溶栓药物研究进展

从两个方面综述了溶栓药物的研究进展 ,包括组织纤溶酶原激活剂的突变体 (rPA、Monteplase、TNK tPA、nPA、K1K2 Pu嵌合体 )以及一些其它来源的纤溶酶原激活剂比如尿激酶原、葡激酶、吸血蝙蝠唾液纤溶酶原激活剂、蚓激酶、纳豆激酶和蛇毒纤溶酶原激活剂等     

急性心肌梗死溶栓治疗概述

急性心肌梗死是严重危害人类健康的疾病，及时有效地溶栓治疗，可挽救生命并改善预后。目前溶栓药有UK和SK等非选择性纤溶酶原激活剂。本对目前选择纤溶酶原激活剂（t-PA,Pro-uk）的大规模临床试验进行综述。     

急性心肌梗死几种溶栓药物治疗比较

目的比较尿激酶(Urokinase,UK)、链激酶(Streptokinase,SK)和重组组织型纤溶酶原激活剂(Rearrangement tissue-type plasminogen activator,r-tPA)对急性心肌梗死患者进行静脉溶栓治疗的临床疗效。方法628例入选患者随机分为3组,UK组222例,SK组205例,R-tPA组201例。分别给予3种溶栓药物静脉输入,观察血管再通的临床指标,同时观察有无出血、心衰、休克等并发症。结果3组的再通率分别为R-tPA组81.3%,SK组66.1%,UK组58.7%。而死亡率则反之,即r-tPA组为8.7%,SK组为9.2%,UK组为10.3%。r-tPA组重度出血发生率明显高于SK组和UK组(依次为6.2%、1.5%、0.6%);而轻度出血以SK组和UK组多见。血管再通后,死亡率、休克、心力衰竭、严重心律失常及再缺血等并发症明显低于血管未通组。结论r-tPA再通率高,溶栓疗效好。如患者经济允许,对急性心肌梗死应首选,但对高血压及老年患者应慎重,以防重度出血的发生。     

新型溶栓药物瑞替普酶治疗急性心肌梗死3例

溶栓治疗急性心肌梗死（AMI）已广泛应用于临床，目前国内常用溶栓药物尿激酶（UK）、链激酶（SK）及重组组织型纤溶酶原激活剂（rt-PA）为溶栓剂。笔者采用新型溶栓药物瑞替普酶（派通欣）治疗，取得较好疗效，现将资料完整的3例报告如下。     

不同溶栓药物治疗急性心肌梗死疗效比较

目的研究不同溶栓药物对急性心肌梗死（Acute myocardiac infarction,AMI）的疗效。方法回顾性分析以链激酶（Staphylokinase,SK）,重组组织型纤溶酶原激活剂（Recombination tissue—type plasminogen activator,r—tPA）和替奈普酶（Tenecteplase,TNK—tPA）治疗共317例住院患者临床情况及疗效。结果TNK-tPA治疗血管再通率最好,出血并发症较少,r-tPA次之,SK组血管再通率最低,出血并发症最多。结论TNK—tPA用于AMI溶栓效果最好。     

急性心肌梗死重组组织型纤溶酶原激活剂溶栓治疗的观察及护理

目的探讨重组组织型纤溶酶原激活剂（rt-PA）溶栓治疗急性心肌梗死的疗效及静脉溶栓的护理要点。方法入选54例急性心肌梗死患者,常规应用阿司匹林和肝素等药物,静脉注射重组组织型纤溶酶原激活剂（rt-PA）100mg,同时予积极护理干预。观察患者溶栓后的冠状动脉开通率（根据临床判定）,出血等并发症和发病30d左室射血分数。结果冠状动脉开通率为81．5％（44例）;30d左室射血分数为（51．6±7．8）％;54例患者中20例出现穿刺处皮下淤血,2例肉眼血尿,29例心律失常,9例低血压。结论重组组织型纤溶酶原激活剂（rt—PA）溶栓治疗急性心肌梗死具有较好疗效,同时结合有效的心理护理,溶栓前、中、后的观察及护理和正确合理的生活护理可防止患者溶栓后出血,心肌再灌注性心律失常等并发症。     

急性心肌梗死重组组织型纤溶酶原激活剂溶栓疗效分析

静脉溶栓治疗是当前治疗急性心肌梗死(AMI)，使冠状动脉血管再通的有效方法之一。本研究分析了48例使用重组组织型纤溶酶原激活剂(rt-PA商品名actilyse，爱通立)静脉溶栓治疗AMI的疗效。     

