瑞香素抗血栓作用

瑞香素80 mg/kg iv对大鼠实验性血栓形成有明显的抑制作用,抑制率54%,在试管内当浓度为0.025,0.05及0.1 mg/ml时,可抑制ADP诱导的家兔血小板聚集。iv 80 mg/kg 5 min,对ADP诱导的家兔血小板聚集也有明显的抑制作用。iv 40及80 mg/kg 20 min,皆可使血小板粘附性降低;并能延长小鼠凝血时间。iv 80 mg/kg 5 min,对家兔纤维蛋白原含量,全血粘度及血浆比粘度均无明显影响。     

刺五加茎时对血小板聚集功能的影响

刺五加茎叶的乙醇提取液相当于生药量25～70mg/ml,体外实验能明显地抑制ADP、胶原所诱导的家兔血小板聚集。家兔iv 700mg/kg,10min后明显抑制ADP诱导的家兔血小板聚集,大白鼠iv 1000mg/kg,30min后明显抑制ADP诱导的血小板聚集。体外实验可使家兔血浆复钙时间明显延长。     

单甘酯对血小板功能及纤维蛋白原含量的影响

目的 :研究单甘酯对血小板聚集、粘附功能及出血时间和纤维蛋白原含量的影响。方法 :比浊法观察血小板聚集功能 ,玻瓶法观察血小板粘附功能 ,小鼠剪尾法观察出血时间 ,比色法测定纤维蛋白原含量。结果 :单甘酯 2 5、5 0mg/kg对血小板粘附有明显抑制作用 ,2 5、5 0、10 0mg/kg(iv)能明显抑制胶原和花生四烯酸诱导的血小板聚集 ,对ADP诱导的血小板聚集无抑制作用 ;40、80mg/kg(ip)可明显延长小鼠尾出血时间 ;2 5mg/kg(iv)即可降低大鼠血浆纤维蛋白原含量。结论 :单甘酯有明显的抑制血小板功能和降低血浆蛋白原含量的作用。     

BM13505对血小板聚集和血栓形成的影响

BM13505在体外对花生四烯酸(AA)诱导的家兔血小板聚集有抑制作用且呈剂量依赖性,其IC_(50)为20μmol/L;对 ADP 和胶原诱导的血小板聚集则无显著影响。大鼠 ivBM13505 0.23mg/kg 能显著,延长血管闭塞时间,与阿司匹林30mg/kg 药效相近。小鼠 ivBM13505 1.13mg/kg 可明显延长尾出血时间效应与阿司匹林30mg/kg 相近。     

夏天无总碱对大鼠血小板功能的影响

夏天无总碱(COAMTA)体外实验和体内给药都明显抑制ADP诱导的大鼠血小板聚集,并明显抑制血栓的形成和血小板粘附。COAMTA iv 0.3mg/kg对大鼠实验性血栓形成有明显的抑制作用,抑制率为31.3%。提示上述作用可能是该药治疗脑血管栓塞等疾病有效的机理之一。     

溶栓1号抗血小板聚集及抗血栓形成作用

溶栓 1号是从蚯蚓中提取的酸性蛋白酶 ,并经进一步纯化 ,可静脉给药考察对ADP诱导的家兔血小板聚集的抑制作用 ;并采用小鼠肺血栓模型 ,电刺激致家兔颈动脉血栓模型及穿线法形成家兔颈动脉血栓模型 3种实验性血栓模型 ,考察溶栓 1号的抗血栓形成作用。实验结果表明 :溶栓 1号静脉注射给药 (1 5 0、3 0 0、60 0u/kg)可明显抑制ADP诱导的家兔血小板聚集作用 ,并可明显抑制小鼠肺血栓、家兔颈动脉血栓的形成。溶栓 1号抑制血栓形成可能与抑制血小板活性有关     

尼群地平的抗血小板聚集和抗血栓作用

国产尼群地平(1)对凝血酶(0.15u/ml)诱导的血小极聚集的 IC_(50)是47.5μmol/L,对 ADP(4μmol/L)诱导作用的 IC_(50)是93.9μmol/L。大鼠 iv 1 0.8μg/g 对凝血酶诱导血小板聚集的抑制率为89.8%,对 ADP、AA 诱导血小板聚集的效应也有非常显著的抑制作用。1尚可明显抑制血栓形成。     

