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PubMed2001

Impaired platelet function among platelet donors.

BACKGROUND: Platelet transfusions are effective for the prevention and treatment of bleeding in patients with disorders of platelet number and/or function. In recent years plateletpheresis concentrates have outnumbered pooled platelet concentrates, albeit with significant differences between nations. Thus, the platelet quality of individual donors has become increasingly important. The aim of this study was to gain an estimate for the prevalence of impaired platelet function among platelet donors. STUDY DESIGN AND METHODS: We determined the inter-donor variability in platelet plug formation with a PFA-100 analyzer, the prevalence of impaired thromboxane formation, and effects of the density in alpha2 integrin polymorphism and density. RESULTS: (i) Collagen-epinephrine induced closure time (CEPI-CT) showed a great inter-subject variability in platelet donors and was higher than in healthy controls (p = 0.008). One-fifth of donors had abnormal CEPI-CT values and 11% exceeded >300 s (max measurable value). (ii) Decreased serum thromboxane B2 levels were found in 9% of all donors, compatible with surreptitious intake of cyclooxygenase inhibitors or with an aspirin-like defect. CEPI-CT correlated inversely with TxB2-levels in donors and controls. (iii) The density of the alpha2-integrin correlated negatively with CEPI-CT and CADP-CT values in controls, but was not responsible for the observed impaired platelet function in donors. (iv) Finally, the ABO blood group system modulates closure times. CONCLUSION: In sum, a large number of platelet donors present with prolonged closure times. Decreased thromboxane formation and frequent platelet donation partly account for this observation.

Adenosine Diphosphate↗
PubMed2002

[Study on blood compatibility of polyurethanes for catheters].

In this article, the blood compatibility of polyurethanes (PUs) made by ourselves for catheters is studied by hemolysis test, platelets adhesion test, kinetic thrombus time test and dynamic clot formation. The results showed that these PUs all have excellent blood compatibility. Among these PUs, H50-100 and H60-100 have best blood compatibility. Additionally, the relationship between the structure and blood compatibility is discussed.

Animals↗
PubMed1992

Activation of platelet concentrate during preparation and storage.

This review will discuss how stored platelets become activated and will examine their ability to function and survive in vivo, posttransfusion. Experimental methods which have been shown to alter platelets during storage will be detailed. Using beta-thromboglobulin (beta-TG) and surface adhesion receptors as markers, investigators have examined the activation changes in platelet concentrates during preparation and storage. Resuspension of the platelet pellet after isolation of platelet-rich plasma appears to play a major role in producing platelet activation and beta-TG release during preparation. However, there is a significant amount of interdonor variability in platelet activation even at this early stage of storage. Over 5 days of storage, platelets release approximately 50% of their beta-TG contents. Furthermore, between 40% and 60% of the platelets express the alpha-granule membrane protein, P-selectin (GMP-140), during storage, which is also indicative of platelet activation. These activation changes correlate to some degree with platelet recovery posttransfusion but clearly do not explain the full lesion of platelet storage. The surface density of two platelet membrane receptors, glycoproteins (GP) Ib and IIb/IIIa, also change with activation, although in opposite directions. Platelet surface GPIb decreases initially with storage and then recovers, perhaps due to its relocation to the platelet surface from an intracellular pool. In contrast to GPIb, mean platelet surface GPIIb/IIIa increases slightly during storage, probably as a consequence of platelet activation and release of alpha-granule GPIIb/IIIa to the surface. Some hypotheses are offered regarding how these activated platelets can continue to circulate after transfusion. Further exploration of the platelet storage lesion will hopefully provide needed answers and thus permit better treatment of hemostatic disorders in the future.

Biomarkers↗
PubMed2003

Unexpected persistence of platelet hyporeactivity beyond the neonatal period: a flow cytometric study in neonates, infants and older children.

Previous studies, using flow cytometry, have reported a lower platelet reactivity in neonates compared to adults. Only few studies were carried out in older children, and results were controversial in terms of age to reach adult platelet function. We studied a total of 125 healthy neonates, infants and older children, and 15 adults. alphaIIbbeta3 expression on resting and activated platelets was lower in all children, with an impaired capability of alphaIIbbeta3 activation (PAC1 and bound fibrinogen). This defect was observed until the age of fifteen with a gradual recovery with age. In neonates, we observed a defect of GPIalpha internalization, and demonstrated that this defect persisted in older children as well. In contrast with alphaIIbbeta3 integrin activation, we did not observe a gradual age-dependent recovery. These unexpected results point out the need for reference values in childhood.

