速效救心丸对大鼠血小板聚集率及环磷腺苷水平的影响

目的探讨速效救心丸对血小板聚集的作用及机制。方法采用比浊法测定速效救心丸、阿司匹林、阿魏酸哌嗪对二磷酸腺苷(ADP)、胶原和花生四烯酸(AA)诱导的大鼠血小板聚集率和环磷腺苷(cAMP)水平的影响。结果与空白组比较,速效救心丸中、高剂量组可显著抑制ADP、胶原、AA诱导大鼠的血小板聚集(P0.01);速效救心丸高剂量组对AA诱导的大鼠血小板聚集抑制作用较阿司匹林组好;速效救心丸可提高大鼠血小板内cAMP的含量(P0.05)。结论速效救心丸能够抑制大鼠ADP、胶原和AA诱导的血小板聚集,其机制可能通过增加cAMP的含量而发挥作用。     

不同抗血小板药物治疗不稳定型心绞痛患者血小板聚集功能的观察

目的:比较联合应用阿司匹林(ASA)和噻氯匹啶(TP)与单独应用ASA治疗不稳定型心绞痛(UAP)患者时血小板对不同诱聚剂诱导的聚集性改变及其临床意义。方法:选择UAP患者68例,随机分为ASA组(32例)和联合用药组(36例),服药后14 d应用比浊法测定由二磷酸腺苷(ADP)、花生四烯酸(ACA)和胶原(Coll)(终浓度分别为2.5 mmol/L、1.5 mmol/L、100 mg/L)诱导的血小板聚集功能;正常对照组20例,检测方法同其他两组。结果:联合用药组和ASA组ADP诱导的最大血小板聚集率均显著低于正常对照组(P<0.01与P<0.05),但ASA组仍显著高于联合用药组(P<0.05);联合用药组和ASA组ACA诱导的最大血小板聚集率差异无显著性意义(P>0.05),但均显著低于正常对照组(P<0.01);联合用药组Coll诱导的最大血小板聚集率显著低于ASA组(P<0.01),后者与正常对照组差异无显著性意义(P>0.05)。结论:UAP患者急性期联合应用ASA和TP抑制血小板聚集功能优于单独应用ASA。     

高血压患者血小板聚集功能与纤维蛋白原基因多态性的相关性研究

目的观察高血压患者血小板聚集功能变化是否与Bβ纤维蛋白原(Fib)基因启动子区-455G/A多态性有关。方法选取108例未经治疗的高血压患者,采用全血电阻抗法测定二磷酸腺苷(ADP)及花生四烯酸(AA)诱导的血小板聚集功能,并用聚合酶链反应-限制性片段长度多态性分析(PCR-RFLP)方法测定BβFib基因启动子区-455G/A多态性,将其分为GG组和GA+AA组,比较两组血小板聚集功能变化。结果GA+AA组Fib浓度高于GG组(P<0.05),ADP诱导的血小板聚集能力GA+AA组低于GG组(P<0.05);而AA诱导的血小板聚集能力呈现GA+AA组高于GG组的趋势(P>0.05)。结论ADP诱导的血小板聚集功能与BβFib基因启动子区-455G/A多态性有关,GG基因型患者血小板聚集功能强于AA及GA基因型患者。但AA诱导的血小板聚集功能与其的关系呈现相反的趋势。     

阿司匹林、肝素对血小板活化及表达CD40L的影响

目的探讨血小板活化与表达CD40L的关系以及阿司匹林、肝素对此过程的影响.方法体外分离健康人血小板,经不同浓度二磷酸腺苷(ADP)、凝血酶诱导后,应用流式细胞术测定血小板活化指标P选择素和炎性标志CD40L表达水平,观察二者随诱导时间延长的变化过程,并分析阿司匹林、普通肝素、低分子肝素对血小板活化及表达CD40L的影响.结果 ADP、凝血酶均呈浓度依赖方式增加血小板P选择素、CD40L表达,二者表达水平随诱导时间延长而同步增减,呈显著正相关(P<0.05).阿司匹林(2.5 μg/ml)对ADP(4 μmol/L)和凝血酶(1U/ml)诱导的血小板活化及CD40L表达无任何影响(P>0.05);普通肝素(2.5U/ml)和低分子肝素(2.5U/ml)单独或与阿司匹林合用,均能极显著地抑制凝血酶诱导的血小板活化及CD40L表达(P＜0.001),但对ADP的诱导过程无影响(P>0.05).结论炎性介质CD40L可表达在活化血小板表面,在多种诱导剂存在的情况下,阿司匹林及肝素能部分抑制血小板的活化及CD40L表达.     