当归及其成分阿魏酸对大鼠血小板聚集和5-HT释放的影响

本文报告当归及其成分阿魏酸对大鼠血小板聚集性和5-HT释放反应的影响。结果表明,当归水剂在试管内当浓度为200～500mg/ml,阿魏酸0.4～0.6mg/ml时抑制ADP和胶原诱导的大鼠血小板聚集。静脉注射当归20g/kg 5分钟后对ADP和胶原诱导的大鼠血小板聚集有明显的抑制作用。阿魏酸钠0.2g/kg和0.1g/kg静脉注射时分别抑制ADP和胶原诱导的大鼠血小板聚集。用³H-5HT标记血小板,观察血小板聚集和释放反应的关系。当归水剂500mg/ml和阿魏酸钠1～2mg/ml对凝血酶诱导的血小板聚集有明显抑制作用,同时也抑制³H-5HT从血小板中释放。     

哒嗪酮类新化合物9612的抗血小板聚集作用

研究了新型哒嗪酮类化合物 96 12对家兔和大鼠血小板聚集的影响 .结果发现 ,96 12在体外能明显抑制花生四烯酸 (AA) ,腺苷二磷酸 (ADP)和凝血酶 (thrombin)诱导的家兔血小板聚集 ,其IC50 分别为 3 2 0 ,9 44和 7 10 μmol/L .96 12 .灌胃给药 (ig) ,能显著抑制AA和ADP诱导的大鼠血小板聚集 ,其作用与同等剂量 (15 0mg/kg)的阿斯匹林 (ASA)相比无明显差异 (P >0 0 5 ) .     

香草酸抗血小板聚集作用的体内外研究

目的香草酸是一种酚酸类化合物,具有抗氧化、抗炎等药理作用,其抗血栓作用尚未有报道。本实验室前期通过筛选发现香草酸具有良好的抗血小板聚集作用,因此本研究通过体内外实验对香草酸抗血小板聚集的作用进行系统评价。方法采用花生四烯酸(arachidonic acid,AA)、二磷酸腺苷(adenosine diphosphate,ADP)、凝血酶(thrombin,THR)诱导体内外血小板聚集模型,结合凝血四项检测评价香草酸抗血小板聚集及抗血栓的作用。结果体外实验中,香草酸对ADP和AA诱导的血小板聚集具有显著抑制作用,并剂量依赖性抑制ADP诱导的血小板聚集;体内试验中,香草酸(10、30和100 mg/kg)能够剂量依赖性抑制ADP和AA诱导的血小板聚集;同时,香草酸(100 mg/kg)能显著降低纤维蛋白原、增加凝血酶原时间,对活化部分凝血活酶时间和血浆凝血酶时间无明显影响。结论本研究首次发现香草酸对ADP和AA诱导的血小板聚集具有抑制作用,为研发具有自主知识产权的抗血小板聚集药物提供了实验依据。     

清脑胶囊对家兔体内血栓形成的影响

目的研究清脑胶囊在家兔体内对血栓的溶栓作用和对血小板聚集的影响。方法采用家兔颈动脉穿线法形成颈动脉血栓模型,观察清脑胶囊对家兔血栓形成以及胶原诱导的血小板聚集作用的影响。结果清脑胶囊能明显降低家兔颈动脉血栓的湿重,并对血小板聚集有明显的抑制作用。结论清脑胶囊具有显著的抗血栓形成的作用。     

Anti-thrombotic effects of higenamine

The anti-platelet and anti-thrombotic effects of higenamine, a benzyltetrahydroisoquinoline alkaloid of the roots of Aconitum japonicum (Ranunculaceae), were investigated. The degree of platelet aggregation was measured with platelet rich plasma (PRP). An acute thrombotic condition was induced in mice by the injection of the mixture of collagen and epinephrine. The thrombus formation was induced inside the arterio-venous shunt tube installed between an abdominal aorta and the renal vein of rats. Higenamine showed inhibitory activities to both human and rat platelet aggregation induced by ADP, collagen and epinephrine. It was more inhibitory to epinephrine induced aggregation (IC(50); 19 and 7.2 microM to human and rat platelets respectively) than ADP- or collagen-induced aggregation. The anti-thrombotic effects of higenamine were also observed in both mouse acute thrombosis model and rat arterio-venous shunt (AV-shunt) models. The oral administration of higenamine (50 or 100 mg/kg) increased the recovery rates from the acute thrombotic challenge in mice and lowered the weight of thrombus formed inside the AV-shunt tube in rats.     

