阿司匹林联合氯吡格雷抗血小板治疗后循环脑梗死的效果观察

目的 观察阿司匹林联合氯吡格雷治疗后循环脑梗死的疗效.方法 306例后循环脑梗死患者随机分为对照组和研究组,分别采用阿司匹林或氯吡格雷联合阿司匹林治疗3周.比较两组凝血指标、血脂、疗效、治疗后30d改良Rankin量表(mRS)及B arthel指数的变化.结果 与对照组比较,研究组凝血酶原时间、活化部分凝血酶原时间、高密度脂蛋白胆固醇水平增加,而纤维蛋白原、三酰甘油、总胆固醇和低密度脂蛋白胆固醇水平降低(P＜0.01).研究组的疗效、mRS评分和Barthel评分均优于对照组(P＜0.01或0.05).结论 阿司匹林联合氯吡格雷抗血小板治疗后循环脑梗死可有效改善血凝状态,疗效确切.     

不同剂量阿司匹林和波立维对阿司匹林抵抗患者血小板聚集功能的影响及护理

目的 观察不同剂量阿司匹林和波立维对冠心病阿司匹林抵抗患者血小板聚集功能的影响,并提出相应护理对策.方法 筛选出冠心病患者中发生阿斯匹林抵抗的患者48例入选本研究,随机分为3组,分别给予阿司匹林100、300 mg和阿司匹林100 mg 波立维75 mg,14 d后采用全血电阻法检测血小板聚集功能.结果 阿司匹林100 mg和阿司匹林300 mg患者的血小板聚集功能比较差异均无统计学意义(P＞0.05);加服波立维可使二磷酸腺苷诱导的血小板聚集功能显著抑制(P＜0.01),但对花生四烯酸诱导的血小板聚集无明显影响.结论 加大阿司匹林剂量或合用波立维不能明显改善冠心病患者的阿司匹林抵抗,对该类患者应加强临床观察和护理.     

田七总皂苷对兔全血血小板聚集的影响

目的观察田七总皂苷对凝血酶或ADP诱导的兔全血血小板聚集的影响。方法兔全血与田七总皂苷孵育5min,然后用凝血酶或ADP作用1min,用全血血小板聚集仪观察兔全血血小板聚集情况。结果田七总皂苷50、100和200μmol/L作用兔血小板后,用凝血酶诱导时对血小板聚集的抑制率分别为39%、60%和61%;用ADP诱导时抑制率分别为65%、79%和60%。结论田七总皂甙对凝血酶和ADP诱导的兔全血血小子板聚集都有抑制作用。     

有氧康复运动、替格瑞洛与阿司匹林联合在PCI术后的应用

目的 探讨有氧康复运动、替格瑞洛、阿司匹林三者联合在PCI术后的应用价值.方法 100例急性ST段抬高型心肌梗死(STEMI)患者随机分为观察组和对照组,对照组采用替格瑞洛联合阿司匹林治疗,观察组在对照组基础上采用有氧康复运动.比较两组心功能指标、成纤维细胞生长因子-21(FGF-21)、基质细胞衍生因子-1(SDF-...     

舒心饮对急性心肌缺血小鼠血小板影响的研究

目的：研究舒心饮对急性心肌缺血小鼠血小板的影响.方法建立小鼠急性心肌缺血再灌注模型,随机选取45只雄性ICR小鼠,依据随机数字表法将这些小鼠分为假手术组、模型组、舒心饮大剂量组、舒心饮小剂量组、抵克立得组5组,每组9只.连续灌胃1个月后造模、采血.运用流式细胞术、单克隆抗体对小鼠CD62 P的阳性表达率进行测定,运用比浊法对小鼠PAR、Fg浓度进行测定,运用放射免疫法对小鼠TXB2和6-keto-PGF1α及其比值进行测定.结果模型组小鼠的CD62 P阳性表达率、PAR、Fg浓度、TXB2/6-keto-PGF1α均显著高于假手术组、舒心饮大剂量、舒心饮小剂量组、抵克立得组（P〈0.05）.结论舒心饮能够对急性心肌缺血小鼠的血小板活化进行有效抑制,从而能对冠心病进行有效防治.     

