,康复医疗组红细胞压积下降显著(P<0.05),余项指标均无统计学意义,治疗3个月两组对比,康复医疗组肢体运动功能明显优于对照组(P<0.05),全血比粘度、全血还原粘度、红细胞压积均降低(P<0.01),TXB_2下降(P<0.05),6-keto-PGF_(1a)升高(P<0.05)。康复医疗间接地引起这些变化,对脑血栓形成患者肢体运动功能的恢复有促进作用。     

血栓的形成及中药抗栓溶栓概况

血栓形成是由于正常的凝血机制的扰乱而促使某些血细胞和蛋白质被激活相互作用而最终导致血小板－纤维蛋白血栓的形成．ＡＴ－Ⅲ、ＰＣ、ＴＭ是体内重要的抗凝物质．白细胞与血小板的相互作用、ＰＧＩ２／ＴＸＡ２值以及许多疾病状态是影响血栓形成的诸因素．许多中药具有抗血小板聚集、抗血栓形成的作用，包括生物碱类，如小檗碱、北豆根碱和钩藤碱；中药蒲黄、花椒、沙棘、大蒜的提取物；一些中药复方等．     

MC-001对大鼠脑缺血-再灌注损伤的保护作用及机制

目的:研究4-O-(2’-亚甲基-3’5’6’-三甲基吡嗪基)苯甲酸(MC-001)对大鼠脑缺血-再灌注损伤的保护作用及机制。方法:采用大鼠大脑中动脉缺血-再灌注模型(cerebral ischemia-reperfusioninjury,CIRI),观察MC-001对脑缺血的影响,测定MC-001各剂量组(16、8、4 mg/kg)对脑水肿程度、组织内超氧化物歧化酶(SOD)、丙二醛(MDA)、血栓烷B2(TXB2)、6-酮-前列腺素(6-Keto-PGF1α)等生化指标的影响;采用在体动静脉血栓法,观察MC-001对血栓形成的影响。结果:MC-001(16、8 mg/kg)可显著降低脑水肿(P<0.05和P<0.01vs溶酶组),并增加CIRI大鼠脑组织SOD(P<0.05和P<0.01vs溶酶组)、降低MDA水平(P<0.05和P<0.01vs溶酶组);呈剂量依赖性地降低脑组织TXB2含量,升高6-Keto-PGF1α及6-Ke-to-PGF1α/TXB2比值(P<0.05和P<0.01vs溶酶组);显著抑制大鼠被动、静脉搭桥后形成的血栓。结论:MC-001对脑缺血-再灌注损伤有明显保护作用,其机制可能...     

维拉帕米对血栓形成及血清一氧化氮水平的影响

目的:探讨维拉帕米(Verapamil)对于血栓形成以及血小板聚集率的影响及其可能的机制.方法:大鼠体内分别给予不同剂量的维拉帕米(5,10,20 mg/kg)、赖氨匹林(4.5 mg/kg)以及溶剂(生理盐水2 ml).利用大鼠颈总动脉-颈外静脉血流旁路法观察维拉帕米对血栓形成的影响,并与赖氨匹林比较;同时观察维拉帕米对于血小板聚集率的影响;提取血清,通过硝酸还原酶法测定一氧化氮(NO)代谢产物,以反映NO的水平.结果:维拉帕米可以呈浓度依赖性的降低血小板的聚集率,明显降低血栓的形成,结论:维拉帕米可能通过提高NO的水平来改善血小板的功能.     

单甘酯抗血栓形成作用研究

目的观察单甘酯对血栓形成的影响。方法采用动静脉旁路血栓形成方法观察血栓形成并称重。颈总动脉血栓采用电刺激大鼠颈总动脉方法。小鼠肠系膜血管微血栓采用激光照射。肺栓塞采用小鼠尾静脉注射花生四烯酸。测定大鼠血浆纤维蛋白原含量。结果单甘酯25,50 mg.kg-1能够明显减轻动静脉旁路内丝线上血栓重量;单甘酯25,12.5 mg.kg-1能明显延长血管阻塞时间;单甘酯35.7和71.4 mg.kg-1明显延迟小鼠肠系膜血管微血栓出现时间。单甘酯40,80 mg.kg-1能明显降低花生四烯酸所致的小鼠死亡,单甘酯25,50和100 mg.kg-1显著降低大鼠血浆纤维蛋白含量。结论单甘酯具有明显的抗血栓形成作用。     

