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PubMed2000

Platelet and platelet-derived microparticle surface factor V/Va binding in whole blood: differences between neonates and adults.

Platelet-derived microparticles (PDMP) appear to play a major role in the generation of procoagulant activity. In this study, we describe a novel flow cytometric method that allows direct evaluation of the procoagulant activity of PDMP and platelets in the physiological milieu of whole blood. The percent PDMP generated in response to calcium ionophore A23187 and calcium was increased in preterm neonates (67.5+/-3.4%, mean +/- S.E.M., n = 8, p <0.05) and term neonates (67.2+/-2.7%, n = 7, p<0.05) compared with adults (49.5+/-3.4%, n = 13). However, in preterm neonates A23187/calcium-induced binding of factor V/Va to PDMP and platelets (22.8+/-5.6 fluorescence units) was markedly reduced (p <0.05) compared to term neonates (58.2+/-7.2) and adults (50.6+/-6.3). In preterm blood, A23187/calcium-induced binding of factor V/Va to PDMP and platelets returned to adult levels when: a) adult plasma, rather than autologous preterm neonatal plasma, was added; or b) factor V, but not factor VIII, was added to autologous preterm neonatal plasma. In summary: 1) We have developed a flow cytometric method for the direct detection of procoagulant PDMP and platelets in whole blood. 2) Compared to adults and term neonates, PDMP and platelets of preterm neonates bound markedly less factor V/Va (reflecting reduced procoagulant activity), because of a relative lack of factor V in preterm neonates. 3) This procoagulant defect in PDMP and platelets may contribute to the propensity of preterm neonates, but not term neonates, to intraventricular hemorrhage. 4) The percent PDMP does not necessarily reflect the degree of procoagulant activity of PDMP or platelets.

Adult↗
PubMed1975

Correction of poor platelet transfusion responses with leukocyte-poor HL-A-matched platelet concentrates.

Matching donor-recipient pairs for HL-A antigens provides a logical starting point for selecting donors for recipients with extensive prior transfusion histories. However, during the course of continued exposure to even HL-A-matched platelet concentrates, further sensitization occurs, as indicated by progressively poorer post-transfusion increments and transfusion reactions. There is evidence that such sensitization may be due to non-HL-A antigens. Finally, it is postulated that the poor post-transfusion platelet increments obtained when standard platelet concentrates are used result from the leukoagglutinin antigen-antibody reaction involving the platelet as an "innocent bystander." The standard platelet concentrate can be purified by a simple method of centrifugation (178 g times 3 min), removing about 96% of the contaminating white blood cells with concomitant loss of about 21% of the platelets. The use of these leukocyte-poor platelet concentrates can restore compatible transfusion increments in highly alloimmunized thrombocytopenic recipients. The luekocyte-poor concentrates can diminish undesirable transfusion reactions following imcompatible platelet transfusions.

Anemia, Aplastic↗
PubMed2002

[CD62p expression in platelet during the preparation course of Cryopreservated platelet-rich plasma].

In order to explore the factors that affect CD62p expression in platelet during the whole course of cryopreservated platelets preparation, CD62p expression of platelet was evaluated by flow cytometry assay. The whole course of cryopreservated platelets preparation in order included whole blood collection, centrifugation for fresh platelet-rich plasma preparation, addition of dimethyl sulfoxide, and freeze in -80 degrees C refrigerator and thaw in 38 degrees C water bath. Result showed that the CD62p expressed slowly from whole blood collection to addition of dimethyl sulfoxide, but expressed abruptly after freeze and thaw and it occupied 82 per cent of the whole expression. It was concluded that the whole blood collection, centrifugation for fresh platelet enriched plasma preparation and addition of dimethyl sulfoxide were optimized in the whole course, but the damage to platelets in the whole course of cryopreservation could not be avoided. It suggests that improved techniques are needed to reduce the damage to cryopreservated platelets.

Blood Platelets↗
PubMed2006

Megakaryocytic cells synthesize and platelets secrete alpha5-laminins, and the endothelial laminin isoform laminin 10 (alpha5beta1gamma1) strongly promotes adhesion but not activation of platelets.

