白膜法手工制备血小板与机制血小板的质量分析

目的比较手工分离及机器分离两种方法制备血小板的相关质量指标。方法对来源于街头采集的400 ml全血60袋,分别采用机器及手工分离白膜层,比较两种制备方法的白膜层血小板回收率、终产品血小板回收率、血小板含量、红细胞混入量、产品容量。结果机器分离血小板白膜层的血小板回收率及产品血小板回收率均高于手工分离制备(P<0.05)。两种制备方法的红细胞混入量的差异无统计学意义(P>0.05)。手工分离血小板终产品容量变异系数高于机器制备血小板(P<0.05)。结论机器制备浓缩血小板所收集的血小板回收率及容量均优于手工制备血小板。

毒结清口服液对Lewis肺癌小鼠血小板活化机制的影响

目的:探讨毒结清口服液对Lewis肺癌小鼠血小板活化标志物表达的影响。方法:建立Lewis肺癌小鼠模型,按分组情况分别干预21 d,观察各组瘤质、抑瘤率及CD62P、CD63表达和v WF水平的变化。结果:毒结清组小鼠体质量显著性高于模型组(P<0.05),毒结清组的抑瘤率为63.2%,化疗组的抑瘤率为38.1%;模型组的CD62P、CD63和v WF水平显著高于正常组(P<0.05);毒结清组的CD62P、CD63表达和v WF水平明显低于模型组和化疗组(P<0.05),显著高于正常组(P<0.05)。结论:毒结清口服液可抑制Lewis肺癌小鼠的肿瘤增殖,保持体质量,可能与其抑制血小板活化机制相关的CD62P、CD63表达和降低v WF水平有关。

治疗骨关节与运动损伤疾病运用自体富血小板血浆的机制与应用

目的:探讨在骨关节与运动损伤疾病使用自体富血小板血浆机制的效果.方法:使用计算机对1990年-2018年万方数据库、知网数据库以及PubMed数据库中涉及的骨关节与运动损伤疾病中使用自体富血小板血浆机制的相关资料进行检索,仔细阅读实验室文献和临床数据报告等内容,并对其相关疾病、数据等现状进行归纳和综述.结果:(1)自体富血小板血浆修复骨关节和软组织损伤等机制尚不明确,现今关于其猜测、推理等内容较多.(2)各种骨关节与运动损伤性疾病治疗中,自体富血小板血浆治疗方法、使用剂量、治疗疗程以及给药方法等尚未完善、规范化,国内外相关疾病无明确的指南和参考文献.(3)对骨关节与运动损伤性疾病治疗中自体富血小板血浆治疗具有较优的发展前景,但在现今临床上仍处于初始探究时间,并对其进行有效实验,充分的分析、总结相关有效证据,为临床治疗提供重要依据.(4)近几年国内外对骨关节与运动损伤性疾病治疗中自体富血小板血浆治疗研究资料较少,缺少明显的对照数据,因此需谨慎进行相关研究,其需经长期检验,根据其结果作为最终的研究结果.结论:在骨关节与运动损伤疾病使用自体富血小板血浆机制,经研究证实,效果明显,因现今临床上缺乏相关研究证实,还需经长时间研究作出最后结果.

硝普钠对急性左心衰竭患者血小板止血机制的影响

血小板的机能状态,其聚集性和粘附性是决定血液流变学特点的重要因素.缺血性心脏病患者血液聚集性和粘附性升高对高纤维蛋白原血症、高脂蛋白血症等有一定影响. 在进行硝普钠对急性心肌梗死后急性左心衰竭患者血小板的聚集性和粘附性影响的研究时,我们对11例上述患者进行了观察,年龄为45～60岁,男9例,女2例.全部患者心肌梗死均位于前壁.其中中度左心衰竭6例,心源性哮喘发作5例,均伴有动脉性高血压.

4℃冷藏贮存血小板体内清除机制研究进展

血小板输注是临床上防治出血性疾病的重要手段之一,临床上常用(22±2)℃振荡保存,但其贮存期短,易受微生物污染,故极大地影响了临床血小板输注的可用性和安全性。近年来国内外多项研究显示,4℃冷藏贮存可以延长血小板贮存时限,但是同时也会加重血小板贮存损伤(PSL),这种血小板输注人体后会被机体加速清除,严重制约了4℃冷藏血小板的临床应用。本文就4℃冷藏贮存导致的PSL,以及输注体内的清除机制研究进展做一综述。