Adolescent↗
PubMed1992

[The radioisotope labelling of thrombocytes using a monoclonal antibody against membrane glycoproteins IIb-IIIa and the measurement of thrombocyte adhesion/aggregation on the substrate surface].

A new method for platelet labeling based on binding of monoclonal antibody to human platelets has been suggested in this study. Monoclonal antibody VM16a against membrane glycoproteins IIb-IIIa was labeled by 125I and then incubated with platelets. About 70% of added antibody was bound when it was used at the concentrations corresponding to the linear part of the concentration curve (0.5 and 1.0 micrograms/ml). Due to high efficiency of binding 125I-VM16a-labeled platelets were used for the measurement of adhesion/aggregation to the substrate in platelet-rich plasma without washing of the free label. Experiments with washed platelets double labeled with 51Cr and 125I-VM 6a showed high correlation between the data obtained with both labels. The method of platelet labeling has been applied for the assessment of drug action on platelet adhesion/aggregation. Measurements were performed in platelet-rich plasma and adhesion/aggregation was stimulated by ADP and analogue of thromboxane A2, U46619. It was shown/that antianginal drug trapidil strongly inhibited and antiatherogenic drug probucol did not affect platelet adhesion/aggregation stimulated by both agonists.

Adenosine Diphosphate↗
PubMedDate not supplied

[Familial occurrence of Glanzmann thrombasthenia].

Glanzmann's thrombasthenia, known also as Glanzmann's disease, is an autosomally inherited hemorrhagic disease with unique abnormalities of platelet functions. Authors present a large family in which Glanzmann's disease was diagnosed in the father and two sons. An analysis of platelet membranes enabled diagnosis of Glanzmann's thrombasthenia type II. A decrease in clot contractibility, fibrinogen binding to blood platelets, and decreased glycoprotein IIb and IIIa levels with marked impairment of GP IIb and IIIa complexes formation were characteristic for affected family members. One daughter died 8 days after birth with the symptoms of hemorrhagic diathesis. Mother and remaining three sons are healthy without the signs of Glanzmann's disease.

Adolescent↗
PubMed2003

Assessment of in vitro platelet activation by Advia 120 platelet parameters.

The Advia 120 Hematology System provides new platelet parameters that have been proposed as useful markers of platelet activation. The aim of this study was to investigate platelet parameter variations after adenosine diphosphate (ADP) activation of platelet-rich plasma (PRP) in vitro, with particular interest in the mean platelet component (MPC), which was compared with two well-known degranulation antigens. Changes in platelet parameters that were induced by the activation of PRP with different concentrations of ADP were examined first. The time course of parameter values up to 60 minutes after maximal ADP activation and the relationships between the MPC and P-selectin and granulophysin expression as determined by flow cytometry were then investigated. After 10 minutes of ADP stimulation, the MPC presented a dose-dependent increase. At the maximal ADP concentration, the initial increase of the MPC was followed by a progressive decrease, leading the MPC to become significantly lower with respect to the baseline after 60 minutes of incubation. Significant variations in other parameters are also described. Finally, a negative correlation was found between the MPC change with respect to time 0 and both P-selectin and granulophysin expression. The present study suggests that platelet parameter variation, particular in the MPC, may be used to assess platelet activation in PRPs stimulated by ADP.

Adenosine Diphosphate↗
PubMed2005

[Application of cationic propyl gallate as inducer of thrombocyte aggregation for evaluating the platelet function of platelet donors].