Following vascular injury, basement membrane (BM) components of the blood vessels are exposed to circulating cells and may contribute to hemostasis and/or thrombosis. Laminins 8 (LN-8) (alpha4beta1gamma1) and 10 (LN-10) (alpha5beta1gamma1) are major laminin isoforms of the endothelial BM, and LN-8 is also secreted by activated platelets. In the present study, we demonstrate synthesis of alpha5-laminins LN-10 and LN-11 (alpha5beta2gamma1) by megakaryocytic cells, and intracellular expression of these laminin isoforms in blood platelets. In contrast to platelet LN alpha4 chain that had an apparent molecular weight of 180 kDa and associated mostly to LNbeta1 chain, platelet LNalpha5 consisted of 300/350 kDa polypeptides and associated mainly to LNbeta2. Both alpha4- and alpha5-laminins were secreted by platelets following stimulation. When compared to recombinant human (rh) LN-8, rhLN-10 was much more adhesive to platelets, though adhesion to both proteins was largely mediated via alpha6beta1 integrin. In spite of their adhesive properties, rhLN-8 and rhLN-10 induced neither P-selectin expression nor cell aggregation, two signs of platelet activation. This study demonstrates synthesis/expression of heterotrimeric alpha5-laminins in hematopoietic/blood cells, and provides evidence for the adhesive, but not activating, role of endothelial laminin isoforms in platelet biology.

Blood Platelets↗
PubMed2006

Expression of cellular prion protein on platelets from patients with gray platelet or Hermansky-Pudlak syndrome and the protein's association with alpha-granules.

The cellular prion protein (PrPc) is a membrane glycoprotein expressed on many human cells including platelets. We investigated the cellular localization of platelet PrPc. In resting platelets most PrPc was localized inside the cells. The correlation of PrPc and P-selectin surface up-regulation after platelet activation suggested its association with alpha-granules. This was confirmed by normal expression of PrPc on Hermansky-Pudlak syndrome platelets, which lack dense granules, and failure of gray platelet syndrome platelets, which lack alpha-granules, to up-regulate PrPc. Our results warrant further studies on the role of platelet PrPc in the transmission of prion diseases by blood transfusion.

Blood Platelets↗
PubMed1976

C1 and human platelets. III. Role of C1 subcomponents in platelet aggregation induced by aggregated IgG.

Studies have been performed with platelets using C1 haemolytic assays and platelet aggregation induced by anti-C1q, anti-C1s and aggregated IgG in the presence of C1 subcomponents C1q, C1r and C1s. C1q was removed by EDTA or modified by collagenase from human platelets while after the same treatment C1s remained bound to the platelets. EDTA treated platelets were no longer aggregated by aggregated IgG. The addition of C1q restored the reactivity of the platelets to aggregated IgG while the addition of C1r or C1s was without effect. Furthermore, the addition of C1r or C1s to C1q inhibited the action of C1q in platelet aggregation induced by IgG.The possible association between the different C1 subcomponents and human platelets is discussed.

Complement C1↗
PubMed1990

Binding of annexin V/placental anticoagulant protein I to platelets. Evidence for phosphatidylserine exposure in the procoagulant response of activated platelets.

Proteins of the annexin/lipocortin family act as in vitro anticoagulants by binding to anionic phospholipid vesicles. In this study, we investigated whether annexin V (placental anticoagulant protein I) would bind to human platelets. Annexin V bound to unstimulated platelets in a reversible, calcium-dependent reaction with an apparent Kd of 7 nM and 5000-8000 sites/platelet. Additional binding sites could be induced by several platelet agonists in the following order of effectiveness: A23187 greater than collagen + thrombin greater than collagen greater than thrombin. However, neither ADP nor epinephrine induced additional binding sites. Three other proteins of the annexin family (annexins II, III, and IV) competed for annexin V platelets binding sites with the same relative potencies previously observed for binding to phospholipid vesicles. Phospholipid vesicles containing phosphatidylserine completely inhibited binding of annexin V to platelets. Annexin V completely blocked binding of 125I-factor Xa to thrombin-stimulated platelets. These results support the hypothesis that phosphatidylserine exposure occurs during platelet activation and may be necessary for assembly of the prothrombinase complex on platelet membranes.

Annexin A5↗
PubMedDate not supplied

[Evaluation of the stability of vincristine binding to blood platelets by the method of spin labeling of platelet membrane].

N-(1-oxyl-2,2,6,6-tetramethylpriperyd-4-y) maleimide (MSL) labels SH or NH2 groups of blood platelets membrane proteins in covalent bonds. Then EPR spectrum of MSL labeled platelets solutions can be measured. Pre-incubation + of the platelets with vincristine prior to MSL labeling induces SH and NK2 groups blocking, decrease in MSL binding to the platelets membrane and EPR spectrum modification of labeled platelets solution. The vincristine effect on platelets membrane lasts until platelets disintegrate. These data confirm, the stability of vincristine bond with platelets membrane.