二肽基肽酶-IV抑制剂的最新研究进展

二肽基肽酶（DPP-IV）抑制剂是最新一代抗糖尿病药物,该文针对DPP-IV抑制剂的最新进展进行综述,主要介绍了它们的作用机制、研究进展和结构类型等。     

A review of the long term effects of thrombolytic agents

Unequivocal evidence exists that reperfusion therapy, when given within 12 hours after onset of symptoms, saves the lives of patients with acute myocardial infarction (MI). As a result, the routine use of such treatment has increased rapidly since the mid-1980s but the rates of utilisation have been relatively static over the last decade at approximately 50% of patients with acute MI. The major question arising in this respect is: is the benefit of reperfusion therapy, which is achieved during the acute phase in evolving MI, maintained on the long term? The main thrombolytic agents currently in use are streptokinase, alteplase, anistreplase, urokinase and reteplase. Other studies compared coronary angioplasty with thrombolytic therapy and investigated the effect of an additional angioplasty procedure after failed thrombolytic therapy. Furthermore, several studies have been performed to investigate the effect of initiation of reperfusion therapy before hospital admission. It is generally agreed that, in particular, patients receiving early treatment within 6 hours from onset of symptoms and patients with ST elevation benefit most from thrombolytic therapy. One would theoretically expect that infarct size reduction achieved by reperfusion therapy would also have a beneficial effect on the survival, not only during the hospital stay but also afterwards, resulting in diverging survival curves between patients who received reperfusion therapy and those who did not. However, the survival curves run perfectly parallel after hospital discharge from 1 year up to year 10 in most studies. The explanation for a lack of extra benefit may be a net result of combining the results of several subgroups. For example, thrombolytic therapy results in more frequent reinfarction especially in the first year, or patients with low left ventricular ejection fraction could survive the hospital phase because of effective thrombolytic therapy, but they survive at high risk. Although several trials suggest that primary percutaneous transluminal coronary angioplasty may be more beneficial than thrombolytic therapy in acute MI, these data should be interpreted cautiously unless confirmed by larger studies with long term results. In addition, evidence exists to suggest that administration of fibrinolytic treatment, under certain conditions, before hospital admission may lead to further improvement of a patient's prognosis. Again, further investigation is warranted. The conclusion is that clear evidence exists that the early improved survival after thrombolytic therapy has been shown to be maintained beyond a decade. However, the expected theorectical additional benefit of reperfusion therapy after hospital discharge has not been observed.     

溶血栓药物在急性脑梗死中的应用进展

脑梗死是导致人类致残和死亡的主要疾病之一,在发生脑梗死的超急性期,积极给予溶栓治疗,开通闭塞的血管,恢复缺血区的再灌注是治疗的关键。目前只有重组组织型纤溶酶原激活剂(rt-PA)被FDA批准应用于急性脑梗死的溶栓治疗,其他的许多药物如瑞替普酶,替奈普酶,去氨普酶、安克洛酶等在脑梗死治疗应用方面正在探索中。本文将针对上述几种主要的溶血栓药物及其已经开展的相关临床研究进行论述。     

Targeted delivery of thrombolytic agents: role of integrin receptors

Blood clotting (formation of thrombus) plays a critical role in the evolution of a number of cardiovascular diseases. Targeted delivery of thrombolytic agents reduces the risks of hemorrhage and toxicity associated with systemic drug administration, thus offering a promising, minimally invasive approach to controlling and treating thrombosis. Platelets play a major role in the progression of thrombosis on vascular injury. Platelet integrin αIIbβ3 (GP IIb/IIIa) serves as a receptor for various proteins such as fibrinogen, vWF, fibronectin and vitronectin, as well as contributing to the adhesion and aggregation of platelets in a variety of conditions. These receptor-based targeted therapies are currently under clinical studies. Integrins and RGD-based ligands for integrins are currently being investigated in imaging and drug delivery related areas of research. RGD-targeted drugs and imaging agents have been developed either by direct conjugation of the homing peptide to the drug or by conjugation of the RGD-peptide to a carrier device containing drug molecules. This review describes the role of integrin receptors in the pathophysiology of thrombosis and its use in the targeted delivery of thrombolytic agents.