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张石革 《中国医院用药评价与分析》2012,(6):490-495
目的:抗血小板药围绕血栓形成机制,对血小板聚集各个环节进行抑制而成为对抗血栓和心血管事件的一线用药,受到临床和患者的青睐,本文总结二磷酸腺苷(ADP)P2Y12受体阻断剂的研究进展与临床评价。方法:采用国内、外文献综述方法。结果与结论:在大量临床研究中,ADP-P2Y12受体阻断剂显示了良好的疗效,其可选择性、不可逆地抑制ADP所诱导的血小板聚集,各种临床结果已被多项循证医学的系统研究所证实。对于冠状动脉介入治疗前的急性冠状动脉综合征者,ADP-P2Y12阻断剂可使患者死亡、非致死性心肌梗死、非致死性脑卒中的发生率降低。 相似文献
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血小板膜糖蛋白GPⅡb/Ⅲa受体拮抗剂的进展与临床评价 总被引:1,自引:0,他引:1
张石革 《中国医院用药评价与分析》2006,6(6):332-335
目的:本文介绍血小板膜糖蛋白GPⅡb/Ⅲa受体拮抗剂的进展与评价。方法:采用国内、外文献综述方法。结果及结论:作为抗血小板药中的一支奇葩,血小板膜糖蛋白GPⅡb/Ⅲa受体拮抗剂进展十分迅速,对膜糖蛋白GPⅡb/Ⅲa受体选择性高,在治疗血栓、急性心肌梗死、急性冠脉综合征、非ST段抬高心肌梗死者方面展现了良好的治疗前景。 相似文献
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近些年来,无论是从治疗还是发病机制的角度,血小板功能活性在急性冠状动脉综合征(ACS)中的作用都越来越得到确认,目前已证实血小板膜糖蛋白(GP)Ⅱb/Ⅲa受体是一个理想的治疗动脉血栓的药物靶点.巴替非班属于新一代人工合成的血小板GPⅡb/Ⅲa受体拮抗剂,主要药理作用为降低血小板聚集功能,对血小板聚集抑制作用也有明显影响. 相似文献
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β-受体阻断剂是近年来心血管疾病治疗中广泛应用的一种药物。它通过阻断心肌细胞膜上的β受体,而引起心率减慢、心肌收缩力减弱,心输出量减少,从而使血压下降、心肌耗氧量下降;β受体阻断剂还有抗血小板聚集、稳定冠状动脉内斑块的作用,故可降低急性冠脉综合征的发生率;对于慢性充血性心衰的病人,长期应用β受体阻断剂可明显延长病人的寿命;β受体阻断剂还可用于心律失常的防治。 相似文献
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多种蛇毒蛋白具有与血小板表面整合素、膜糖蛋白Ⅰb(GPⅠb)或血管性血友病因子(VWF)相互作用而影响血栓形成的功能。影响血小板血栓形成的蛇毒蛋白目前分为3类:去整合素、VWF调节蛇毒蛋白及GPⅠb结合蛋白。其中,去整合素具有高效抑制血小板聚集的功能;VWF调节蛇毒蛋白具有体外介导VWF依赖型血小板聚集的功能;而GPⅠb结合蛇毒蛋白又分为2组:GPⅠb激动剂和GPⅠb拮抗剂,分别起诱导血小板聚集与抑制VWF介导的血小板聚集的功能。本文将对上述影响血小板血栓形成的蛇毒蛋白的结构、功能及其在临床上的研究与应用进行综述。 相似文献
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抗癌化疗止吐药的研究进展 总被引:2,自引:0,他引:2
目的:通过对5-HL受体阻断剂,NK-1受体阻断剂,皮质类固醇等药物的研究进展进行阐述,了解用于预防恶心呕吐的药物,为预防和治疗化疗后的恶心呕吐反应寻找或开发出更安全、有效、经济的药物,从而减少或避免在化疗过程中的依从性差,疗效不稳定等情况。方法:通过回顾性研究国内外相关的临床试验和调研相关的文献,展开对其作用机制、药代动力学、临床应用等方面的阐述。结果:5-HT3受体阻断剂和NK-1受体阻断剂对急性呕吐均有较好的疗效,但后者对延迟性呕吐的效果优于前者,而与皮质激素合用疗效会增加,减少不良反应。结论:5-HT3受体阻断剂广泛应用于临床,对急性呕吐有效,但这些止吐药不能做到完全控制化疗引起的恶心呕吐反应(chemotherapy-induced nausea and vomiting,CINV)。 相似文献
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Jararhagin is a 52 kDa hemorrhagic P-III metalloproteinase isolated from the venom of the medically important Brazilian pit-viper Bothrops jararaca. It is a member of the reprolysin family of zinc metalloproteinases containing a catalytic metalloproteinase domain followed by a disintegrin-like and a cysteine-rich domain. The impact of jararhagin on hemostasis has been extensively studied using in vitro and in vivo model systems as well as in clinical studies. Jararhagin-induced hemorrhage is the result of the degradation of sub-endothelial matrix proteins leading to the disruption of the blood vessel endothelium, with accompanying disturbances in platelet function. The versatility of jararhagin is further demonstrated by its direct action on von Willebrand factor, the degradation of fibrinogen, by its