The purpose of study was to investigate the feasibility of the application of cationic propyl gallate (C-PG) as inducer of platelet aggregation for evaluating the platelet function of single-donor plateletpheresis and identifying the incidence of defective platelet function among donors. Experiments were as follows: 3 healthy volunteers' platelet aggregation induced by 100-300 micromol/L C-PG was determined by LG-PABER analyzer to observe the effect of C-PG concentration on platelet aggregation; 30 healthy volunteers' platelet aggregation before and 24 hours after administration of 200-400 mg acetylsalicylic acid (ASA) was examined after induction by 200 micromol/L C-PG for determining the cut-off value to discriminate platelet dysfunction donors; the platelet aggregation of 483 platelet donors was detected and the activated plasma clotting time (APCT) of donors who have deficiency in platelet aggregation was examined for investigating the incidence of defective platelet function among donors. The results showed that platelets were activated by C-PG induction in a dose dependent manner, when concentration of C-PG reached 200 micromol/L, the percentage of platelet aggregation was highest. It significantly decreased after 24 hours with ASA than that before the administration (P < 0.001), especially in 180 seconds induced by C-PG. If cut-off point was fixed on the platelet aggregation < 20% in 180 seconds, donors of platelet dysfunction can be selected effectively. 25 of defective platelet aggregation function among 483 donors were detected, and 11 out of 25 platelet dysfunction donors had the deficiency in procoagulant activity with prolonged APCT. It is concluded that C-PG as inducer of platelet aggregation is feasible to screen the platelet function of donors. Five percent of platelet donors has function defect examined by C-PG as inducer of platelet aggregation.

Antioxidants↗
PubMed2005

Anti-thrombotic action of clopidogrel and P1(A1/A2) polymorphism of beta3 integrin in patients with coronary artery disease not being treated with aspirin.

Individual variability in response to clopidogrel is known but its mechanism is poorly understood. We examined the relationship between glycoprotein IIIa polymorphism P1(A1/A2) and anti-thrombotic actions of clopidogrel. Clopidogrel (75 mg/d; 2 weeks) was administered to 48 normolipemic patients with coronary artery disease. Bleeding time, thrombin generation at the site of microvascular injury, platelet function under high shear, using PFA-100 with ADP cartridge, and platelet surface activation markers (P-selectin and fibrinogen binding sites on GPIIb/IIIa complex detected by PAC-1 antibody), were studied both before and after clopidogrel treatment. Both unstimulated and low-dose (0.02 microM and 1 microM) in vitro ADP-stimulated platelets were examined. GP IIIa polymorphism was assessed by polymerase chain reaction and restriction fragment length polymorphism analysis. We identified 32 P1(A1/A1) homozygotes, 15 P1(A1/A2 heterozygotes and one P1(A2/A2) homozygote. Clopidogrel significantly prolonged bleeding time in all subjects, but this effect was greater in P1(A2 carriers (p < 0.01). Furthermore, clopidogrel only depressed thrombin generation at the site of microvascular injury (p < 0.01) in P1(A2) patients and prolonged closure time measured in vitro by PFA-100 (p < 0.05). At baseline spontaneous expression of PAC-1 and P-selectin was higher in P1(A2) subjects as compared to P1(A1) homozygotes (p < 0.05 for both antigens). Clopidogrel lowered the expression of both markers affecting more P1(A2) carriers, so that the difference in binding PAC-1 antibody between platelets from P1(A1) and P1(A2) carriers disappeared, while the difference in P-selectin expression slightly diminished. Anti-thrombotic effects of clopidogrel are more pronounced in CAD patients carrying the P1(A2) allele than in P1(A1) homozygotes.

Aspirin↗
PubMed2005

[Identification of human platelet specific functional antibody and its fragments].

OBJECTIVE: To study the immunoreactivity of the specific anti-platelet glycoprotein (GP) IgG antibody and its F(ab')2 fragments from patients with chronic idiopathic thrombocytopenic purpura (ITP) and to investigate their effects on platelet aggregation function. METHODS: Peripheral blood samples were collected from 84 patients with ITP. Modified monoclonal antibody immobilization of platelet antigen assays was used to detect the IgG antibodies specific for GP I b/II a, GP I b/IX and GP VI. The IgG antibody and its F(ab')2 fragments in the positive plasma inhibiting platelet aggregation function were prepared and purified. Plate-rich Peripheral blood sample was collected from a normal person with O type blood and platelet-rich plasma (PRP) and platelet-poor plasma (PPP) were prepared. Plasma pf ITP patient or purified IgG or F(ab')2 fragments of different concentrations were added into PRP, and then inducers of platelet aggregation ADP, ristocetin, or collagen were added. The platelet aggregation was measured. Platelet GP II b/III a specific human-rat chimeric antibody 7E3 and GP I b specific antibody SZ2 were used as positive controls and PBS was used as negative control. RESULTS: GP II b/III a and/or GP I b/IX and/or GP VI specific antibodies were found in 48 (57.1%) patients. The plasma, purified IgG and F(ab')2 fragments of 7 of these 48 patients (14.6%) with positive autoantibody showed significant activity against GP II b/III a (4 patients), GP I b/IX (2 patients), or GP VI (one patient). The purified IgG and F(ab')2 fragments of 2 patients positive in GP II b/ III a autoantibody out of the 7 patients significantly inhibited the platelet aggregation induced by ADP, the purified IgG and F(ab')2 fragments of 1 patients positive in GP I b/IX out of the 7 patients significantly inhibited the platelet aggregation induced by ristocetin, and the purified IgG and F(ab')2 fragments of 1 patients positive in GP VI out of the 7 patients significantly inhibited the platelet aggregation induced by collagen. CONCLUSION: A functional fragment, F(ab')2 portion of IgG is responsible for the autoantibody interaction with platelet GPs in ITP, and some of them also affect the platelet function. It can be used to develop completely humanized anti-GP small molecular phage antibody.

