蚯蚓纤溶酶夺犬纤溶酶活性和血小板聚集功能的影响

研究口服蚯蚓纤溶酶对纤溶系统的和血小板聚集功能的影响。方法 正常雄性Ｂｅａｇｌｅ犬，体重６．５－９ｋｇ，经口给蚯蚓纤溶酶，经前肢静脉取血，以Ｓ－２２５１为发色底物，测定血浆纤溶酶活性；５０μｍｏｌ／Ｌ ＡＤＰ为诱导剂测定血小板聚集率。结果（１）单剂量ＥＦＥ４０，８０ｍｇ／ｋｇ后血浆纤溶酶活性升高，８０ｍｇ／ｋｇ组高于４０ｍｇ／ｋｇ组。连续给药１０ｄ，４０，８０ｍｇ／ｋｇ组均有多个时间点纤溶酶活性各     

蚯蚓纤溶酶的分离纯化及其动力学性质研究

目的：建立一种高效的蚯吲纤溶酶（ＥＦＥ）的分离纯化技术,并研究其特性。方法：蚯蚓经组织匀浆、缓冲液抽提与选择性热变性,再经抑制剂１,６－己二胺（ＨＤ）偶联的Ｓｅｐｈａｒｏｓｅ ４Ｂ亲和层析,ＤＥＡＥ－Ｓｅｐｈａｒｏｓｅ离子交换层析。结果及结论：分离纯化得到具有强烈纤溶活性的酶组分（ＥＦＥ－Ｆ１、２,ＥＦＥ－Ｆ３）。其中ＥＦＥ－Ｆ３对合成底物Ｓ－２２８８和Ｃｈｒｏｍｏｚｙｍ Ｐ的Ｋｍ分别是０．０１ｍｍｏｌ／Ｌ和０．０２ｍｍｏｌ／Ｌ,ＨＤ的Ｋｉ为１ｍｍｏｌ／Ｌ;该酶热稳定性强,能抗４ｍｏｌ／Ｌ脲。     

蚯蚓纤溶酶对家兔溶栓、纤溶和抗凝作用的影响

本实验表明蚯蚓纤溶酶(QM_(85))不仅具有体外溶解血栓的作用,而且口服300万mm~2/kg或静注10万mm~2/kg可加速急性肺动脉栓塞的溶栓效应,与生理盐水组比较有显著性差异。QM_(85)还能使兔血浆纤维蛋白原含量下降,“3P”试验阳性,凝血时间,复钙时间和凝血酶原时间延长。     

穿心莲对冠心病患者血小板功能及纤溶功能的影响

目的：为了探讨穿心莲在冠心病防治的作用。方法：本文采用随机分组，将冠心病患者（７７例）随机分配到穿心莲治疗组，阿斯匹林组及安慰剂组中去，比较穿心莲对冠心病患者血小板聚集率，血浆ＴＸＢ２，６－Ｋ－ＰＧＦ１α及优球蛋白溶解时间的影响，并与阿斯匹林治疗组及安慰剂组所得结果进行比较。结果穿心莲能显著抑制冠心病患者血小板１ｍｉｎ及５ｍｉｎ聚集率（Ｐ〈０．０１），显著抑制冠心病患者血浆ＴＸＢ２浓度（Ｐ〈０．０     

高活力蚯蚓纤溶酶的纯化及性质研究

由电泳得知赤子爱胜蚓ＥｉｓｅｎｉａＦｏｅｌｉｄｅ有６种纤溶酶同工酶。经纯化从中得到一种具强纤溶活性的单组分酶。收率为粗酶粉总活力的１９．１％。该酶分子量为３００００Ｄ,比活为６６６７Ｕ／ｍｇ,在ｐＨ４～１１及２５℃～５５℃温度范围内稳定。     

各型冠心病纤溶酶原及血小板聚集功能的临床意义

本文总结了纤溶酶原、血小板集聚功能在不同类型冠心病的改变。结果:①纤溶酶原在不稳定型心绞痛组和陈旧性心肌梗塞组较正常组明显降低,急性心肌梗塞组与正常组相比,差别尤为显著。②血小板最大聚集率在陈旧性心肌梗塞组高于不稳定型心绞痛组。在急性心肌梗塞组连续三次检测中显示聚集率有逐渐增高趋势。     

THE IMPAIRMENT OF PLATELET FUNCTION IN FIBRINOLYSIS AND PRESERVING EFFECT OF APROTININ

Platelet adhesion depends on the platelet membrane glycoprotein Ib (GPIb) and plasma von Willebrand Factor (vWF), which can be reflected by ristocetin-induced aggregation. Here we report damage effect of fibrinolysis and preserving effect of aprotinin on platelet function. Addition of 40 U/ml urokinase and 0.3 U/ml plasmin to PRP or washed platelets made the ristocetin-induced aggregation decline to 31.6% and 38.5% of control value respectively. The extent of declining was positively correlated with the concentration of urokinase and plasmin. Meanwhile, the platelet GPIb decreased to 76.4% of control value. The results showed that the fibrinolysis impaired the platelet function and this effect may be associated with the hydrolysis of GPIb. Further research found that by adding the same dose of urokinase or plasmin to aprotinin-pretreated PRP or washed platelets, the aggregation did not change statistically and decrement of GPIb is much less marked. We concluded that the aprotinin could relieve the platelet dsfunction effectively by its inhibitory effect on fibrinolytic activity.     