inhibition of platelet adhesion to collagen and by its inability to be affected by the plasma inhibitor 2-macroglobulin. Collagen-induced platelet aggregation is inhibited by jararhagin though the binding of the molecule to the 2 subunit I domain of the platelet surface 2β1 integrin (collagen receptor). Jararhagin also cleaves the β1 subunit of the same integrin, inhibiting platelet interaction and ultimately causing impairment of signal transduction. The effect of jararhagin on cell systems other than platelets is evaluated; in fibroblasts, jararhagin functions as a collagen-mimetic substrate and, in endothelial cells, it causes apoptosis and indirectly inhibits cell proliferation by release of angiostatin-like compounds. Jararhagin induces a strong pro-inflammatory response characterized by intense leukocyte accumulation at the site of the injection. Although hemorrhage and edema are a response to the direct effect of jararhagin, jararhagin-induced inflammation and necrosis are dependent on macrophages and key pro-inflammatory cytokines or their receptors. Some data also indicate that the toxin possesses anti-tumorgenic properties. Methods for inhibiting jararhagin are reviewed; this encompasses the use of synthetic peptides to the isolation of naturally occurring mammalian peptides and the development of toxin-specific antibodies through DNA immunisation and monoclonal antibody technologies. The availability of jararhagin makes it an important tool for research into the mechanisms of action of similar toxins, for insights into cellular interactions and for clinical investigations into the treatment of envenomings from B. jararaca. 相似文献
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目的:探讨早期护理干预对急性心肌梗死(AMI)患者便秘的影响.方法:将68例患者随机分为对照组和于预组各34例,对照组给予常规护理和宣教,干预组于入院当日起在进行常规护理的基础上即采用心理支持、饮食指导等护理方法.结果:观察组的便秘、焦虑和抑郁的发生率均低于对照组,具有统计学意义(P<0.05).结论:对AMI患者采取有效的护理干预,能显著降低便秘的发生率. 相似文献
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目的:观察氯吡格雷治疗急性冠脉综合征(ACS)的临床疗效。方法:120例ACS患者随机均分为治疗组和对照组。对照组采用阿司匹林常规治疗,治疗组在对照组的基础上口服氯吡格雷75mg·d-1,qd。2组均治疗6个月后评价临床疗效,治疗前、后测定血清血小板P选择素和C反应蛋白水平。结果:治疗组临床疗效总有效率为93.3%,显著高于对照组(75.0%),差异有统计学意义(P<0.05)。治疗后,治疗组血小板P选择素和C反应蛋白水平显著降低,与治疗前和对照组治疗后比较,差异有统计学意义(P<0.05)。2组均未见不良反应发生。结论:氯吡格雷治疗ACS临床疗效好,可以抑制血小板活化和炎性反应达到抗血栓目的。 相似文献
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花生壳提取物对家兔血小板聚集的影响 总被引:1,自引:0,他引:1
目的:研究花生壳提取物体内、外给药对血小板活化因子(PAF)诱导家兔血小板聚集的影响。方法:分别采用体内和体外给药,比浊法测定血小板的聚集率,观察花生壳提取物对PAF诱导的家兔血小板聚集的抑制作用。结果:花生壳提取物在20、10mg·mL-1浓度下体外给药对PAF诱导血小板聚集有明显抑制作用(P<0.05),抑制率分别为47.13%、33.48%;在100mg·kg-1剂量下体内给药对PAF诱导血小板聚集有明显抑制作用(P<0.01),抑制率为21.78%。结论:花生壳提取物对PAF诱导的血小板聚集有抑制作用,其作用机制可能与拮抗PAF受体有关。 相似文献