六种中药生物碱对LPS作用下猪血管内皮细胞分泌细胞因子的影响

通过研究6种中药生物碱对细菌内毒素（LPS）作用下猪血管内皮细胞分泌细胞因子血栓素B2（TXB2）,内皮素-1（ET-1）和E-选择素（E-selectin）的影响,拟探讨生物碱抗LPS的药理作用机制。培养猪血管内皮细胞至单层融合状态,加入LPS刺激,3 h后加入高、中、低3种浓度的6种中药生物碱青藤碱、防己诺林碱、水苏碱、川芎嗪、苦参碱和吴茱萸碱,继续培养21 h后收集细胞上清液,用ELISA测定TXB2,ET-1和E-selectin的含量。结果,水苏碱高剂量组和川芎嗪高剂量组的TXB2含量极显著低于LPS对照组,川芎嗪中剂量组和吴茱萸碱高剂量组显著低于LPS对照组;苦参碱高剂量组的ET-1含量极显著低于LPS对照组,青藤碱高剂量组显著低于LPS对照组;防己诺林碱高剂量组和吴茱萸碱中剂量组的E-selectin含量显著低于LPS对照组。结果提示六种中药生物碱具有明显的抗细菌内毒素作用,可在由TXB2,ET-1和E-selectin介导的机体凝血、休克和炎症等病理损伤过程中发挥治疗作用。     

白头翁汤及其主要成分对内皮细胞分泌细胞因子TNF-α,TXB_2和6-keto-PGF_(1α)的影响

为探讨白头翁汤及其主要成分对细菌内毒素(LPS)导致的机体炎症等病理损伤的治疗作用。培养内皮细胞至单层融合状态,加入内毒素刺激,3 h后加入高、中、低3种浓度的白头翁汤、白头翁皂苷B4、白头翁素、小檗碱、药根碱、巴马汀、秦皮甲素和秦皮乙素,继续培养21 h后收集细胞上清液,用ELISA方法测定TNF-α,TXB2和6-keto-PGF1α的含量。结果表明:白头翁汤高剂量组、白头翁皂苷B4高剂量组和小檗碱高剂量组的TNF-α含量极显著低于LPS对照组(P0.01);白头翁汤中剂量组、白头翁皂苷B4中剂量组、小檗碱中剂量组、药根碱中剂量组和秦皮甲素高剂量组显著低于LPS对照组(P0.05);白头翁汤高剂量组和巴马汀高剂量组的TXB2含量极显著低于LPS对照组(P0.01);白头翁汤中剂量组、白头翁素高剂量组、小檗碱中剂量组、药根碱高剂量组和中剂量组、巴马汀中剂量组显著低于LPS对照组(P0.05);秦皮乙素高剂量组的6-keto-PGF1α含量显著低于LPS对照组(P0.05)。说明白头翁汤及其主要成分对LPS体外诱导内皮细胞产生炎性细胞因子具有明显的抑制作用,可能对TNF-α,TXB2和6-keto-PGF1α介导的机体炎症、凝血和休克等病理损伤具有治疗作用。     

pH与盐度胁迫对鼠尾藻光合作用及抗氧化系统的影响

为研究鼠尾藻(Sargassum thunbergii)在逆境胁迫条件下光合作用能力的变化及抗氧化系统的调节机理,利用液相氧电极技术和抗氧化酶试剂盒,检测了pH、盐度胁迫对鼠尾藻表观光合作用、色素含量、丙二醛(MDA)含量及抗氧化酶活性的影响。结果表明:(1)pH 6.0与pH9.5胁迫处理24 h后鼠尾藻表观光合速率均大幅下降,48 h后均与对照组(pH 8.5)差异显著(P0.05);(2)pH 9.5胁迫处理48 h后SOD、CAT活性均显著升高(P0.05),MDA含量呈先上升后下降趋势;(3)盐度15胁迫处理24 h,盐度20与25胁迫处理48 h后表观光合速率显著低于对照组(盐度31,P0.05),胁迫72 h后3个处理组表观光合速率有一定幅度的上升;(4)盐度20胁迫处理24 h后MDA含量先上升后下降(P0.05),SOD、CAT活性由24 h至48 h时有一定幅度的上升。盐度15胁迫处理72 h后MDA显著上升(P0.05),而SOD、CAT活性较低。可以得出pH胁迫使鼠尾藻光合作用能力降低,强碱性使藻体受到活性氧损伤。盐度为15时,鼠尾藻抗氧化酶活力较低,当高于15时,抗氧化系统对活性氧有较高的清除能力。     