Adolescent↗
PubMed1990

[Effect of erythrocyte contamination on thrombocyte storage].

The influence of red cells on the storage of platelet concentrates (PC) is still questionable. Therefore, we investigated 40 PCs with 4 different red cell concentrations (less than or equal to 5000, 10,000, 50,000 and 100,000/microliters), but equal leukocyte contamination, in a paired study during 5 day storage. In correlation to the red cell contamination, there was a significant reduction of platelets, discoids and especially "functional active" platelets already after addition of the red cells, which was due to a spontaneous platelet aggregation. The difference increased during the storage (p less than 0.05 and p less than 0.001). The other parameters investigated (pH, aggregation, adherence, beta-TG) showed the well-known storage alterations, but no special influence of the red cells. Therefore, PCs should contain the least red cell contamination for storage purposes.

Blood Preservation↗
PubMed1990

Separation of platelet concentrates (PC) from buffy coat (BC) using the bottom and top drainage (BAT) system.

By the preparation of platelet concentrates (PC) from buffy coat (BC), the blood component separation may be improved considerably. One can use new bag systems with bottom and top drainage (BAT) which allow partial automation of the separation procedure. Thus, it is possible to produce very pure red cell concentrates (RCC) and FFP, as well as BC, by one separation step under well standardized conditions. Several preparative factors influence the quality of the PCs, especially the storage of the whole blood and the BC. Optimal yields (0.72-0.78 x 10(11) platelets), separation efficiency (67.7-70.8%) and lowest cell contamination (leukocytes 0.1-0.2 x 10(8), red cells 0.2-0.3 x 10(8) per concentrate) were obtained with whole blood stored for 1 h and BC for 2-4 h before resuspension by 30 min face-over-face-rotation. In respect to the release of leukocyte proteases during the storage, the BC should not rest for more than 2-3 h before separation of the platelets in order to prevent potentially functional impairment of the platelets by leukocyte proteases.

Blood Component Removal↗
PubMed1990

Preparation of a monoclonal antibody, SZ-51, that recognizes an alpha-granule membrane protein (GMP-140) on the surface of activated human platelets.

To identify the changes on the platelet plasma membrane after platelet activation, we prepared monoclonal antibodies specific for activated platelets. Hybridoma cell line SZ-51 was screened for antibodies which bound to thrombin activated platelets but not to resting platelets. 125I-SZ-51, and IgG1, bound 780 molecules/platelet on resting platelets. However, it bound 11,000 molecules/platelet on thrombin activated platelets with high affinity (4.2 nmol/L). The isolated protein using affinity chromatography showed a single band in both periodic acid-Schiff and Coomassie blue staining. Immunoblot analysis revealed that SZ-51 reacted with a 140,000 molecular weight protein which was identified to be alpha-granule membrane protein (GMP-140) in radioimmunoassay. These results demonstrate that the antigen recognized by SZ-51 is GMP-140, which is expressed on the plasma membrane of activated platelets.

Antibodies, Monoclonal↗
PubMed2006

Platelet microparticle formation and thrombin generation under high shear are effectively suppressed by a monoclonal antibody against GPIba.