糖尿病患者血小板信号转导机制的前沿性研究

令血小板活化的生物化学途径迄今已被完全阐明,而未受控制的其活性则可导致一过性的局部缺血、不稳定心绞痛、心肌梗死和脑血管事件等诸多病变。众所周知,糖尿病以血小板功能异常为特征,包括Ca^(2+)移动增强、与膜流动性相关的异常。

高胆固醇血症患者血小板膜表达CD40配体

研究高胆固醇血症患者血小板膜表达CD4 0配体 ,以探讨高胆固醇血症促动脉粥样硬化、血栓形成的机制。选择 2 5例高胆固醇血症患者及 2 5例年龄性别相匹配的健康对照者 ,采用流式细胞术测定血小板膜CD4 0配体和P选择素的表达 ,用酶联免疫吸附法测定血浆单核细胞趋化蛋白 1水平。结果发现 ,高胆固醇血症患者血小板膜CD4 0配体和P选择素的表达及血浆单核细胞趋化蛋白 1水平明显高于对照组 (P <0 .0 1) ,CD4 0配体表达与总胆固醇 (r=0 .4 1,P =0 .0 2 )及低密度脂蛋白胆固醇 (r=0 .5 6 ,P =0 .0 1)呈正相关 ,P选择素的表达与低密度脂蛋白胆固醇也呈正相关 (r=0 .79,P =0 .0 1)。结果提示 ,高胆固醇血症患者血小板膜表达CD4 0配体增加 ,高胆固醇血症可能是通过激活CD4 0配体而促进炎症反应、血栓形成 ,加速动脉粥样硬化的发生发展。

The Potential Pathway of L-arginine·L-aspartate for Inhibition of Platelet Function

Aim L-Arginine· L-aspartate, a double salt, has been recently reported toinhibit platelet aggregation and thrombosis, but its action mechanism is not clear yet. This studywas conducted to investigate its effect on FITC-PAC-1, an anti-glycoprotein IIb/IIIa monoclonalantibody binding to activated platelets, and on correlative autacoid levels in plasma or inplatelets in order to explore its potential pathway of inhibiting platelet aggregation andthrombosis. Methods Monoclonal antibody binding to activated platelets was assayed by flowcytometry; NO was assessed by colorimetric method. cAMP, TXB_2 or 6-keto-PGF_(1α) levels wereassessed by radioimmunoassay. Results Gavaged 30 mg·kg^(-1) of L-arginine·L-aspartate increasedboth concentration of NO in plasma and 6-keto-PGF_(1) in incubated supernatant of aortic segment ofrats ex vivo (P < 0.05), but it did not influence cAMP content in platelets and the level of TXB_2or 6-keto-PGF_(1) in plasma of rats, whereas ASA significantly lowered TXB_2 or 6-keto-PGF_(1α) inplasma. Both 100 μmol-L^(-1) of L-arginine ·L-aspartate and ASA inhibited FITC-PAC-1 binding toactivated platelets in vitro. Conclusion The increase in NO and PGI_2 release from endo-thelialcells and consequent inhibition of platelet activation may contribute to the inhibition of plateletaggregation and thrombosis by L-arginine· L-aspartate; whereas arachidonic acid or cAMP metabolicpathway is not closely correlative with the studied effect.

基于功能代谢学分析血液环境异常情况下血小板变化及中医药治疗现状

血液循环系统环境易受内外因素影响,引发缺氧、缺血或炎症等异常情况,导致血液循环障碍。血小板是由骨髓中巨核细胞细胞质脱落而成,在维持血管完整性和调节止血方面具有关键作用,是血液系统中的重要组成。血小板形态功能的正常是其进行代谢的基础,而正常的代谢是维持形态功能的必然要求,两者相辅相成。血液环境的改变会导致血小板的功能障碍和代谢紊乱,中医药对于血小板功能和代谢的异常变化均具有显著治疗作用,通过抑制血小板活化和聚集、降低血小板黏附性和影响血小板释放等途径,使异常状态的血小板回归正常,从而减轻患者症状、优化治疗效果和提高生活质量。文章以功能学和代谢学为切入点分析血液环境异常情况下血小板变化的机制,整理和阐述中医药治疗研究现状,以期为血小板研究和中医药抗血小板治疗提供理论基础和参考依据。