The effect of flow and mass transport in thrombogenesis

The paper presents a mathematical analysis of the contributions of flow and mass transport to a single reactive event at a blood vessel wall. The intent is to prepare the ground for a comprehensive study of the intertwining of these contributions with the reaction network of the coagulation cascade. We show that in all vessels with local mural activity, or in “large” vessels (d>0.1 mm) with global reactivity, events at the tubular wall can be rigorously described by algebraic equations under steady conditions, or by ordinary differential forms (ODEs) during transient conditions. this opens up important ways for analyzing the combined roles of flow, transport, and coagulation reactions in thrombosis, a task hitherto considered to be completely intractable. We report extensively on the dependence of transport coefficient k_L and mural coagulant concentration C_w on flow, vessel geometry, and reaction kinetics. It is shown that for protein transport, k_L varies only weakly with shear rate in large vessels, and not at all in the smaller tubes (d<10⁻² mm). For a typical protein, k_L∼10⁻³ cm s⁻¹ within a factor of 3 in most geometries, irrespective of the mural reaction kinetics. Significant reductions in k_L (1/10–1/1,000) leading to high-coagulant accumulation are seen mainly in stagnant zones vicinal to abrupt expansions and in small elliptical tubules. This is in accord with known physical observations. More unexpected are the dramatic increases in accumulation which can come about through the intervention of an autocatalytic reaction step, with C_w rising sharply toward infinity as the ratio of reaction to transport coefficient approaches unity. Such self-catalyzed reactions have the ability to act as powerful amplifiers of an otherwise modest influence of flow and transport on coagulant concentration. The paper considers as well the effect on mass transport of transient conditions occasioned by coagulation initiation or pulsatile flow. During initiation, instantaneous flux varies with diffusivity and bulk concentration, favouring the early adsorption/consumption of proteins with the highest abundance and mobility. This is akin to the ‘Vroman effect’ seen in narrow, stagnant spaces. The effect of flow pulsatility on k_L has the potential, after prolonged cycling, of bringing about segregation or accumulation of proteins, with consequences for the coagulation process.     

Accumulations of von Willebrand factor within ECMO oxygenators: Potential indicator of coagulation abnormalities in critically ill patients?

Clot formation within membrane oxygenators (MOs) remains a critical problem during extracorporeal membrane oxygenation (ECMO). The composition of the clots—in particular, the presence of von Willebrand factor (vWF)—may be an indicator for prevalent nonphysiological flow conditions, foreign body reactions, or coagulation abnormalities in critically ill patients. Mats of interwoven gas exchange fibers from randomly collected MOs (PLS, Maquet, Rastatt, Germany) of 21 patients were stained with antibodies (anti‐vWF and anti‐P‐selectin) and counterstained with 4′,6‐diamidino‐2‐phenylindole. The extent of vWF‐loading was correlated with patient and technical data. While 12 MOs showed low vWF‐loadings, 9 MOs showed high vWF‐loading with highest accumulations close to crossing points of adjacent gas fibers. The presence and the extent of vWF‐fibers/“cobwebs,” leukocytes, platelet–leukocyte aggregates (PLAs), and P‐selectin‐positive platelet aggregates were independent of the extent of vWF‐loading. However, the highly loaded MOs were obtained from patients with a significantly elevated SOFA score, severe thrombocytopenia, and persistent liver dysfunction. The coagulation abnormalities of these critically ill patients may cause an accumulation of the highly thrombogenic and elongated high‐molecular‐weight vWF multimers in the plasma which will be trapped in the MOs during the ECMO therapy.     

Interactions Between Endothelial Secretogogues

Among endothelial secretogogues prostacyclin (PGI₂), nitric oxide (NO) and tissue plasminogen activator (t-PA) play a crucial role in maintaining thromboresistance, tone and structure of the vascular wall. Most receptor agonists, such as B₂ kinin receptor agonists, or shear force produce a coupled release of all three secretogogues, and therefore interactions between them are to be expected. Essentially, PGI₂ is a platelet suppressant, NO a vasodilator and t-PA a fibrinolytic agent. These and other properties of endothelial secretogogues supplement each other in protecting the cardiovascular system from injuries. It is not surprising that disturbances of the secretory function of endothelial cells are associated with atherosclerosis, diabetes, thrombosis or hypertension. Traditionally, PGI₂, NO, t-PA or their substitutes are used individually for the treatment of peripheral arterial disease, angina pectoris or acute myocardial infarction. In light of recent findings, their joint administration can be advocated. For instance, NO donors will potentiate platelet-suppressant action of PGI₂ analogues, whereas exogenous PGI₂ or TXA₂ synthase inhibitors (i.e. following increase in endogenous PGI₂) will abolish a paradox of prothrombotic action of t-PA or streptokinase. The replacement therapy with PGI₂, NO or t-PA should match as closely as possible the physiologically coupled release of these secretogogues.     

去氨加压素对大隐静脉曲张围手术期出血和血栓形成的影响

目的评价大隐静脉曲张围手术期应用去氨加压素(DDAVP)对围手术期出血和血栓形成风险的影响。方法本项前瞻性随机试验纳入2015年1月至2016年9月期间在6个医学中心接受大隐静脉曲张手术的166例患者,随机分为去氨加压素治疗组(n=81)和空白对照组(n=85)。比较两组患者血红蛋白(Hb)、血小板(PLT)、丙氨酸氨基转移酶(ALT)、血肌酐(SCr)、活化部分凝血酶原时间(PT)、D-二聚体(D-dimer)、vWF因子、术后肢体疲斑面积、是否发生下肢深静脉血栓事件以及是否有大出血事件等指标。实验数据采用软件SPSS 22.0进行分析。根据数据类型分别采用t检验、秩和检验(Mann-Whitney U检验)、X~2检验或Fisher确切概率法比较组间差异。结果治疗组术后瘀斑面积[1.92(0.42,10.83)cm~2]显著低于对照组[6.00(1.82,19.60)cm~2],差异有统计学意义(P0.05)。DDAVP在老年人群(≥60岁)中能有效较少大面积瘀斑的出现。对照组观察到1例下肢深静脉血栓事件,治疗组未见。两组术后Hb、PLT、ALT、SCr、PT、D-dimer,vWF因子等指标差异均无统计学意义(P0.05)。结论围术期使用DDAVP可有效减少大隐静脉曲张围手术期瘀斑面积,且不增加术后出血和下肢深静脉血栓发生率。