血细胞分析仪测定血小板的影响因素分析

目的：分析血细胞分析仪测定血小板的影响因素．为临床提供可靠的诊治依据。方法：按照BC3000全自动血液分析仪的血小板计数原理及血小板直方图,把干扰的标本分成3组,A组：在血小板直方图上。后蜂翘起始处在25fl以外的标本;B组：后蜂翘起始处在20～25fl之间的标本;C组：后峰翘起始处在20fl之内的标本。每组检测30份标本,分别行血细胞分析仪及显微镜计数血小板．对两法结果作配对t检验。同时对正常与异常血小板直方图的血小板聚集及大血小板的例数、血细胞分析仪及镜检计数血小板的结果作比较。结果：B、C两组血细胞分析仪计数血小板的结果均比显微镜直接计数血小板的结果偏高（P〈0．05～0．01）;异常血小板直方图的血小板聚集以及大血小板的例数均明显高于正常图形者．其血细胞分析仪计数血小板明显则偏低（P〈0．01）。结论：小红细胞数量、血小板凝集及大血小板等均可影响血细胞分析仪对血小板的计数;对血小板计数与直方图不符的标本．应行手工计数或重新采血检测．以使血小板计数结果可靠．为临床诊断治疗提供有参考意义的数据。     

5-羟色胺对断奶腹泻仔鼠小肠组织学结构的影响

为研究5-羟色胺(5-HT)增多是否通过影响肠黏膜屏障引起断奶仔鼠的腹泻,检测断奶腹泻仔鼠小肠绒毛高度(VH)、隐窝深度(CD)变化。采用21d刚断奶ICR仔鼠,分为6组,第1组为正常对照组,第2组为应激腹泻组,番泻叶(0.4kg/L)按体重15mL/kg灌胃同时后肢束缚应激处理,第3组为氢溴酸西肽普兰(CH)对照组,用CH进行腹腔注射处理,第4组CH+腹泻组,CH药物处理4h后进行应激腹泻处理;第5组对氯苯丙氨酸(PCPA)对照组,PCPA腹腔注射;第6组PCPA+应激腹泻组,PCPA药物处理4h后进行应激腹泻处理。连续处理5日后处死小鼠,取十二指肠、空肠、回肠,4%多聚甲醛固定、石蜡包埋,制作石蜡切片,HE染色,测量肠绒毛高度、隐窝深度。由HE染色结果发现,应激腹泻组、CH+应激腹泻组和PCPA+应激腹泻组与正常对照组相比,肠绒毛顶端出现充血,绒毛变短,裸露固有层等病理现象。与正常对照组相比,应激性腹泻组小鼠肠绒毛高度降低:十二指肠,空肠,回肠分别降低14.80%(P0.01),6.89%(P0.01)和19.31%(P0.01),隐窝深度分别升高14.09%(P0.01)、4.85%(P0.05)、11.53%(P0.01),故VH和CD的比值(V/C)降低:CH处理组与应激腹泻组小鼠变化趋势相同;而PCPA处理组则无明显变化。与应激腹泻小鼠相比,CH+应激腹泻组小鼠肠绒毛高度降低,尤其空肠显著降低11.18%(P0.01),隐窝深度升高,尤其十二指肠显著升高4.86%(P0.05),故V/C值也降低,而PCPA+应激腹泻组小鼠绒毛高度升高,分别为4.83%(P0.05),4.15%(P0.01),10.60%(P0.01),隐窝深度降低,分别为27.46%(P0.01)、19.21%(P0.01)、16.74%(P0.01),故V/C值升高。断奶腹泻仔鼠小肠黏膜机械屏障遭到破坏,而肠道内5-HT含量的升高也会使断奶仔鼠出现腹泻现象,同时小肠绒毛高度降低,隐窝深度增加。因此5-HT升高可能通过损伤断奶仔鼠小肠的绒毛高度和隐窝深度,从而引发腹泻。     