异亚丙基莽草酸抗血栓作用的实验研究

目的研究异亚丙基莽草酸(ISA)对大鼠动静脉环路血栓、大脑中动脉栓塞及血小板聚集的对抗作用及机制。方法用动静脉环路血栓及三氯化铁致大脑中动脉栓塞(MCAT)模型观察药物作用;并研究了ISA体内、外给药对血小板聚集的影响。结果ISA 25,50,100及200 mg·kg^-1 ig均可显著降低大鼠体外血栓重量;ISA 50,100,200 mg·kg^-1 ig可明显改善MCAT模型大鼠神经症状;ISA 100及200 mg·kg^-1 ig MCAT模型大鼠脑梗塞范围分别下降27.8%和31.6%;另外,ISA体内、外给药对ADP和胶原诱导的血小板聚集有明显的抑制作用。结论ISA可能通过抗血小板聚集作用抑制血栓的形成。     

迷迭香酸抗血栓和抗血小板聚集作用

迷迭香酸是丹参水溶性成分之一。大鼠体内实验(iv)表明,它能抑制静脉血栓形成。阻抑胶原诱导的血小板聚集,促进纤维蛋白溶解活性。当剂量为50及100 mg/kg时,血栓形成的抑制率分别为41.9和54.8%(P<0.vv05)。当剂量为100及150mg/kg时,血小板聚集的抑制率分别为30.4%(P<0.05)和46.4%(P<0.01),血浆优球蛋白溶解时间缩短(P<0.05)。纤维蛋白原含量无明显变化。以上结果说明,迷迭香酸有温和的抗血栓作用。其机理可能与抗血小板聚集和增强纤维蛋白溶解活性有关。     

三种蝮蛇抗栓酶注射剂对大鼠和家兔血小板聚集的影响

用比浊法研究三种蝮蛇抗栓酶注射剂对大鼠和家兔血小板聚集的影响,结果表明蝮蛇抗栓酶注射剂在试管内浓度0.045u/ml 时对大鼠和家兔血小板聚集无明显抑制作用。静脉注射蝮蛇抗栓酶注射剂1u/kg 对家兔血小板聚集有明显抑制作用。尤其是蛇岛蝮蛇抗栓酶注射剂抑制作用最为显著。     

瑞香素对血清脂质及脂蛋白胆固醇含量的影响

Daphnetin is one of the components of Daphne koreana Nakai and the sample used in the experiment is the synthesized product. The compound was shown to possess obvious effect on lipid and lipoprotein cholesterol contents in the serum of normal and hyperlipidemic mice or rats. When daphnetin was given orally to rats, the serum level of high density lipoprotein cholesterol and the ratio of high density lipoprotein cholesterol to total cholesterol of normal rats were raised, whereas no significant effect on the level of lipid in normal mice was observed. Daphnetin (800 mg/kg, po for 1 week) decreased significantly the total cholesterol content in the serum of yolk(0.5 ml) treated mice. In addition, when daphnetin was given orally at a dosage of 800 mg/kg day for 2 weeks, the serum level of total cholesterol decreased. The sernm concentration of high density lipoprotein cholesterol and the ratio of high density lipoprotein cholesterol to total cholesterol in rats with hyperlipidemia increased significantly.     

