参芪注射液对血小板表面活性和超微结构的影响

本文应用电镜观察了一次静脉注射参芪液60ml 前后对冠心病心气虚患者血小板聚集的影响。结果提示用药前冠心病心气虚患者与正常相比血小板扩聚型和聚集数都明显增加,用药后一小时上述异常现象明显好转。用家兔血小板体外实验表明参芪液对ADP 诱导的血小板聚集也有抑制作用。血小板超微结构的初步观察提示对血小板的伪足形成及颗粒释放也可能有一定抑制作用。     

麝香保心丸对急性心肌梗死患者血小板聚集的影响

目的观察麝香保心丸对急性心肌梗死患者血小板聚集的影响。方法选取120例急性心肌梗死患者,随机分为两组,每组60例。试验组口服麝香保心丸加阿司匹林和氯吡格雷,对照组口服阿司匹林加氯吡格雷,测定患者服药前及服药1个月后血浆血小板聚集率及血小板活化因子水平,观察其变化。结果用药前试验组血小板聚集率为（55．38±10．35）％,血小板活化因子水平为（41．85±10．64）nmol／L;对照组血小板聚集率为（53．29±10．22）％,血小板活化因子水平为（42．79±11．04）nmol／L,两组间无统计学意义;用药后试验组血小板聚集率为（28．60±8．09）％,血小板活化N子水平为（18．65±8．84）nmol／L;对照组血小板聚集率为（35．27±9．03）％,血小板活化因子水平为（25．37±9．13）nmol／L,较基线水平均有明显下降（P〈0．05）,试验组下降更为明显（P〈0．05）。结论麝香保心丸可有效抑制急性心肌梗死患者血小板聚集。     

人参总皂甙对兔血小板聚集和环核苷酸代谢的影响

本文观察了人参总皂甙(GS)对兔血小板聚集和环核苷酸代谢的影响。结果表明,GS12mg/kg静脉注射后,可明显抑制花生四烯酸、ADP及胶原诱导的血小板聚集,同时也使血小板cAMP含量升高,两条时效曲线均大致呈双峰型,高峰出现的时间均在给药后15及120min。提示GS可能通过升高血小板cAMP含量而抑制血小板激活。体外实验证明,GS能激活腺苷酸环化酶,并抑制磷酸二酯酶活性,这可能是GS体内给药后升高血小板cAMP含量的作用机理。     

升血小板胶囊结合泼尼松治疗原发免疫性血小板减少症临床观察及对Treg细胞和Th17细胞的影响

目的:分析探讨原发免疫性血小板减少症(ITP)的治疗中采用升血小板胶囊与泼尼松联合用药的临床观察以及对Treg细胞(调节性T细胞)和Th17细胞(辅助性T细胞17)的影响。方法:ITP患者60例,随机分为对照组和观察组各30例,对照组仅给予泼尼松治疗,观察组在泼尼松治疗基础上加用升血小板胶囊,比较两组治疗前后血小板数(Plt)、Treg细胞计数、Th17细胞计数、IL-10(白介素10)含量、IL-17(白介素17)含量。结果:治疗后,观察组治疗效果(96.67%)显著高于对照组(70.00%);观察组血小板数(132±70)×10~9/L、Treg细胞计数(4.54±1.4)%、IL-10含量(29.36±7.48)ng/L明显高于对照组血小板数(90±53)×10~9/L、Treg细胞计数(3.23±0.90)%、IL-10含量(35.64±8.16)ng/L,差异有统计学意义(P0.05)。但治疗后两组Th17计数、IL-17含量比较差异无统计学意义(P0.05)。结论:升血小板胶囊与泼尼松联合应用治疗原发免疫性血小板减少症疗效显著,可有效改变Treg含量,调节ITP作用,同时也证实了ITP发生可能与Treg细胞和Th 17细胞的缺陷有关。     