Blood Platelets↗
PubMed1990

The kinetics and quantitation of platelet deposition on control (CPC) and heparin-bonded polyurethane angio-catheter (HBPC) with indium-111 labeled platelets in a dog model.

The dynamics of platelet deposition on CPC and HBPC was evaluated with In-111 labeled platelets (In-PLT) with a computerized gamma camera (CGC). Ten non-heparinized dogs (18-25 kg) were catheterized in both femoral arteries with 10 cm of CPC and HBPC (5 Fr., Cordis, Inc.) 24 hours post-injection of 300-420 microcuries of In-PLT, and imaged for 3 hours with gamma camera. The regional platelet deposition on three segments of catheters and puncture site was determined. The catheters were harvested and radioactivity on the catheter segments (proximal: PROX, middle: MID, distal: DIST and puncture site: PS) of both was determined. From the platelet count in blood, radioactivity in blood and segments of catheters, adjacent artery and area of artery and catheter, the platelet-density [X10(3)] (mean +/- S.D.) on catheter and artery were calculated and tabulated: (table; see text) The large standard deviation of retained platelets is due to embolization. The platelet-density and regional counts on catheter segments were lower in the HBPC than CPC. The rate of platelet-deposition was lower in the HBPC than CPC. Most of the thrombi were lost during pullout of the catheter. Both in vivo (dynamic) and in vitro studies were necessary for evaluation of CPC thrombogenicity.

Animals↗
PubMed1989

Platelet and shear rate promote tumor cell adhesion to human endothelial extracellular matrix--absence of a role for platelet cyclooxygenase.

Blood platelets are thought to be involved in certain aspects of malignant dissemination. To study the role of platelets in tumor cell adherence to vascular endothelium we performed studies under static and flow conditions, measuring tumor cell adhesion in the absence or presence of platelets. We used highly metastatic human adenocarcinoma cells of the lung, cultured human umbilical vein endothelial cells (ECs) and extracellular matrices (ECM) prepared from confluent EC monolayers. Our results indicated that under static conditions platelets do not significantly increase tumor cell adhesion to either intact ECs or to exposed ECM. Conversely, the studies performed under flow conditions using the flat chamber perfusion system indicated that the presence of 2 x 10(5) pl/microliters in the perfusate significantly increased the number of tumor cells adhered to ECM, and that this effect was shear rate dependent. The maximal values of tumor cell adhesion were obtained, in presence of platelets, at a shear rate of 1,300 sec-1. Furthermore, our results with ASA-treated platelets suggest that the role of platelets in enhancing tumor cell adhesion to ECM is independent of the activation of the platelet cyclooxygenase pathway.

Adenocarcinoma↗
PubMed1988

Platelet antibody detection using frozen pooled human lymphocyte antigen-typed platelets as target cells.

The immunoreactivity of five sera containing either iso-, auto- or allo-antiplatelet antibodies to frozen-thawed human lymphocyte antigen (HLA)-typed pooled platelets was assessed to determine the practicality of using such a platelet preparation in an immunofluorescent platelet antibody system. The platelet reagent was analyzed over an 8-week period after initial freezing and storage. Mixtures of platelets with each serum or dilutions of it were initially incubated for 1 hour, then extensively washed and incubated with fluorescein-conjugated goat F(ab')2 antihuman IgG, A, M. After repeat washing, each mixture was then analyzed using a flow cytometer to determine the relative amount of fluorescent antibody bound. Not only was each of the five sera consistently positive for the presence of an anti-platelet antibody, but the extent of immunoreactivity for each remained relatively stable over the 8-week period of analysis. The results suggest that frozen pooled HLA-typed platelets should be an invaluable reagent for screening serum samples for the presence of antiplatelet antibodies in patients who are thrombocytopenic or who are refractory to platelet transfusion therapy.

Blood Platelets↗
PubMed1988

[Experience of HLA-matched platelet transfusion in patients who are refractory to random donor platelets].

Platelets collected from random and multiple donors were as effective on transfusion as those obtained from single donor by platelet pheresis if patients were not alloimmunized. In alloimmunized patients, effects of platelet transfusion were correlated with the HLA-matching grade; 100% effective in A-match, 92% in B-match and 65% in C-match. This correlation was not observed if the patient had infection. The transfusion of A- or B-matched platelets resulted in a lowering or disappearance of HLA antibody activities in most patients. However, the transfusion of C-matched platelets caused increasing or appearance of HLA antibody activities in some patients. The ABO-incompatibility did not show a significant effect on platelet transfusion when anti-A or anti-B antibody activities in donors and antiglobulin tests on patients' red cells were negligible. Non HLA, platelet specific antibodies were produced in some patients and presumed to be participated in the destruction of transfused HLA-matched platelets.