Antiplatelet and antithrombotic activities of timosaponin B-II, an extract of Anemarrhena asphodeloides

1. Antithrombotic agents are effective in the treatment of ischaemic stroke. Timosaponin B-II (TB-II) is a major active component of Anemarrhena asphodeloides Bunge (Liliaceae; rhizome) that has protective effects against cerebral ischaemic damage. The present study examined the antiplatelet and antithrombotic actions of TB-II. 2. In in vitro experiments, TB-II (20, 40 and 80 mg/mL) potently and dose-dependently inhibited ADP-induced platelet aggregation. Furthermore, 1, 3 and 6 mg/kg TB-II prolonged activated partial thromboplastin time by 9.29, 16.86 and 25.50%, respectively, but had no effect on the prothrombin time. Furthermore, 1, 3 and 6 mg/kg TB-II significantly reduced the wet weight, dry weight and length of the thrombi (%inhibition (based on wet weight): 13.6, 19.8 and 24.7%, respectively). 3. In a rabbit arteriovenous shunt model, 1, 3 and 6 mg/kg, i.v., TB-II had no effect on thrombus formation. Plasma euglobulin lysis time and fibrin degradation product were not affected by 1, 3 and 6 mg/kg TB-II, but plasminogen levels were decreased significantly by 14.4, 18.3 and 29.0%, respectively. 4. The results of the present study demonstrate significant antiplatelet and anticoagulation effects of TB-II and suggest that these actions could contribute to its neuroprotective effect against damage following cerebral ischaemia damage.     

Studies on antiplatelet effect of OP-41483, a prostaglandin I2 analog, in experimental animals. I. Effect on platelet function and thrombosis

Antiplatelet and antithrombotic effects of OP-41483, a PGl2 analog, were studied in experimental animals, and the following results were obtained: 1) With 10 min-intravenous infusion to guinea pigs, OP-41483 inhibited platelet adhesiveness and platelet aggregation at 300-1000 ng/kg/min and 1000 ng/kg/min, respectively. In these effects, OP-41483 was 1-3 times more potent than carbacyclin and 3 times less potent than PGl2. 2) With oral administration to guinea pigs, OP-41483 given as its alpha-cyclodextrin clathrate (OP-41483 alpha-CD) inhibited platelet adhesiveness at doses higher than 1.0 mg/kg (expressed in terms of OP-41483), whereas PGl2 and carbacyclin did not at 10 mg/kg. OP-41483 alpha-CD also inhibited platelet aggregation after a single dose of 3 mg/kg and repeated doses of 3 mg/kg/day for 7 days. 3) In the electrically induced thrombosis model of guinea pig mesenteric artery, OP-41483 (300-1000 ng/kg/min, i.v.-infusion) and OP-41483 alpha-CD (1.0-3.0 mg/kg, p.o.) inhibited thrombus formation, but heparin (1.0-10 U/kg/min, i.v.-infusion) did not. 4) In the rabbit extracorporeal circulation thrombosis model, OP-41483 (100 and 300 ng/kg/min, i.v.-infusion) inhibited thrombus formation in the extracorporeal shunt and prevented the decrease in platelet count, hematocrit and fibrinogen level in circulating blood. Heparin (1.0-3.0 U/kg/min, i.v.-infusion) also inhibited the thrombus formation and the decrease in fibrinogen level, but did not inhibit the decrease in hematocrit and platelet count.     

抗人血小板膜糖蛋白Ⅲa单克隆抗体抑制兔血栓形成的实验研究

目的　评价抗人血小板膜糖蛋白Ⅲa单克隆抗体SZ21抑制兔血栓形成的能力。方法不同浓度的SZ21（0、10及20μg／ml）分别加入兔富血小板血浆（PRP）中,进行二磷酸腺苷（ADP）诱导的兔血小板聚集试验;体内注射SZ21（1.5mg／kg）,注射前及注射后5、30及60分钟时制备兔PRP,分别进行聚集试验;用颈动静脉旁路血栓模型研究SZ21对兔血栓形成的作用,20只新西兰兔随机分成4组,体内注射SZ21,剂量为A组0.1mg／kg,B组0.4mg／kg,C组0.75mg／kg,D为对照组（SZ391mg／kg）,然后测定血栓重量。结果　体外20μg／ml的SZ21对兔血小板抑制率为80％;SZ21体内注射60分钟时完全抑制血小板聚集功能;血栓模型分组试验,各组平均栓重为A组31mg,B组21mg,C组20.2mg,D组31mg,B、C组与对照组间有明显统计学差异（P＜0.01）。结论　单克隆抗体SZ21能有效抑制兔动静脉旁路血栓形成。