参芪注射液对家兔血小板内环核苷酸含量的影响

根据我院临床和实验研究,益气中药参芪注射液具有抑制血小板聚集作用。为探讨其作用机理,我们测定了用药前后血小板内环核苷酸含量的变化。材料和方法 1.药物和试剂:参芪注射液系我院制剂室生产。采用内蒙古黄芪(A Stragalusmangholicus Bge,产地河北)、路党参(CodonopsisPilosula(Franch)Nannf,产地山西),水煎醇提而     

活士辛对血管收缩功能及血小板环核苷酸含量的影响

目的：研究洛土辛（Lot）对血管收缩功能及血小板环核苷酸含量的影响。方法：采用血管收缩张力记录和放射免疫测定法。结果：Ｌot、罂栗碱（Ｐap)和氨力农（Am）0．3－100μmol/L可剂量依赖地松弛5－HT30μmol/L诱发的血管的收缩反应，Lot对大鼠主动脉、犬隐静脉和猪冠状动脉松驰作用的负对数摩尔浓度ED50分别为5．5、5．4、5．2，Pap对前两的ED50分别为5．3、5．6，Am对前的ED50为5．4；美蓝使它们松驰血管的作用量效曲线右移。Lot和Am还增加异丙肾上腺素松弛大鼠主动脉的作用。Lot拮抗Meth激动α受体引起的大鼠主动脉血管收缩反应的pA2值仅为4．6。Lot 10、100μmol/L可显地提高血小板内cAMP含量，略升cGMP。结论:Lot有舒张血管、提高血小板环核苷酸作用，此可能与磷酸二酯酶抑制有关。     

桃核承气汤对动物血栓形成及血小板聚集的影响

目的:以血栓形成、血小板聚集、凝血酶原时间为药效学指标,对桃核承气汤活血化瘀相关的功效进行研究。方法:分别测定桃核承气汤对大鼠血栓形成及对家兔ADP诱导的血小板聚集和凝血酶原时间的影响;测定大黄酸对ADP诱导的血小板聚集的影响。结果:大鼠灌服桃核承气汤10 g生药/kg后,可减轻血栓干重(P<0.05或P<0.01),家兔灌服桃核承气汤5 g生药/kg后,可抑制ADP诱导的血小板聚集(P<0.05)。大黄酸体外给药(0.1μg/mL和1μg/mL),对ADP诱导的血小板聚集也具有抑制作用(P<0.01)。结论:桃核承气汤具有抑制血栓形成和血小板聚集的作用,大黄酸为桃核承气汤在体内产生活血化瘀的重要药效成分之一。     

芦丁抑制家兔血小板激活因子诱导血小板活化作用的实验研究

目的：观察芦丁对家兔血小板激活因子（PAF）诱导血小板聚集、5－羟色胺（5－HT）释放、血小板内游离钙离子浓度的影响及其机理。方法：以比浊法测定家兔洗涤血小板（WRR）聚集率，邻苯二甲醛（OPT）荧光分光光度法测定5－HT含量，以Fura-2荧光分光光度法测定血小板游离钙离子浓度的变化。结果：芦丁体外呈浓度依赖性抑制PAF（9．55×10^-9mol/L)诱发的WRP聚集、5－HT释放作用，IC50分别为0．73、1．13mmol/L；同时68．3、274、545μmol/L芦丁剂量依赖地抑制PAF（4．78×10^-9mol/L)引起的血小板内游离钙浓度增高。结论：芦丁可抑制PAF诱导的血小板聚集、5－HT释放及血小板内游离钙浓度增加。     

心钠素在心肺气虚诊断中的意义

42例心肺气虚患者血浆心钠素含量为82.24±68.85pg/ml,较健康人显著降低(P<0.01);18例阴虚患者血浆心钠素含量为591.33±202.36pg/ml、较健康人显著升高(P<0.01);9例心肺气虚患者服用生脉饮25天后,其血浆心钠素含量由135.22±97.54 pgm 升高为416.22±277.62 pg/ml,用药前后比较有显著性差异(P<0.05)。提示血浆心钠素含量可以作为心肺气虚诊断和评价其治疗效果的参考标准之一。     