Anemia, Aplastic↗
PubMed1987

Characterization of a tubular flow chamber for studying platelet interaction with biologic and prosthetic materials: deposition of indium 111-labeled platelets on collagen, subendothelium, and expanded polytetrafluoroethylene.

A plastic (Plexiglas) chamber for evaluating platelet deposition under controlled hemodynamic conditions has been developed. The perfusion chamber has been designed to retain the cylindrical shape typical of the vasculature, to be flexible enough to accept a variety of biologic and prosthetic materials, and to simulate a broad range of physiologic flow conditions in either an ex vivo or in vitro perfusion system. Three type of surfaces were exposed to blood flowing directly from the carotid artery of a heparinized pig through the perfusion chamber: de-endothelialized pig aorta, collagen strips from rabbit Achilles tendon, and an expanded polytetrafluoroethylene material (Gore-Tex). Platelets, previously radiolabeled with indium 111 and injected into the animal, were quantified on the material surface, and the total number of deposited platelets determined for a range of blood flow rates (5 to 40 ml/min) and exposure times (0.5 to 20 minutes). The deposition rates were correlated with theory for describing the mass transport of platelets to the test surface. At the wall shear rates investigated (105 to 850 sec-1), the deposition of platelets on subendothelium was strongly dependent on the local flow conditions. Values of deposition on Gore-Tex obtained at similar flow conditions (105 to 425 sec-1) were reduced compared with that observed on subendothelium and showed a markedly weaker dependence on the shear rate. In contrast, deposition of platelets on collagen was more than an order of magnitude greater than on subendothelium and showed a dependence on flow only at the lowest flow rate studied (10 ml/min). The results indicate that collagen is much more reactive than subendothelium and Gore-Tex with respect to the growth and stability of platelet aggregates and moreover suggest that flow mechanisms for depositing platelets on various surface may be substantially different.

Animals↗
PubMed1979

Elemental composition of platelets. Part III. Determination of Ag, Au, Cd, Co, Cr, Cs, Mo, Rb, Sb, and Se in normal human platelets by neutron activation analysis.

The elements Ag, Au, Cd, Co, Cr, Cs, Mo, Rb, Sb, and Se were determined in platelets from seven normal donors. The results, in ng/g wet weight, for plasma-free platelets follow: "Pure" platelets: Ag = 29 +/- (18), au = 0.22 +/- (0.22), Cd = 6.2 +/- 3.4, Cs = 54.8 +/- 19.2, Cr = 6.1 +/- 2.5, Co = 7.5 +/- (5.0), Mo = 3.4 +/- 1.3, Rb = 10400 +/- 3000, Sb = 18 +/- (26), and Se = 782 +/- 127. "Impure" platelets: Au = 0.23 +/- (0.28), Cd = 6.4 +/- 2.6, Cs = 35.2 +/- 13.8, Cr = 8.2 +/- 2.9, Co = 2.9 +/- (3.0), Mo = 3.2 +/- 0.8, Rb = 8700 +/- 1700, Sb = 13.2 +/- (8.7), and Se = 679 +/- 57. To our knowledge, none of these 10 trace elements has been determined in platelets before. The selenium concentration in platelets exceeds that in other tissues (e.g., liver). We suggest that glutathione peroxidase or other unknown selenoenzymes are particularly important in platelet metabolism. Platelets are crucial for triggering thrombosis, and so may be involved as links between selenium deficiency and the concomitant increased death rate from cardiovascular disease.

Antimony↗
PubMed1979

Relationship between packed cell volume, platelets, and platelet survival in red blood cell-hypertransfused mice.

In this study we have measured platelet and megakaryocyte concentration, blood volume, and platelet survival of mice after RBC hypertransfusion to PCVs of 62% to 90%. The platelet concentration of mice with PCVs up to 75% was decreased by up to one half. At higher PCVs a more severe thrombocytopenia developed, with platelet concentrations decreased to less than 10% of baseline in approximately one half of the mice. Blood volumes of the hypertransfused mice were increased up to twofold. Megakaryocyte concentrations were normal or increased. Platelet survival in mice with PCVs less than 75% was normal but was sharply decreased for mice with higher PCVs. The decrease in platelet concentration at moderately elevated PCVs may be explained by hemodilution in the larger blood volume. However, hemodilution alone cannot explain the severe thrombocytopenia at higher PCVs. The presence of decreased platelet survival with normal or increased megakaryocyte concentrations in this latter group suggests that the severe thrombocytopenia is the result of more rapid platelet destruction. In summary, elevation of the PCV by RBC hypertransfusion produces thrombocytopenia. The severity of the thrombocytopenia and the mechanisms involved in producing it change abruptly when the PCV exceeds 75%. These findings should be considered in interpretations of the influence of RBC hypertransfusion on hematopoiesis and in clinical and experimental studies of thrombopoiesis in polycythemic subjects.