粉防己碱,牛磺酸和阿斯匹林对血小板聚集及血栓形成影响的研究

粉防己碱（Ｔｅｔ）和牛磺酸（Ｔａｕ）均能抑制ＡＤＰ、胶原和凝血酶诱导的大鼠血小板聚集及血栓形成。Ｔｅｔ抑制ＡＤＰ诱导的血小板聚集作用较强。Ｔａｕ则对胶原诱导的作用强。阿斯匹林较二药合用弱。     

EFFECT OF PLATELET HEPARIN AFFINITY MATERIALS ON ENDOTHELIAL CELL FIBRINOLYTIC ACTIVITY AND SECRETION OF PROSTACYCLIN

Platelets and endothelial cells play an important role in initiation anddevelopment of atherosclerosis. Much attention has been paid to investigate effect ofplatelet release products on endothelial cells, it is unknown whether platelet products canaffect endothelial cell fibrinolytic activity. We extracted platelet heparin affinity materials(PHAM) from platelet lysate using Heparin-Sepharose CL 6B column, and treated cul-tured human umbilical endothelial cells with PHAM to imitate conditions in vivo. As a re-suit, PHAM could increase endothelial cell PAI activity without change of t-PAantigen. No free t-PA activity was detected in conditioned medium from either stimulatedor nonstimulated endothelial cell cultures. Addition of 10μg/ml PHAM to endothelialcells induced nearly one fold increase of PAI activity (P<0.001). Such increase was timeand dose dependent. Moreover, treatment with PHAM resulted in a dose dependent in-crease of the secretion of prostacyclin (measured by 6-keto-PGF_(1α)), 10μg/ml PHAMcaused six fold increase of prostacyclin (P<0.001). The above results showed thatPHAM could inhibit endothelial cell fibrinolytic activity but increase secretion ofprostacyclin. It is assumed that this could be the negative feedback for protecting thehuman body from thrombus formation. Break of this feedback mechanism may beresponsible for thrombotic diseases.     

支气管哮喘发作时PAdT与PAgT的改变

通过对32例支气管哮喘急性期患者血小板功能的测定,结果显示支气管哮喘急性期患者血小板粘附性(PAdT)与聚集性(PAgT)明显增高,与缓解期相比有明显差异(P<0.01),提示血小板功能异常与支气管哮喘的常规发病机理有关。     

普疏舒对血小板聚集功能的影响

本文观察了普疏舒对大白鼠血小板聚集功能的影响。结果表明,连续灌胃给予普疏舒(105.8mg/kg和282.2mg/kg)对牛凝血酶诱导的大鼠血小板聚集有明显抑制作用,抑制率分别为0.86和0.67(P<0.01)。同样剂量的普疏舒亦可使ADP诱导的血小板聚集率降低0.67和0.44(P<0.01)。提示普疏舒具有对抗血小板聚集的作用。     

海洋假单胞菌碱性蛋白酶的纤溶及抗血栓形成作用

①目的　探讨海洋假单胞菌碱性蛋白酶 (MPAP)的纤溶作用及对血栓形成和血小板聚集功能的影响。②方法　通过纤维蛋白平板实验 ,观测MPAP的纤溶活性 ;建立大鼠颈动脉血栓形成模型 ,观察静脉应用MPAP后血栓形成时间及血小板最大聚集率的变化。③结果　MPAP具有较强的直接溶解纤维蛋白的作用 ;MPAP(1 0 0、2 0 0mg/kg体质量 )静脉用药后 ,血栓形成时间明显延长 (F =4 .72 ,q =3.78、4 .97,P <0 .0 5 ) ,血小板的最大聚集率显著降低 (F =4 0 .5 6 ,q =8.4 2、1 3.85 ,P <0 .0 5 )。④结论　MPAP具有明显的抗血栓形成作用     

肽6A对纤溶系统及血小板聚集功能的影响

P6A(10~(-6)—10~(-4)mol/L)体外实验显著减弱ADP诱导的大鼠血小板聚集,明显增加血小板的有效解聚率。20～30μmol/kg的 P 6 A动脉注射后,3～6分钟时大鼠血浆t-PA、PAI活性无变化。0.25～1.0μg/ml的P6A亦不能使兔血浆纤维蛋白平板出现溶解。实验结果提示,P 6 A对血栓闭塞性血管再通的作用主要依赖其抗血小板聚集及促血小板解聚的作用。     

血管内皮素对人类血小板功能影响的研究

实验表明,血管内皮素不引起血小板胞浆游离钙离子的变化和血小板聚集;血管内皮素与血小板活化剂(胶原、凝血酶、血小板激活因子)联合实验表明,血管内皮素对血小板活化剂引起的反应亦无明显影响。