心舒口服液对大鼠主动脉血管平滑肌细胞增殖和家兔体外血小板聚集功能的影响

 目的探讨心舒口服液治疗动脉硬化,抑制血管平滑肌增生和抗血小板聚集作用。方法通过血清药理学方法,考察心舒口服液对大鼠血管平滑肌体外增殖作用及家兔体外血小板聚集功能的影响。结果心舒口服液不同时间点含药血清能够明显抑制血管平滑肌细胞的增殖,对花生四烯酸(AA)和ADP诱导的体外血小板聚集功能均有明显的抑制作用。结论心舒口服液治疗心肌缺血作用机制与抑制血管平滑肌细胞增殖和抗血小板聚集有关。     

蝙蝠葛酚性碱对血小板聚集的影响及其机制研究

 目的观察蝙蝠葛酚性碱(PAMD)对血小板聚集的影响,探讨其抗血小板聚集的作用机制。方法用比浊法测定血小板聚集度;放免法测定兔血小板内环腺苷酸(cAMP)和环鸟苷酸(cGMP)的浓度;荧光探针Fura-2/AM标记测定兔血小板内游离钙离子浓度。结果体内外实验表明,PAMD对由二磷酸腺苷(ADP),花生四烯酸(AA)和凝血酶(THR)诱导的大鼠和兔血小板聚集的抑制作用具剂量或浓度依赖性;PAMD能明显升高兔血小板内cAMP,cGMP的浓度,并抑制由THR诱导的血小板内游离钙离子浓度的升高。结论PAMD具有抗血小板聚集的作用,其机制可能与增加血小板内cAMP和cGMP的含量和抑制血小板[Ca²⁺]_i浓度的升高有关。     

Anti‐platelet Activity of Erythro‐(7S,8R)‐7‐acetoxy‐3,4,3′,5′‐tetramethoxy‐8‐O‐4′‐neolignan from Myristica fragrans

Platelets play a critical role in pathogenesis of cardiovascular disorders and strokes. The inhibition of platelet function is beneficial for the treatment and prevention of these diseases. In this study, we investigated the anti‐platelet activity of erythro‐(7S,8R)‐7‐acetoxy‐3,4,3′,5′‐tetramethoxy‐8‐O‐4′‐neolignan (EATN), a neolignan isolated from Myristica fragrans, using human platelets. EATN preferentially inhibited thrombin‐ and platelet‐activating factor (PAF)‐induced platelet aggregation without affecting platelet damage in a concentration‐dependent manner with IC₅₀ values of 3.2 ± 0.4 and 3.4 ± 0.3 μM, respectively. However, much higher concentrations of EATN were required to inhibit platelet aggregation induced by arachidonic acid. EATN also inhibited thrombin‐induced serotonin and ATP release, and thromboxane B₂ formation in human platelets. Moreover, EATN caused an increase in cyclic AMP (cAMP) levels and attenuated intracellular Ca²⁺ mobilization in thrombin‐activated human platelets. Therefore, we conclude that the inhibitory mechanism of EATN on platelet aggregation may increase cAMP levels and subsequently inhibit intracellular Ca²⁺ mobilization by interfering with a common signaling pathway rather than by directly inhibiting the binding of thrombin or PAF to their receptors. This is the first report of the anti‐platelet activity of EATN isolated from M. fragrans. Copyright © 2013 John Wiley & Sons, Ltd.     

青心酮对慢性阻塞性肺病患者血流动力学及血浆心钠素和环磷酸苷类水平的影响

为了解青心酮对慢性阻塞性肺病（慢阻肺）患者血流动力学的影响，用右心漂浮导管检测了１１例慢阻肺患者应用青心酮前、后血流动力学某些参数，同时采用放射免疫分析法测定了血浆心钠素及环磷酸苷类水平。结果：静脉注射青心酮后，肺动脉平均压及肺循环阻力、体循环阻力均下降（Ｐ＜０．０５）．体动脉压及动脉血气指标无明显变化（Ｐ＞０．０５），心输出量在正常范围内增加。血浆心钠素、环磷酸鸟苷水平下降（Ｐ＜０．０１，Ｐ＜０．０５）。表明青心酮可能通过调节环磷酸腺苷、环磷酸鸟苷的比值而达到扩血管目的，其心钠素降低可能是一种继发性反应。     