硫氢化钠药物后处理对心肌细胞缺氧/复氧损伤的影响及机制的探讨

目的从贵州省遵义市正安县产野木瓜中提取并纯化野木瓜多糖(stauntonia chinensis polysaccharides,SCP),对其特征进行初步研究。以体外模型观察SCP对血小板聚集和释放的影响,为野木瓜的进一步研发利用提供基础资料。方法①用水提醇沉法提取纯化SCP,Molish反应定性鉴定SCP,红外光谱分析SCP结构特征。②以Born''s比浊法测定SCP对胶原、ADP、花生四烯酸和凝血酶诱导的家兔血小板聚集的影响。③荧光分光光度法测定SCP对胶原诱导的血....     

复方丹参滴丸对冠心病患者阿司匹林抵抗的作用

目的:探讨复方丹参滴丸对冠心病阿司匹林抵抗患者二磷酸腺苷(ADP)、花生四烯酸(AA)诱导的血小板聚集率的影响。方法:根据AA和ADP作为诱导剂测定的血小板聚集功能,将39例阿司匹林抵抗患者随机分为2组。A组为常规阿司匹林治疗组(n=19),B组为阿司匹林联合复方丹参滴丸治疗组(n=20)。分别在治疗前以及治疗1个月后测定由ADP、AA诱导的血小板聚集率,比较2组治疗前后及治疗后不同组别上述指标的差异。结果:阿司匹林联合复方丹参滴丸治疗1个月后,可使冠心病阿司匹林抵抗患者血小板聚集率下降,与治疗前比较有显著性差异[(49.46%±5.18%)比(73.81%±2.86%),P=0.048 9];可使冠心病患者血尿酸水平下降,B组治疗后血尿酸水平为(421.69±34.01)μmol/L,较治疗前[(444.69±50.88)μmol/L]明显下降(P=0.038 9),与A组治疗后[(444.88±21.32)μmol/L]相比明显下降(P=0.042 2)。2组患者在治疗中未出现不良临床事件。结论:复方丹参滴丸对冠心病阿司匹林抵抗患者有抗血小板聚集作用,并且治疗后可降低血尿酸水平。     

冠心病患者支架置入术后监测血小板聚集率的临床意义

目的观察冠心病患者支架置入术后应用阿司匹林和氯吡格雷联合抗血小板治疗后,监测血小板聚集率并探讨其临床意义。方法测定562例冠心病患者,术前,术后3、7天,1、3、6个月二磷酸腺苷(ADP)和花生四烯酸(AA)诱导的血小板聚集率。ADP和AA分别按照血小板抑制率<40%和≥40%进行分组。ADP诱导血小板抑制率<40%组(75例)和≥40%组(487例)。AA诱导血小板抑制率<40%组(67例)和≥40%组(495例)。观察支架术后冠心病患者6个月的主要心脑血管事件。结果ADP和AA诱导的血小板抑制率<40%和≥40%两组分别比较一般临床资料,差异无显著性意义。随访6个月主要心脏事件的发生率:ADP诱导血小板抑制率<40%组高于≥40%组(30.7%vs12.9%,P<0.05);AA诱导血小板抑制率<40%组也高于≥40%组(28.1%vs11.7%,P<0.05)。出血不良事件没有显著差异。结论冠心病患者支架置入术后的血小板抑制率与6个月的主要心脑血管事件相关。     

达肝素钠对兔血小板功能的影响及阿司匹林和氯吡格雷的干预作用

目的 研究达肝素钠对兔血小板活化的影响以及阿司匹林和氯吡格雷的干预.方法　纯种新西兰家兔12只,给予阿司匹林或氯吡格雷或二者合用喂饲,静脉注射达肝素钠前及注射后20、30 min检测ADP、AA诱导的血小板聚集、血浆CD62P和vWF的水平.结果 应用达肝素钠后血小板聚集、CD62及vWF无明显增加;与基线水平比较,阿司匹林组加用氯吡格雷两药合用,静脉注射达肝素钠前(9.50±4.18 vs 2.67±1.63)及注射后20 min(10.50±3.21 vs 2.83±1.66)ADP 诱导的血小板聚集均明显降低.单用阿司匹林喂饲7 d,应用达肝素钠后血小板聚集增加(7.00±4.10 vs 12.50±4.04).结论 达肝素钠不会引起血小板激活;阿司匹林与达肝素钠合用增加血小板聚集;氯吡格雷与阿司匹林两药合用明显降低血小板聚集.     