We studied the inhibition of platelet microparticle (MP) formation and thrombin generation under high shear forces. We hypothesized that an inhibitor of the GPIb a -von Willebrand factor (vWF) interaction would be more effective in suppressing MP formation and thrombin generation than GPIIb/IIIa inhibitors. Platelet-rich plasma (PRP) anticoagulated with PPACK (D-Phe-Pro-Arg chloromethyl ketone) was exposed in a cone-and-plate viscometer (shear: 5,000 s(-1) for 5 min) in the presence of antagonists to GPIb a (the monoclonal antibody [Mab] Ib-23) or to GPIIb/IIIa (abciximab, tirofiban, eptifibatide) at their IC90 determined in platelet aggregometry with ristocetin or ADP, respectively. We used double labeling (CD41-PE and annexin-V-FITC) for flow cytometric detection of MP and their aminophospholipid exposure. Thrombin generation was measured using PRP prepared from ACD anticoagulated blood. About 40% of the thrombin generation was found to be mediated by the MP fraction of the PRP. Blockade of GPIb a with Mab Ib-23 reduced MP formation and thrombin generation by 50%, and was more effective than any GPIIb/IIIa antagonist. The combination of Mab Ib-23 with one of the GPIIb/IIIa inhibitors further reduced the MP formation to ~ 30%. The antibody also partially inhibited thrombin induced platelet aggregation. Epitope mapping suggested that Mab Ib-23 binds between the amino acids 201 and 268 of GPIb a , explaining the interference with vWF and thrombin interaction. In contrast to the commonly used GPIIb/IIIa antagonists, the blockade of GPIb a with Mab Ib-23 effectively reduces the prothrombotic MP generation and thrombin formation at shear rates typically found in arterial stenoses.

Abciximab↗
PubMed2006

The relationship of platelet reactivity to the occurrence of post-stenting ischemic events: emergence of a new cardiovascular risk factor.

The reactivity of platelets to agonists plays a central role in the genesis of thrombosis following percutaneous coronary intervention (PCI) and spontaneous plaque rupture. Antiplatelet therapy has reduced the occurrence of thrombotic events following PCI, including myocardial infarction and stent thrombosis. Because the platelet is a fundamental component in the generation of an arterial thrombus and the stimulus for thrombosis is marked in PCI, it is logical to predict that patients with superior platelet inhibition would have the best outcomes with respect to ischemic events post PCI. However, until recently there was little information linking measurements of high ex vivo platelet reactivity to the occurrence of ischemic events. An emerging body of data, mostly from small studies, supports the pivotal link between periprocedural platelet physiology and increased risk of adverse thrombotic events. This review explores the available information linking platelet reactivity during and after PCI to the occurrence of adverse events, including myocardial infarction, recurrent ischemia within 6 months, and stent thrombosis.

Angioplasty, Balloon, Coronary↗
PubMedDate not supplied

A study of aspirin induced changes in bleeding time, platelet aggregation, and Sonoclot coagulation analysis in humans.

The purpose of this study was to determine whether or not a newer test of platelet function, Sonoclot coagulation analysis, can identify the patients who develop significant prolongation of bleeding time after aspirin ingestion. Template bleeding time, platelet aggregation in response to arachidonic acid, collagen, epinephrine, adenosine diphosphate, and ristocetin, and Sonoclot coagulation analysis were performed before and after ingestion of aspirin in 22 adult volunteers. Mean bleeding time increased from 5.32 +/- 2.16 min to 7.34 +/- 2.1 min, but remained within normal range (2.5 to 9 min). There was marked intersubject variability in the effect of aspirin on bleeding time, and difference between men and women was not significant. There was significant decrease in platelet aggregation in response to arachidonic acid, collagen and epinephrine. Sonoclot coagulation analysis did not show significant effect of aspirin administration. There was no correlation among changes in bleeding time, platelet aggregation, and Sonoclot coagulation analysis. Five patients with known platelet function disorders and prolonged bleeding times (mean = 18.5 min, range 14 to 22) without any other coagulation abnormalities were also studied. In four of these patients who had normal platelet count, Sonoclot graphs were morphologically similar to those in the volunteers with normal bleeding times, but in one patient with thrombocytopenia, morphology was altered. It is our conclusion that Sonoclot coagulation analysis is unlikely to identify patients with prolonged bleeding time in whom platelet count and other coagulation factors are normal.

Adult↗