党参、黄芪对血小板聚集的临床及实验研究

近年来,我院气血研究室在中医气血相关理论的指导下,应用现代科学方法开展了对益气药党参、黄芪的研究,取得了较大的进展。为进一步研究党参、黄芪益气行血的作用机理及其物质基础,本文在原有研究的基础上,试图以党参、黄芪的不同制剂,不同剂量及服药后不同时间对血小板聚集功能的影响,从一个侧面来探讨益气行血理论的实质所在。先后进行下列的研究:     

Anti‐Platelet Activity of Water Dispersible Curcuminoids in Rat Platelets

Curcuminoids are active principle of turmeric with plethora of health beneficial properties. In this study, we have evaluated for the first time the effect of water dispersible curcuminoids on rat platelet aggregation. Curcuminoids (10–30 µg/mL) significantly inhibited platelet aggregation induced by agonists viz., collagen, ADP and arachidonic acid. Curcuminoids were found to be two‐fold more potent than curcumin in inhibiting platelet aggregation. Intracellular curcuminoid concentration was relatively higher than curcumin in rat platelets. Curcuminoids significantly attenuated thromboxane A₂, serotonin levels in rat platelets which play an important role in platelet aggregation. Curcuminoid treatment increased nitric oxide (NO) levels in platelets treated with agonists. Curcuminoids inhibited free radicals such as superoxide anion released from activated platelets, which ultimately inhibits platelet aggregation. Further, curcuminoids inhibited 12‐lipoxygenase activity and formation of 12‐hydroperoxyeicosatetraenoic acid (12‐HPETE) in activated rat platelets which regulates platelet aggregation. The results suggest that curcuminoids have remarkable anti‐platelet activity by modulating multiple mechanisms involved in platelet aggregation. Thus curcuminoids may have a therapeutic potential to prevent platelet activation related disorders. Copyright © 2015 John Wiley & Sons, Ltd.     

冠心病患者血浆p-选择素与血小板参数的表达意义

目的探讨冠心病患者血浆p-选择素(CD62p)与血小板聚集率(PAGM)及血小板参数变化之间的关系。方法128例患者根据冠脉造影结果分为冠心病组和正常组,采用流式细胞术(FCM)三色荧光标记技术检测血小板膜CD62p的阳性百分率和血小板的四项参数。结果冠心病组94例中CD62p阳性分率(3.707±2.526)%,正常组34例中CD62p阳性分率(1.043±1.016 3)%,2组比较有显著性差异(P<0.01)。冠心病组血小板平均体积(MPV)、血小板分布宽度(PDW)、血小板最大聚集率均明显高于正常组(P均<0.01),血小板计数(Plt)冠心病组小于正常组,血小板比容(PCT)2组比较无显著性差异(P>0.05)。结论CD62p是血小板活化的敏感和特异指标,可用于冠心病的监测和抗血小板药物疗效的疗效。     