野黄芩苷抗血小板活化效应的评价

目的评价野黄芩苷对血小板的聚集与活化的影响。方法在人洗涤血小板中进行血小板聚集实验,分别用胶原(1.00μg/ml)、U46619(0.30μM)、ADP(10.00μM)、凝血酶(0.04U/ml)作为诱导剂,对比在0.04mg/ml、0.10mg/ml、0.20mg/ml三种不同预孵浓度状态下野黄芩苷对血小板聚集的影响。并进一步研究三种不同浓度的野黄芩苷对血栓素类似物(U46619)引起的血小板纤维蛋白原结合的影响。结果胶原、U46619、ADP、凝血酶均可明显促进血小板聚集,而血小板预孵育野黄芩苷可以抑制诱导剂引起的聚集,并且抑制作用呈现浓度依赖关系。血小板预孵育野黄芩苷可以减少U46619引起的血小板纤维蛋白结合,并且抑制作用呈现浓度依赖关系。结论野黄芩苷可以抑制血小板的聚集和活化,很可能是通过阻断血栓素A2诱导血小板聚集的某一个中间环节产生作用。     

氯吡格雷联合阿司匹林对老年不稳定性心绞痛患者血小板聚集的影响

目的观察氯吡格雷联合阿司匹林对老年不稳定性心绞痛患者血小板聚集功能的影响。方法选择老年不稳定性心绞痛患者120例,随机分为阿司匹林组、低剂量联合组(氯吡格雷25 mg)、中剂量联合组(氯吡格雷50mg)、高剂量联合组(氯吡格雷75 mg),每组30例。观察时间为8周,治疗前后测患者血小板颗粒膜蛋白140(GMP-140)浓度及分别用二磷酸腺苷(ADP)和花生四烯酸(AA)为诱导剂的血小板聚集率,记录临床疗效及不良反应发生情况。结果与治疗前比较,治疗8周后,阿司匹林组、低、中和高剂量联合组GMP-140浓度、ADP介导的血小板聚集率显著降低[(15.3±2.9)μg/L vs(9.7±1.5)μg/L、(16.7±3.4)μg/L vs(8.9±2.3)μg/L、(14.9±3.0)μg/L vs(5.1±1.4)μg/L、(16.4±3.5)μg/L vs(7.8±2.2)μg/L,(43.5±9.8)%vs(24.3±8.9)%、(41.0±7.8)%vs(20.3±8.1)%、(44.3±9.2)%vs(21.5±8.7)%、(43.9±7.6)%vs(20.6±8.0)%,P0.05];AA介导的血小板聚集率4组治疗后较治疗前明显降低[(28.7±9.1)%vs(16.1±7.4)%、(29.2±9.3)%vs(17.2±8.5)%、(30.1±10.1)%vs(17.9±9.4)%、(28.8±8.5)%vs(25.7±8.6)%,P0.05],4组比较无显著差异(P0.05)。低、中、高剂量联合组总有效率均高于阿司匹林组(93.33%、96.67%、96.67%vs 86.67%,P0.05)。仅高联合组出现2例不良反应。结论应用氯吡格雷50mg联合阿司匹林对老年不稳定性心绞痛患者双联抗血小板聚集治疗最为适合。     

Impaired cytoplasmic ionized calcium mobilization in inherited platelet secretion defects

