维持性血液透析患者血小板参数和血小板聚集功能的研究

目的 观察血液透析对尿毒症患者血小板功能、血小板参数的影响并探讨其作用机理.方法 应用血小板聚集仪观察尿毒症患者血液透析前后,血小板聚集功能和血小板参数的变化.结果 血液透析前,尿毒症组的血小板聚集率明显低于正常对照组;其血小板参数与对照组相比无明显差异.血液透析后,患者血小板聚集率无明显增加,但其血小板参数无明显变化.结论 血液透析不能改善尿毒症患者血小板功能.     

血小板聚集试验在尿毒症透析患者诊治中的应用

目的探讨血小板聚集试验在尿毒症透析患者诊治中的临床意义。方法以APACT2型血小板聚集仪用ADP为诱聚剂,检测60例正常人(对照组)及60例尿毒症患者(观察组)透析前、透析后血小板聚集率。结果观察组血液透析前的血小板最大聚集率为(32.4±8.2)%,透析后为(36.2±9.2)%,均明显低于对照组的(62.7±16.1)%(P<0.01);而透析前、后血小板聚集率差异无统计学意义(P>0.05)。结论血小板聚集试验简便、实用,可作为评价血小板聚集功能的初筛试验。血液透析不能改善尿毒症患者血小板功能。     

无肝素血液透析的临床应用

要进行血液透析，必须建立体外循环，并要使用抗凝剂以防止血液凝结在体外循环，又不导致出血的发生。但是，尿毒症病人由于代谢产物肥类及酚类在体内蓄积，抑制了血小板的功能，造成血小板聚集能力降低。由于凝血功能障碍，常合并出血倾向。透析时使用肝素，使血小板、补体被激活，造成尿毒症血液透析患者的出血倾向加重，甚至可能大出血死亡。本文对有出血倾向维持性血液透析患者，行无肝素血液透析32例次，使用血仿膜透析器。透析前，肝素盐水透析超滤，使肝素充满膜内外及膜孔中；血流量维持在200mL／min以上，仅2例次因血流量＜160mL…     

肺心病急性发作期病人的体外血小板聚集功能变化

本文测定34例肺心病息性发作期病人体外血小板聚集率,血小板计数和动脉血气分析。结果显示肺心病急性发作期病人的血小板5分钟聚集率和血小板最大聚集率明显高于健康对照组(P<0.01),血小板最大聚集率与二氧化碳分压有显著直线相关性(r=0.7999;P<0.01),与氧分压,血小板计数无相关性。说明肺心病急性发作期病人的体外血小板聚集功能增强,并随二氧化碳分压升高而增高。     

透析膜生物相容性的研究

血液透析是尿毒症病人维持生命的替代疗法之一，但透析膜的生物相容性对患者不良反应的发生率和死亡率有一定的影响。评价透析膜生物相容性的指标主要有补体活化、中性粒细胞黏附聚集活化及功能异常、血小板黏附聚集及释放反应、凝血及纤溶活性的改变及外周血单个核细胞活化及细胞因子的产生与释放。     

血液透析病人消化道出血的护理体会

消化道出血是尿毒症常见并发症之一,尤其是接受血液透析的尿毒症患者,由于肌酐、尿素氮指标均较正常值高出许多,间接刺激胃肠道系统引起出血,再者尿毒症时常合并血小板功能不全引起凝血机能障碍,血小板功能不全又加重了消化道出血。另外在血液透析中抗凝剂的应用常可诱发或加重     

晚期尿毒症血透病人血小板聚集功能变化及其意义

本文报告30例晚期尿毒症患者血透前、首剂肝素化后及血透后24h检测了血小板1min和5min聚集率。结果显示,尿毒症患者血小板1min及5min聚集率均显著低于正常,首剂肝素化后有显著提高,血透后24h较血透前有明显改善。上述结果表明:尿毒症患者血小板聚集功能低下,这可能是该类患者常有出血倾向的主要原因之一;作为抗凝药物的肝素,对血小板功能有活化作用;血透能改善这类患者的血小板功能,是防治其出血倾向的有效措施。     

Ⅱ型糖尿病病人血小板聚集、第Ⅷ因子相关抗原的临床研究

本文对23例初发Ⅱ型糖尿病病人口服降糖药吡磺环已脲(Glipizide)治疗前后的血小板聚集、第Ⅷ僵因子相关抗原(ⅧR:Ag)和纤维蛋白原进行动态研究。结果表明:Ⅱ型糖尿病病人在临床未发现微血管病变时已有血小板聚集率升高,血小板聚集率与空腹血糖、糖化血红蛋白A1(GHbA1)无相关性,与ⅧR:Ag呈正相关(P<0.001)。吡磺环己脲治疗后血小板聚集率明显下降。提示血小板功能异常可能参与Ⅱ型糖尿病微血管病变的发生;内皮损害会加剧血小板聚集功能;吡磺环已脲对抑制血小板聚集功能有一定作用。     