20(S)⁃原人参二醇止血作用及其机制

目的通过体内和体外实验研究20(S)?原人参二醇对小鼠凝血系统的作用和对人/鼠血小板的活化作用,探讨原人参二醇的止血作用及相关的作用机制。方法小鼠断尾和肝划痕法观察小鼠出血时间;自动血液分析仪检测大鼠血常规;自动凝血分析仪检测大鼠凝血四项指标;酶联免疫吸附法检测血小板中环磷酸腺苷(cAMP)和环磷酸鸟苷(cGMP)水平;Cytation 5多功能酶标仪检测洗涤人血小板内钙离子的浓度([Ca²⁺]i);比色法观察血小板的聚集率;流式细胞术检测洗涤人血小板中CD62P和PAC?1相关表达。结果原人参二醇能缩短小鼠的出血时间;增加红细胞参数中的红细胞数量(RBC)和红细胞压积(HCT),提高血小板参数中血小板数量(PLT)和血小板压积(PCT);缩短大鼠活化部分凝血活酶时间(APTT),中剂量和高剂量组可增加纤维蛋白原的表达。同时,原人参二醇能提高大鼠洗涤血小板cAMP水平、血小板内[Ca²⁺]i和血小板聚集度;增加洗涤人血小板CD62P释放和PAC?1表达。结论原人参二醇具有一定的止血作用,一方面通过激活大鼠的内源性凝血系统,影响体内血小板和红细胞参数,促进血浆中纤维蛋白原生成;另一方面通过影响钙离子和cAMP信号通路,增加血小板Ca²⁺内流、CD62P释放和促进PAC?1的表达,最终诱导血小板聚集,形成血栓,发挥止血作用。     

冰片对三氯化铁诱导的大鼠动脉血栓形成的抑制作用及机制

目的 :探讨冰片的抗血栓作用。 方法 :用血栓形成实验、血小板聚集实验及血小板内钙离子浓度的测定,考察冰片对血栓形成、血小板5-羟色胺(5-HT)含量、血小板聚集率及血小板内游离钙离子浓度 _i的影响。 结果 : ig 冰片粟米油溶液140 mg·kg^-1,7次能抑制三氯化铁诱导的大鼠动脉血栓形成(P<0.05),升高血小板内5-HT含量(P<0.05),抑制5-HT诱导的血小板聚集作用(P<0.05);在有无细胞外钙存在时,冰片血清均能够明显抑制5-HT诱导的血小板胞内 _i升高。 结论 :冰片具有抗血栓作用,其机制可能与抑制血小板5HT释放和血小板聚集,抑制血小板胞浆 _i升高有关。     

Antiplatelet activity of Phellinus baummii methanol extract is mediated by cyclic AMP elevation and inhibition of collagen-activated integrin-α(IIb) β₃ and MAP kinase

Phellinus baumii is a mushroom that has been used as folk medicine against various diseases and is reported to have antidiabetic, anticancer, antioxidant, antiinflammatory and antihypertensive activities. However, information on the effects of P. baumii extract in platelet function is limited. Therefore, the aim of this study was to examine the impact of a P. baumii methanol extract (PBME) on platelet activation and to investigate the mechanism behind its antiplatelet activity. PBME effects on agonist‐induced platelet aggregation, granule secretion, [Ca²⁺]_i mobilization, α_IIbβ₃ activation, cyclic AMP release and mitogen‐activated protein kinase (MAPK) phosphorylations were studied using rat platelets. PBME dose‐dependently inhibited collagen, thrombin and ADP‐induced platelet aggregation with an IC₅₀ of 51.0 ± 2.4, 54.0 ± 2.1 and 53.0 ± 4.3 μg/mL, respectively. Likewise, thrombin‐induced [Ca²⁺]_i and collagen‐activated ATP secretions were suppressed in PBME treated platelets. Aggregation and ATP secretion were also markedly attenuated by PBME alone or in combination with PP2 (Src inhibitor) and U‐73122 (PLC inhibitor) in collagen‐stimulated platelets. Besides, PBME treatment elevated basal cyclic AMP levels and inhibited collagen‐induced integrin‐α_IIbβ₃ activation. Moreover, PBME attenuated extracellular‐signal‐regulated protein kinase 2 (ERK2) and c‐Jun N‐terminal kinase 1 (JNK1) phosphorylations. Further PD98059 (ERK inhibitor) and SP60025 (JNK inhibitor) reduced collagen‐induced platelet aggregation and ATP secretion. In conclusion, the observed PBME antiplatelet activity may be mediated by activation of cyclic AMP and inhibition of ERK2 and JNK1 phosphorylations. Finally, these data suggest that PBME may have therapeutic potential for the treatment of cardiovascular diseases that involve aberrant platelet function. Copyright © 2011 John Wiley & Sons, Ltd.