Defects in platelet cytoplasmic Ca++ mobilization have been postulated but not well demonstrated in patients with inherited platelet secretion defects. We describe studies in a 42-year-old white woman, referred for evaluation of easy bruising, and her 23-year-old son. In both subjects, aggregation and 14C-serotonin secretion responses in platelet-rich plasma (PRP) to adenosine diphosphate (ADP), epinephrine, platelet activating factor (PAF), arachidonic acid (AA), U46619, and ionophore A23187 were markedly impaired. Platelet ADP and adenosine triphosphate (ATP), contents and thromboxane synthesis induced by thrombin and AA were normal. In quin2-loaded platelets, the basal intracellular Ca++ concentration, [Ca++]i, was normal; however, peak [Ca++]i measured in the presence of 1 mmol/L external Ca++ was consistently diminished following activation with ADP (25 mumol/L), PAF (20 mumol/L), collagen (5 micrograms/mL), U46619 (1 mumol/L), and thrombin (0.05 to 0.5 U/mL). In aequorin-loaded platelets, the peak [Ca++]i studied following thrombin (0.05 and 0.5 U/mL) stimulation was diminished. Myosin light chain phosphorylation following thrombin (0.05 to 0.5 U/mL) stimulation was comparable with that in the normal controls, while with ADP (25 mumol/L) it was more strikingly impaired in the propositus. We provide direct evidence that at least in some patients with inherited platelet secretion defects, agonist-induced Ca++ mobilization is impaired. This may be related to defects in phospholipase C activation. These patients provide a unique opportunity to obtain new insights into Ca++ mobilization in platelets.     

Inhibitory effect of aqueous extracts of some herbs on human platelet aggregation in vitro

Effect of aqueous extract of several herbs on human platelet aggregation in vitro was investigated. Out of 28 herbs/nutriceuticals investigated, camomile, nettle alfalfa, garlic and onion exhibited most significant anti-platelet activity (>or=45% inhibition). Aqueous extracts of alfalfa, fresh nettle, and camomile inhibited ADP induced-platelet aggregation by 73, 65 and 60%, respectively, compared with control (P < 0.05). Camomile and alfalfa inhibited collagen-induced platelet aggregation by 84 and 65%, respectively, but nettle could not inhibit collagen-induced aggregation. In contrast, nettle was the most potent inhibitor (66%) of whole blood aggregation induced by collagen, followed by alfalfa (52%), and camomile (30%) compared with control (P < 0.05). None of these three herbs however could inhibit arachidonic acid or thrombin induced platelet aggregation. Camomile and alfalfa strongly inhibited thromboxane B2 synthesis induced by ADP or collagen, but nettle had no effect. Alfalfa and nettle increased cGMP levels in platelets by 50 and 35%, respectively, compared with the control (1.85 +/- 0.23 nM) (P < 0.005). All these data indicate that camomile, nettle and alfalfa have potent anti-platelet properties, and their inhibitory actions are mediated via different mechanisms.     

Subnormal platelet response to thromboxane A2 in a patient with chronic myeloid leukaemia

A new type of acquired platelet dysfunction was found in a chronic myeloid leukaemia patient with petechiae and thrombocytosis. Platelet aggregation induced by arachidonic acid (AA), collagen and A23187 was decreased, secondary aggregation by ADP and epinephrine was defective and ristocetin-induced aggregation was completely reversible. No platelet ATP was released by AA and collagen. Only high concentrations of AA (≤ 2 mM) induced minimal reversible aggregation. ¹⁴C-serotonin uptake by the platelet and platelet adenine nucleotide contents were normal. Normal AA metabolism was demonstrated by thin-layer radiochromatographic analysis of the metabolites of ¹⁴C-AA and the determination of thiobarbituric acid reactive substances produced by the incubation of AA or thrombin with the platelets. Minimal reversible aggregation was observed when patient's platelet-rich plasma was added to a reaction mixture in which thromboxane A₂ (TXA₂) had been generated. TXA₂ produced by patient's platelets showed normal platelet-aggregating activity. These results suggest that a subnormal platelet response to TXA₂ is included as a mechanism for this acquired hypofunction of the platelet.     

Modulation of platelet and leucocyte function by a Chinese herbal formulation as compared with conventional antiplatelet agents