尿毒症患者血液透析中的出血倾向

尿毒症患者血液系统损害主要表现为出血和贫血 ,其出血倾向可表现为鼻黏膜、消化道甚至脑出血。为探讨本病出血的临床防治方法 ,我们检测了尿毒症患者血液透析前后血小板计数、血小板聚集功能、白陶土部分凝血活酶时间 (ＫＰＴＴ)和凝血酶原时间 (ＰＴ)。1　临床资料1 1　一般资料　 1998年 7月至 2 0 0 0年 6月在我科行血液透析的尿毒症患者 30例。均符合第二届全国肾脏病学术会议拟定的诊断标准 :血清肌酐持续 >44 2ｍｍｏｌ/Ｌ,内生肌酐清除率 <0 42ｍｌ/ (ｓ·1 73ｍ2 )。其中男 2 1例 ,女 9例 ,年龄 2 1～6 8岁 ,透析时间 (18± 8)个…     

血液透析患者血小板聚集功能和其它部分血流流变学的变化

对１６例维持性血液透析患者进行了血小板聚集试验和其它部分血流流变学测定。结果显示，ＨＤ组血小板聚集率显著低于正常对照组，表明ＨＤ患者存在血小板功能缺陷。     

HETEROGENEITY OF THROMBASTHENIC PLATELET AGGREGATION INDUCED BY MULTIPLE AGGREGATING AGENTS

The function of platelet aggregation was studied in 12 patientswith congenital thrombasthenia,using multiple aggregating agents.Heterogeneityof aggregation patterns were encountered based upon the response to differentinducers,pattern 1 was characterized by refractoriness to both weak inducers(ADP and epinephrin)and strong inducers(collagen and arachidonate).Pattern 2 demonstrated that deseased platelets responded to the strong agonists.Platelets front one patient showed no response to all the inducers employedin the study including ristocetin,and was referred to pattern 3.The relationshipbetween the aggregating patterns of thrombasthenia and its clinical manifesta-tions is called for further investigation.     

葛根素对家兔肝缺血再灌注损伤时血小板聚集功能的影响

目的:探讨葛根素对家兔肝缺血-再灌注损伤时血小板聚集功能的影响.方法:30只家兔,随机均分为对照组(C组)、缺血再灌注组(IR组)和葛根素组(Pur组).观察血小板最大聚集率(Ptmax)、最大聚集时间(PtT)及聚集坡斜率(PtS)的变化.结果:IR组与C组比较,各时间点Ptmax、PtS明显升高,PtT显著缩短,Pur组与IR组相比较,Ptmax明显降低(P＜0.01),PtT明显缩短(P＜0.05),PtS明显升高(P＜0.05).结论:葛根素可通过抑制血小板聚集功能,改善肝脏微循环,从而防治肝脏缺血再灌注损伤.     

单纯性肥胖儿童血小板聚集反应的变化及其机理研究

采用ADP诱发体外血小板聚集及胆固醇亚组分沉淀法观察22例7～12岁肥胖儿童血小板聚集率及151例肥胖儿童血清胆固醇各组分含量和比值。结果表明,单纯性肥胖儿童血清总胆固醇(TC)和低密度脂蛋白胆固醇(LDL-C)含量明显高于正常儿童(P<0.01),而高密度脂蛋白胆固醇(HDL-C)含量、HDL-C/T-C、HDL_2-C/T-C及HDL_2-C/HDL-C比值显著低于正常儿童(P<0.05)。高脂血症的肥胖儿童1秒与5秒时血小板聚集率较正常儿童和血脂不高的肥胖儿童显著升高(P<0.01)。提示高脂血症肥胖儿童血小板聚集反应增强,似与其T-C和LDL-C增高及HDL_2-C含量下降有关。     

出血性血小板病患者血小板超微结构的研究

未明原因多部位出血性血小板产现是一新型出性血疾病，特征为同一血小板对常规诱导阈值浓度的各种诱导剂可有正常或有缺陷的聚集反应。观察同一患者聚集的、不聚集的和静息的血小板，在电镜下的超向一结构。结果患者血小板超微结构形态学的改变，均符合正常对照者形态变化的规律。     

Platelet function in nephrotic syndrome patients at the Kenyatta National Hospital