双花提取物抗血小板聚集及抗凝血活性研究

[目的]研究玫瑰（Rosa rugosa）、月季（Rose chinensis Jacq.）双花提取物对血小板聚集及血液系统的作用。[方法]考察双花提取物对家兔全血凝血时间、体外血小板聚集率、凝血酶原时间（PT）、活化部分凝血活酶时间（APTT）及大鼠纤溶系统的影响;采用高糖诱导人脐静脉内皮细胞损伤模型,考察其对细胞SOD活性和MDA含量的影响。[结果]双花提取物能抑制全血血小板聚集,延长全血凝血时间和APPT,缩短优球蛋白溶解时间（ECLA）,降低纤维蛋白原（FIB）含量。[结论]双花提取物具有抗血小板聚集及抗凝血活性。     

State of the Hemostatic system in iron-deficient newborn calves

An investigation of 38 newborn calves with iron-deficiency anemia reveals that the most accelerated platelet aggregation occurred under the effect of collagen (19.8 s), slightly later ADP (25.6 s), ristomycin (23.0 s), H₂O₂ (24.7 s), and thrombin (37.5 s), and the latest under the effect of epinephrine (70.6 s). The content of discoid platelets is reduced to 57.8% while increasing the total number of active forms of platelets to 42.2% and number of small and large aggregates to respectively 14.8 and 3.26 per 100 free platelets. These animals are characterized by a decrease in antiaggregation activity of the vascular wall with respect to all inducers and their combinations used with weakening of its anticoagulant activity by 8.3% and fibrinolytic capacity by 9.4%. In this case, there is a significant increase in the activity of blood clotting factors I, II, V, and IX, leading to acceleration of prothrombin time (12.6 s), activated partial thromboplastin time (27.8 s), and thrombin time (16.6 s).     

Activity of platelet hemostasis in newborn calves

Healthy newborn Simmental and Black Pied calves with a normal number of platelets in bloodstream don’t have reliable dynamics of the aggregation function of blood platelets with adenosine diphosphate, collagen, thrombin, ristocetin, epinephrine, as well as combinations of ADP + epinephrine, ADP + collagen, and collagen + epinephrine inducers. The level of discocytes in blood on days 1–2 was 78.5, not reliably changing until the end of the neonatal stage. In this case, the number of disco-echinocytes, spherocytes, spheroechinocytes, and bipolar forms of platelets in the bloodstream remained stably low. Maintenance during colostrum feeding of a low intensity of metabolism of endogenous arachidonic acid in platelets and of a low content of ATP, ADP, actin, and myosin in them can be considered important mechanisms providing stability of platelet aggregation activity in calves in the neonatal stage.     

Platelet thromboxane synthetase inhibitors with low doses of aspirin: possible resolution of the "aspirin dilemma"

Selective pharmacological inhibition of thromboxane A2 synthesis did not prevent arachidonate-induced aggregation of human platelets in vitro. Prevention was instead achieved by a combination of thromboxane A2 inhibitors with low concentrations of aspirin. The latter partially reduced the proaggregatory cyclooxygenase products that accumulated when thromboxane A2 synthesis was blocked. The aspirin concentrations did not affect per se either platelet aggregation or prostacyclin synthesis in cultured human endothelial cells. The combination of thromboxane synthetase inhibitors with low doses of aspirin may offer greater antithrombotic potential than either drug alone.     