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目的:探讨皖南蝮蛇毒血小板抑制因子(AHV-PI)对家兔动脉血栓形成的影响及可能机制。方法:新西兰家兔24只,随机分成假手术组、动脉血栓模型组、阳性对照组(奥扎格雷钠,5mg/kg),AHV-PI(0.1mg/kg)实验组共4组,每组6只。应用70%FeCl3溶液化学损伤的方法来制备家兔颈动脉血栓模型,采用血栓弹力仪(TEG)描计血栓弹力图,比浊法测定家兔血小板聚集率,ELISA测定各组血浆中α颗粒膜蛋白(GMP-140)和血栓素B2(TXB2)水平,光镜和透射电镜分别观察动脉血栓形成和血小板形态的改变。结果:AHV-PI实验组与模型组相比,血栓弹力图凝血时间(R)值和血凝块形成时间(K)值延长(P〈0.01和P〈0.05),Alpha角度、最大幅度(MA)和凝血指数(CI)减小(P〈0.05和P〈0.01);血小板聚集率的各项指标均明显降低(P〈0.05);血浆中GMP-140和TXB2含量降低(P〈0.01)。AHV-PI实验组光镜下动脉内未见血栓形成,血小板电镜显示血小板形态基本规则,与模型组相比伪足较少,α-颗粒和致密颗粒无明显减少,胞浆空泡化现象减轻。结论:AHV-PI可以通过抑制血小板聚集,防止动脉血栓的形成,其机制可能与之保护血小板超微结构,减少血小板脂质代谢和颗粒内容物的释放有关。 相似文献
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Kawano KI Hokamura K Kondo K Ikeda Y Suzuki Y Umemura K 《European journal of pharmacology》2001,417(3):217-222
The advantage of platelet integrin GPIIb-IIIa receptor antagonists in the prevention of thrombotic occlusion was clearly proven in patients who underwent interventional treatment of the coronary artery, but its value in cerebral ischemia is still under investigation. The expectation of intracranial hemorrhage on strong inhibition of platelet function restricts its application in cerebral ischemia. To minimize bleeding while keeping antithrombotic activity, we have tried to find an appropriate approach using a combination of platelet integrin GPIIb-IIIa receptor antagonist and some other antithrombotic agents. The time to thrombotic occlusion was measured using a photothrombotic occlusion model of guinea pig middle cerebral artery. A platelet integrin GPIIb-IIIa receptor antagonist, ME3277 (sodium hydrogen [4-[(4,5,6,7-tetrahydrothieno [3,2-c] pyridin-2-yl) carbonylamino] acetyl-o-phenylene] dioxydiacetate), delayed occlusion time from 7.3 min in vehicle to 15.0, 20.6 and 25.9 min (P<0.05) at 0.1, 0.3 and 1 mg/kg, respectively. ME3277 profoundly inhibited ex vivo platelet aggregation and the highest dose of ME3277 prolonged (3.5 folds, P<0.01) the bleeding time measured in the hind paw. A thromboxane A(2) synthase inhibitor, sodium ozagrel, significantly delayed occlusion time to 19.5 min at 30 mg/kg (P<0.05) while it did not affect bleeding time or platelet aggregation. ME3277 (0.1 mg/kg) in combination with 10 mg/kg sodium ozagrel synergistically delayed occlusion time (sodium ozagrel alone; 7.9 min, combination; 26.1 min, P<0.05 vs. ME3277 alone). Sodium ozagrel did not affect ex vivo platelet aggregation or bleeding time when combined with 0.1 mg/kg of ME3277. This synergy was cancelled by combination with 30 mg/kg aspirin (14.7 min). A thromboxane A(2) receptor antagonist, vapiprost (0.1 mg/kg), did not enhance the antithrombotic efficacy of ME3277. These results imply that local prostacyclin production enhances the in vivo antithrombotic effect of the platelet integrin GPIIb-IIIa receptor antagonist. Therefore, the thromboxane A(2) synthase inhibitor allowed a reduction in the dose level of the platelet integrin GPIIb-IIIa receptor antagonist for cerebral thrombosis, which resulted in a reduced risk of bleeding. 相似文献