Platelet and leucocyte activity are important in the acute development of thrombosis and in the pathogenesis of ischaemic vascular disease. Dan Shen Di Wan (DS, Cardiotonic Pill or Dantonic(R) Pill) is one of the most commonly used Chinese herbal formulations for treating patients with atherosclerotic disease in China and several Asian countries. We studied the effect of DS on platelet and leucocyte function and compared the effects with conventional antiplatelet agents, cangrelor (ADP P2Y(12) receptor antagonist) and aspirin (acetyl salicylic acid, ASA). Measurements were made by platelet aggregation (%) and activation (CD62P %), platelet-monocyte conjugate formation (P/M, CD42a median fluorescence, mf), platelet-neutrophil conjugate formation (P/N, mf), and leucocyte activation (CD11b median fluorescence on monocytes and neutrophils, mf) in response to 3.3 micromol/L adenosine diphosphate (ADP), 1.0 micromol/L platelet activating factor (PAF), 5.0 micromol/L adrenaline and 0.5 microg/mL collagen. We also evaluated the effect of its main component, water soluble extract of salvia miltiorrhiza (SME) on intracellular calcium mobilization in platelets triggered by 10 micromol/L ADP, 10 micromol/L PAF, 2 microg/mL collagen and 15 micromol/L thrombin receptor activating peptide (TRAP). Overall DS showed inhibition of platelet aggregation, platelet activation, platelet-leucocyte conjugate formation and leucocyte activation in response to all the agonists apart from adrenaline (all p < 0.01). DS showed inhibition of platelet aggregation and leucocyte activation equivalent to cangrelor 100 nmol/L and ASA 100 micromol/L. SME dose-dependently inhibited intracellular calcium mobilization in platelets following stimulation with all the platelet agonists with maximum effective at 0.36 mg/mL (all p < 0.01). When used at 0.18 mg/mL its inhibitory effect was equivalent to cangrelor and ASA. We conclude that DS is a potential inhibitor of both platelet and leucocyte activation.     

A new congenital defect of platelet secretion: impaired responsiveness of the platelets to cytoplasmic free calcium

Summary . A 16-year-old boy with a bleeding disorder since infancy has a long bleeding time, normal platelet count and morphology and normal plasma factor-VIII activities. His platelets undergo normal shape change and primary aggregation in response to ADP but show defective 5-hydroxytryptamine (5-HT) secretion and aggregation in response to adrenaline, sodium arachidonate, U44069, PAF-acether, A23187 and low concentrations of collagen. Thrombin and higher concentrations of collagen produce a normal response. Secretion of β-thromboglobulin and platelet factor 4 parallels that of 5-HT. Thromboxane B₂ is produced normally in response to exogenous arachidonate and to stimulation by thrombin, collagen and A23187 in all concentrations tested. The patient's endoperoxides and thromboxane A₂ aggregate aspirin-treated platelets, though his platelets are themselves unresponsive. Cyclic AMP is present at normal concentration in the patient's unstimulated platelet-rich plasma, and PGI₂ inhibits platelet aggregation by ADP and thrombin in a normal dose-related manner. Platelet ultrastructure, 5-HT uptake and content of adenine nucleotides, platelet factor 4 and β-thromboglobulin are all within normal limits. When the patient's platelets were loaded with the fluorescent dye quin 2, which serves as an indicator of cytoplasmic free calcium ions, their responses to thrombin, whether in the presence or virtual absence of extracellular Ca2+, were entirely normal in respect of free calcium ions, secretion, shape-change and aggregation. In response to ionomycin, however, a normal increase in free calcium ions was accompanied by normal shape-change but virtually no aggregation or 5-HT secretion. The platelet calmodulin content was normal. These findings show that the defect in this patient's platelets is of utilization of cytoplasmic Caz+ for secretion and aggregation, rather than of Ca2+ uptake or mobilization of Ca2+ from intracellular storage sites. It is suggested that the most likely site of the defect is the phosphorylation of one of the proteins concerned in the secretory mechanism.     

The Effect of Prostaglandin E1 on Platelet Function in Vitro and in Vivo

S ummary Low concentrations of prostaglandin E₁ (PGE₁) inhibit ADP-induced aggregation in pig and rabbit citrated platelet-rich plasma and in suspensions of washed platelets. Higher concentrations also inhibit the initial change in shape induced by ADP and the release of platelet ATP, ADP and serotonin caused by stimuli such as collagen, thrombin, antigen-antibody complexes and gamma-globulin-coated polystyrene particles. PGE₁ is not taken up by platelets and its effects can be removed by resuspending platelets in fresh medium. Immediately following an intra-arterial injection, ADP-induced platelet aggregation is suppressed, but after 5 min the response returns to normal. PGE₁ inhibits haemostasis in rabbits when given as a continuous infusion. It is concluded that the effect of PGE₁ on haemostasis involves inhibition of the release of ADP from platelets exposed to collagen and thrombin, and inhibition of ADP-induced aggregation.     