Platelet function was assessed in 40 patients with nephrotic syndrome but without renal failure in order to establish whether or not there is any haemostatic disorder lending to hypercoagulable state. The findings were compared with those from 40 normal controls. There was no clinical evidence of thromboembolic phenomena in the patients. Values for the mean platelet counts and clot retraction were similar (P less than 0.05), whereas significant decrease of platelet adhesiveness (P less than 0.001) as well as prolonged platelet aggregation time (P less than 0.001) were noted. This is different from some reports in literature which have frequently reported enhanced platelet function. There may be a difference in the way platelets metabolise arachidonic acid to potent aggregating agents, in the African patients as compared to patients studied elsewhere. The hypercoagulable state in our nephrotic syndrome may be explained by alterations in other haemostatic parameters rather than in platelet function.     

阿魏酸(ferulic acid)对人血小板功能的影响

阿魏酸抑制各种诱导剂引起的人血小板聚集,并表现与 PGE_1有协同作用。我们观察到阿魏酸增加人血小板 c—AMP 含量,抑制凝血酶诱导的血栓素 B_2和丙二醛生成,但对花生四烯酸诱导的产生无抑制作用。我们的结果表明阿魏酸抑制血小板聚集可能通过增加 c—AMP,这一结果尚需进一步研究。     

糖尿病血管并发症的血小板高聚集性及其临床意义

用四种方法在50例糖尿病患者和42名正常人中,检测血小板聚集性的七项指标,用逐步回归分析法,在Intecolor 3621微型电子计算机上进行运算。结果表明糖尿病病人伴血管并发症者血小板聚集性增高明显,并以伴有多种血管并发症者尤其显著。血小板聚集性增高与糖尿病的病程、血糖和血脂水平以及应用胰岛素与否无关。血小板高聚集性的病理因素,在临床上对识别糖尿病伴血管并发症可能有意义。     

川芎嗪对人血小板聚集的抑制作用

研究不同剂量川芎嗪对人血小板聚集ADP,AA,PAF三条激活途径的抑制作用,以期进一步探讨川芎嗪抗血小板作用及活血化瘀机理。结果表明:0.14～0.56mg/ml的川芎嗪均能显著地抑制三条激活途径,且随川芎嗪浓度的增加,其抑制作用呈现量效关系。     

A NEW VARIANT OF PLATELET AGGREGATION DEFECT

This paper presents a group of 200 patients withrepeated occurrence of ecchymosis on the extremities and/or menorrhagia occasionally associated with gum bleeding or epistaxis. 152 were female and 48 male, with age ranging from 16 t0 42 years. The results of laboratory examinations such as blood p!atelet count, bleecling time, platelet morphology, platelet adhesive- ncss and platelet aggregation induced by ADP, epi nephrine and ristocetin were all normal. Using SJAMP as a new platelet aggregating agent, 74 cases failed in platelet aggregation, the abnormality rate being 3770. SJAMP, a new anticoagulant isolation from Chinese sea-cucumbers, can induce a special aggregation tracing on normal platelet-rich plasma. Therefore, we consider that the patients with failure of SJAMP-induced aggregation may suffer from a new variant of platelet aggregation defect.     

Platelet immune complex interaction in pathogenesis of Kawasaki disease and childhood polyarteritis

The role of platelets in the pathogenesis of vasculitis and the formation of coronary artery aneurysms was studied in 19 children with Kawasaki disease and five with polyarteritis. All patients with Kawasaki disease developed thrombocytosis in the third week of illness. The peak platelet count was significantly correlated (p less than 0.005) with the subsequent development of coronary artery aneurysms. The rise in platelet count was associated with the appearance in the circulation of a factor that induced aggregation and serotonin release in normal platelets. This factor was shown to be of high molecular weight, and its activity was lost at low pH--features suggestive of an immune complex. Immune complexes, detected by precipitation with polyethylene glycol, also appeared in the circulation as the platelet count increased. These complexes induced platelet aggregation, and there was a significant correlation (p less than 0.001) between the concentrations of IgG and IgA in the polyethylene glycol precipitated material and the platelet aggregating activity. Similar platelet aggregating activity was also detected in patients with polyarteritis but followed a different time course, persisting in the circulation for several months in association with continued disease activity. These findings imply that different mechanisms have a role in distinct phases of Kawasaki disease. The initial feverish phase (probably infective) is probably followed by an immune complex vasculitis that occurs when antibodies to the initiating agent appear in the circulation. The immune complexes aggregate platelets and induce release of serotonin. Platelet derived vasoactive mediators may increase vascular permeability and facilitate further deposition of complexes in the tissues.