Portal hypertensive colopathy in patients with liver cirrhosis

AIM: In patients with liver cirrhosis and portal hypertension, portal hypertensive colopathy is thought to be an important cause of lower gastrointestinal hemorrhage. In this study, we evaluated the prevalence of colonic mucosal changes in patients with liver cirrhosis and its clinical significance. METHODS: We evaluated the colonoscopic findings and liver function of 47 patients with liver cirrhosis over a 6-year period. The main cause of liver cirrhosis was post-viral hepatitis (68%) related to hepatitis B (6%) or C (62%) infection. All patients underwent upper gastrointestinal endoscopy to examine the presence of esophageal varices, cardiac varices, and congestive gastropathy, as well as a full colonoscopy to observe changes in colonic mucosa. Portal hypertensive colopathy was defined endoscopically in patients with vascular ectasia, redness, and blue vein. Vascular ectasia was classified into two types: type 1, solitary vascular ectasia; and type 2, diffuse vascular ectasia. RESULTS: Overall portal hypertensive colopathy was present in 31 patients (66%), including solitary vascular ectasia in 17 patients (36%), diffuse vascular ectasia in 20 patients (42%), redness in 10 patients (21%) and blue vein in 6 patients (12%). As the Child-Pugh class increased in severity, the prevalence of portal hypertensive colopathy rose. Child-Pugh class B and C were significantly associated with portal hypertensive colopathy. Portal hypertensive gastropathy, esophageal varices, ascites and hepatocellular carcinoma were not related to occurrence of portal hypertensive colopathy. Platelet count was significantly associated with portal hypertensive colopathy, but prothrombin time, serum albumin level, total bilirubin level and serum ALT level were not related to occurrence of portal hypertensive colopathy. CONCLUSION: As the Child-Pugh class worsens and platelet count decreases, the prevalence of portal hypertensive colopathy increases in patients with liver cirrhosis. A colonoscopic examination in patients with liver cirrhosis is indicated, especially those with worsening Child-Pugh class and/or decreasing platelet count, to prevent complications such as lower gastrointestinal bleeding.

Role of platelet-activating factor in pathogenesis of acute pancreatitis

Platelet-activating factor(PAF)is a potentproinflammatory phospholipid mediator that belongsto a family of biologically active,structurally relatedalkyl phosphoglycerides with diverse pathologicaland physiological effects.This bioactive phospholipidmediates processes as diverse as wound healing,physiological inflammation,angiogenesis,apoptosis,reproduction and long-term potentiation.PAF actsby binding to a specific G protein-coupled receptorto activate multiple intracellular signaling pathways.Since most cells both synthesize and release PAFand express PAF receptors,PAF has potent biologicalactions in a broad range of cell types and tissues.Inappropriate activation of this signaling pathway isassociated with many diseases in which inflammationis thought to be one of the underlying features.Acutepancreatitis(AP)is a common inflammatory disease.The onset of AP is pancreatic autodigestion mediatedby abnormal activation of pancreatic enzyme caused bymultiple agents,which subsequently induce pancreaticand systemic inflammatory reactions.A number ofexperimental pancreatitis and clinical trials indicatethat PAF does play a critical role in the pathogenesisof AP.Administration of PAF receptor antagonist cansignificantly reduce local and systemic events that occurin AP.This review focuses on the aspects that are morerelevant to the pathogenesis of AP.

Inhibitory effects and mechanisms of high molecular-weight phlorotannins from Sargassum thunbergii on ADP-induced platelet aggregation

We evaluated the effects of high molecular-weight phlorotannins from Sargassum thunbergii(STP) on ADP-induced platelet aggregation and arachidonic acid(AA) metabolism in New Zealand white rabbits and Wistar rats.The inhibition of STP on platelet aggregation was investigated using a turbidimetric method,and the levels of the terminal products of AA metabolism were measured using the corresponding kits for maleic dialdehyde(MDA),thromboxane B2(TXB2) and 6-keto-prostaglandin F1α(6-keto-PGF1α) by colorimetry and radioimmunoassay,as appropriate.We found that STP could inhibit ADP-induced platelet aggregation,and the inhibitory ratio was 91.50% at the STP concentration of 4.0 mg/mL.Furthermore,STP markedly affected AA metabolism by decreasing the synthesis of MDA(P<0.01) and increasing the synthesis of 6-keto-PGF1α,thus changing the plasma TXB2/6-keto-PGF1α balance when the platelets were activated(P<0.01).Therefore,STP altered AA metabolism and these findings partly revealed the molecular mechanism by which STP inhibits ADP-induced platelet aggregation.

Receptor-mediated inhibitory mechanisms and the regulation of platelet function

Platelets are derived from megakaryocytes;they circulate in mammalian blood vessels and play essential roles in hemostasis and thrombosis.When platelets encounter injury,they respond by triggering the formation of a blood clot to prevent blood loss(hemostasis).While this is vital for survival,