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目的:研究二磷酸腺苷(ADP)诱导的血小板聚集率的测定方法。方法:收集30例急性冠脉综合征(ACS)患者的血样,选择5,10,20μmol·L^-1不同浓度的ADP测定血小板1,3,5min的聚集率和最大聚集率。结果:5μmol·L^-1ADP组不同时间点的血小板聚集率与10,20μmol·L^-1ADP组差异显著(P〈0.01),10μmol·L^-1ADP组不同时间点的血小板聚集率与20μmol·L。ADP组差异无统计学意义。研究发现血小板聚集率有直方双曲线和波形图两组有代表性的图形。结论:对于普利生公司的LBY—NJ4四通道血小板聚集仪,10μmol·L^-1为最适ADP诱导剂浓度。初步推断患者的血小板聚集率的图形为直方双曲线,可能对氯吡格雷的反应较高,氯吡格雷能起到较好的抗血小板作用。 相似文献
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目的:探讨应用流式细胞术全血法检测血小板功能、影响因素及临床意义。方法:应用血小板特异性荧光抗体CD61-FITC标记血小板,并以0.82μm标准微球进行定位对照和设置机器检测条件,调节机器阈值,设门计数血小板微颗粒(PMP)占CD61阳性颗粒的百分比。以ADP及胶原诱导血小板活化,计数活化以后血小板释放的PMP,以未加血小板激活剂的标本作为零聚集对照,激活剂活化的标本以单个血小板数量的减少反应血小板聚集率的多少,并进行方法学的评价。结果:该方法能够有效的检测PMP及低浓度诱导剂诱导下的血小板聚集,检测的血小板聚集功能敏感度明显高于比浊法。应用枸橼酸钠和CTAD抗凝样本,检测结果显示CTAD抗凝的全血静息状态下血小板释放PMP的量显著低于枸橼酸钠抗凝全血释放PMP量。结论:流式细胞术全血法检测血小板功能方法准确、敏感,快速、简便适合于临床常规检测。 相似文献
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目的:探讨血小板糖蛋白Ⅱb/Ⅲa受体拮抗药替罗非班对糖尿病肾病患者血小板活性和肾功能的影响。方法:20例健康体检者为对照组(CON组),33例糖尿病肾病患者随机分为替罗非班治疗组(TM组)和糖尿病肾病组(DN组),分别检测3组治疗前和治疗后1个月的血小板计数(PLT)、平均血小板体积(MPV)、血小板激活复合物-1(PAC-1)、糖化血红蛋白(HbAlc)、尿素氮(BUN)、血肌酐(Scr)、尿微量白蛋白(MAU),并分析3组间的相关性。结果:与CON组比较,DN组的MPV、PAC-1、HbAlc、BUN、Scr、MAU水平明显增高(P<0.05);与DN组比较,TM组的MPV、PAC-1、BUN、Scr、MAU水平明显降低(P<0.05)。结论:糖尿病肾病患者血小板活性增高,小剂量替罗非班治疗能够抑制血小板活化,改善糖尿病肾病患者的肾功能。 相似文献
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Platelet aggregation is mediated by the glycoprotein IIb-IIIa receptor, a member of the integrin superfamily of membrane-bound adhesion molecules. In the activated platelet, binding to the major adhesive proteins, fibrinogen and von Willebrand, occurs due to a conformational change of the glycoprotein IIb-IIIa receptor. Glycoprotein IIb-IIIa receptor antagonists effectively block the binding of these adhesive proteins and thus inhibit platelet aggregation. Large-scale clinical trials have demonstrated the benefits of these agents in patients undergoing percutaneous coronary angioplasty and with acute coronary syndromes compared to conventional antiplatelet therapy. Furthermore, trials are in progress in patients with acute myocardial infarction. The beneficial effects of these agents was first demonstrated with abciximab, a monoclonal antibody to the glycoprotein IIb-IIIa receptor, in patients at risk of coronary arterial thrombosis, and was further illustrated in trials with other IIb-IIIa receptor blocking agents, both with synthetic peptide and non-peptide receptor antagonists. This review focuses on the glycoprotein IIb-IIIa receptor antagonists most advanced in clinical development. 相似文献