Incomplete Inhibition of Platelet Secretion by Low-dose Aspirin

This study determines the effects of low-dose oral acetylsalicylic acid (Aspirin) on platelet aggregation and dense granule secretion in relation to inhibition of thromboxane formation. In addition, possible modifications of inhibition of platelet function by iloprost and linsidomine (SIN-1) were also studied. Aspirin (40 mg/day) was administered to 15 healthy male non-smoking volunteers for 8 consecutive days. Platelet function was measured ex vivo before and 12 h after the last drug intake. At the same times urinary excretion of thromboxane B(2) (TXB(2)) and 6-oxo-PGF(1α) were determined. Asirin treatment resulted in a significant (P < 0.01), by 65%, reduction of urinary TX B(2) excretion, whereas urinary excretion of 6-oxo-PGF(1α) remained unchanged, demonstrating the expected selectivity of low-dose aspirin for the platelet cyclooxygenase. There was also a nearly complete (93-95%) inhibition of collagen (0.3-5 μg/ml)-induced thromboxane formation in platelets. However, collagen-induced ATP-and 5-HT secretion was much less inhibited by aspirin and was reduced by only 20% at 5 μg/ml collagen. Similar results were obtained with ADP while thrombin (> 1.2 IU/ml)-induced 5-HT secretion was not antagonized at all. Also aspirin did not affect the inhibition of platelet function by iloprost and linsidomine (SIN-1). It is concluded that stimulation of platelet secretion by stronger stimuli, such as collagen or thrombin, is largely cyclooxygenase-independent and may not be detected by measuring serum thromboxane levels. This may be relevant for clinical situations with shear-stress-induced platelet activation, for example at carotis stenoses or other types of atherosclerotic plaques.     

Adenosine diphosphate strongly potentiates the ability of the chemokines MDC, TARC, and SDF-1 to stimulate platelet function

Platelet activation is normally induced by primary agonists such as adenosine diphosphate (ADP), thrombin, and collagen, whereas other agonists, such as epinephrine, can play important accessory roles. It is now reported that the macrophage-derived chemokine (MDC), thymus activation-regulated chemokine (TARC), and stromal cell-derived factor one (SDF-1) are highly effective activators of platelet function under a variety of conditions, stimulating platelet shape change, aggregation, and adhesion to collagen or fibrinogen. Chemokine-mediated platelet activation was rapid and maximal (less than 5 seconds) under arterial flow conditions and depended strongly on the presence of low levels of primary agonists such as ADP or thrombin. Concentrations of ADP (0.05-0.25 microM) or thrombin (0.005-0.02 U/mL) that induced minimal aggregation caused major aggregation acting in combination with the chemokines. The ability of apyrase to block chemokine-dependent aggregation or adhesion was consistent with an important role for ADP. Chemokine-stimulated aggregation was also insensitive to indomethacin, suggesting that the activation of cyclo-oxygenase is not involved. TARC, MDC, and SDF-1 increased intracellular calcium concentrations [Ca(2+)](i) when combined with low levels of ADP. The MDC and TARC receptor CCR4 was expressed on platelets, and an anti-CCR4 antibody blocked aggregation induced by TARC or MDC. Treatment of platelets with SDF-1 and MDC rapidly exposed P-selectin (CD62P) on the cell surface but did not induce the secretion of serotonin. These findings suggest that the chemokines MDC, TARC, and SDF-1, which may be produced during inflammatory responses, coupled with low levels of ADP or thrombin, can serve as strong stimuli for activating platelet function.     

Familial and constitutional bleeding disorder due to platelet cyclo-oxygenase deficiency

Three family members from two successive generations had a bleeding tendency. Their template bleeding time was prolonged and platelet aggregation induced by ADP and adrenaline showed no second wave; collagen at low to moderate concentrations failed to aggregate and release ATP, whereas higher amounts aggregated and released. Aggregation and release due to thrombin, ristocetin, and synthetic epoxy derivatives (U 44069 and U 46619) were normal. Arachidonate (AA) was inactive, and was not converted either in thromboxane (TX) A2 activity evaluated on the rabbit aorta strip, nor in TXB2 evaluated by radioimmunoassay and by radiochromatography. The parallel impairment of TXB2 and PGE2 formation by the patient's platelets are compatible with a platelet cyclo-oxygenase deficiency. This study suggests that transmission is autosomal dominant, and confirms that cyclo-oxygenase is not needed for aggregation and ATP release by high amounts of collagen.