抗血栓,抗动脉硬化中草药的筛选

血小板中环氧酶和脂氧酶作用于花生四烯酸代谢系统，可产生形成血栓的血栓烷Ａ２（ＴＸＡ２）及引起过敏性疾病的１２－羟基二十碳四烯酸（１２－ＨＥＴＥ）。ＴＸＡ２不稳定，迅速生成稳定的ＴＸＢ２，因此抑制ＴＸＢ２生成则可抑制血栓生成，抑制１２－ＨＥＴＥ生成则可预防动脉硬化及过敏性疾病。本文利用放射薄层方法，测定兔血中血小板花生四烯酸代谢产物ＴＸＢ２和１２－ＨＥＴＥ的生成量，筛选了４８种中药，其中２３味中药可选择性抑制环氧酶和脂氧酶的活性。浓度为１ｍｇ／Ｌ显示抑制作用强的中药有五倍子、柳叶，浓度为１０ｍｇ／Ｌ抑制作用较强的中药有桂皮、五倍子、茴香、黑加仑、蒲公英、甘草、车前草、柳叶等     

Platelet-activating factor-induced aggregation of human platelets specifically inhibited by triazolobenzodiazepines

Platelet-activating factor (PAF), a naturally occurring phospholipid, is a potent activator of various biological processes, including platelet aggregation. The mechanisms by which PAF acts are largely unknown, partly because of the lack of specific inhibitors for PAF-elicited responses. It was found that in washed human platelets the psychotropic triazolobenzodiazepine drugs alprazolam and triazolam potently inhibited PAF-induced changes in shape, aggregation, and secretion. The effects were specific for PAF activation, since the responses of human platelets to adenosine diphosphate, thrombin, epinephrine, collagen, arachidonate, and the calcium ionophore A23187 were not inhibited by the triazolobenzodiazepines. These psychotropic drugs should be useful in investigating the possibility that PAF or PAF-like phospholipids play a role in neuronal function and in elucidating biochemical mechanisms activated specifically by PAF in a variety of cells.     

Aspirin: its effect on platelet glycolysis and release of adenosine diphosphate

Incubation of human platelets with aspirin inhibited glycolysis and produced a fall in the concentration of adenosine triphosphate. When platelets were exposed to collagen there was an increase in glycolysis and release of adenosine diphosphate. Prior incubation of the platelets with aspirin for 5 minutes did not totally suppress the increase in glycolysis after exposure to collagen but completely inhibited the collagen-induced reaction of the release of adenosine diphosphate. It is suggested that aspirin acts on human platelets by inhibiting both release of adenosine diphosphate and the transport of glucose across the platelet membrane.     

Hemostatic system activity in milk- and plant-fed calves

Experiments were conducted on 36 healthy Simmental and Black Pied calves. Hemostatic indices were determined on days 31, 45, 60, 75, and 90. Maximum increase in platelet aggregation activity was noted on day 45 with the use as inducers ADP + collagen + epinephrine (17.1 s), ADP + thrombin + epinephrine (16.9 s), and ADP + collagen + thrombin + epinephrine (14.1 s). In this case, control of the vessel wall over platelet aggregation in the blood stream increased: the vessel wall antiaggregation activity index (VWAAI) was respectively 1.41, 1.39, and 1.36. An increase in the production by endotheliocytes of antithrombin III and tissue plasminogen activators was revealed in animals at this age. An increase in the level of fibrinogen and factors II, VII, I, X, XI, and XII with stability of factors V and VII and subsequent weakening of activated factors by the end of the examined stage of early ontogeny was established.     

Histamine is an intracellular messenger mediating platelet aggregation

Inhibition of human platelet aggregation by N,N-diethyl-2-[4-(phenylmethyl)phenoxy]ethanamine-HCl (DPPE), a novel antagonist of histamine binding, suggested that histamine might serve a critical role in cell function. Phorbol-12-myristate-13-acetate (PMA) or collagen was found to increase platelet histamine content in parallel with promotion of aggregation. Inhibitors of histidine decarboxylase (HDC) suppressed both aggregation and the elevation of histamine content, whereas DPPE inhibited aggregation only. In saponin-permeabilized platelets, added histamine reversed the inhibition by DPPE or HDC inhibitors on aggregation induced by PMA or collagen. The results indicate a role for histamine as an intracellular messenger, which in platelets promotes aggregation.