Animals↗
PubMed1977

Potentiation by alpha and inhibition by beta-adrenergic stimulations of rat platelet aggregation. A comparative study with human and rabbit platelets.

Epinephrine, known to potentiate and elicit aggregation of human platelets, was shown to inhibit thrombin-induced aggregation of rat platelets, delaying the onset of aggregation from 2 to 12 times. Incubation of rat platelet suspensions with propranolol (1.25--30 micrometer), inactive by itself, totally prevented the inhibitory effect of epinephrine and also permitted a potentiation effect to show up. On the contrary, phentolamine (1.25--30 micrometer) potentiated the inhibitory effect of epinephrine on rat platelets and unmasked an inhibitory effect on human platelets. Finally, isoproterenol (0.25--9 micrometer) produced a marked inhibition of aggregation induced by thrombin, ADP and collagen in the three species studied, but most particularly in the rat. From these results, we conclude that stimulation of the platelet adrenergic receptors may either result in promotion (alpha-stimulation) or inhibition (beta-stimulation) of platelet aggregation. Furthermore, differences in the ratios or responses of alpha/beta receptors may account for species variations in the platelet aggregation response to catecholamine challenge.

Adenosine Diphosphate↗
PubMed1983

Dissociation between hemodynamic and platelet antiaggregant effects of prostacyclin in dogs determined with a rapid platelet isolation technique.

Prostacyclin, a potent vasodilator and inhibitor of platelet aggregation, is being increasingly used in disease states in which platelets may play a pathophysiologic role. A literature review revealed a variable dissociation between the in vitro platelet antiaggregant activity of prostacyclin and both the in vivo hemodynamic and platelet antiaggregant activities. Because widely variable platelet isolation techniques may have contributed to this variability, we investigated the hemodynamic and platelet antiaggregant effects of prostacyclin infusion in the dog, using in vitro techniques limiting the time from blood sampling to aggregometry to 2 1/2 and 10 1/2 min. Using the short technique, we demonstrate complete inhibition of platelet aggregation at a prostacyclin infusion rate that caused only a mild decrease in arterial pressure. In contrast, the longer technique requires an eightfold higher prostacyclin infusion rate to achieve the same degree of antiaggregant activity. The prostacyclin activity apparent half-life was 3 min. Because interspecies differences exist in both the hemodynamic and antiaggregant effects of prostacyclin and in their relationship to each other, we suggest that a closer approximation of in vivo antiaggregant effects may be obtained with in vitro methods that are rapid, thus taking into account the lability of prostacyclin. We conclude that the variable in vitro platelet antiaggregant effects of prostacyclin reported in the literature are due to the variable and longer techniques.

Animals↗
PubMed1981

Inhibition of platelet phospholipid methylation during platelet secretion.

A pathway for the synthesis of membrane phosphatidylcholine involving the N-methylation of phosphatidylethanolamine has been detected in several types of mammalian cells. Furthermore, it has been implicated in the coupling of agonist binding to cell response. We examined whether human platelets exhibit this synthetic pathway and whether platelet agonists influence its activity. When washed platelets were incubated with 0.15 microM L-[methyl-3H]methionine at 37 degrees C, they incorporated methyl-3H into their phospholipids linearly at the rate of 1 pmole/10(9) platelets/hr. When incubated with 20 microM radiolabeled methionine, they incorporated about 15 pmole/10(9) platelets/hr. The radioactivity was found predominantly in phosphatidyl-N-monomethylethanolamine, phosphatidyl-N,N-dimethylethanolamine, and phosphatidylcholine. Thrombin caused an immediate (within 15 sec) and sustained (up to 30 min) decrease in the rate and extent of N-methylation of platelet phospholipids. This was accounted for by a decrease in synthesis of methylated phospholipids rather than an increase in their degradation. This thrombin effect correlated with serotonin release and could be dissociated from platelet aggregation and prostaglandin synthesis. Thrombin also decreased the synthesis of phosphatidylcholine when choline was used as the radiolabeled substrate. Other agonists such as epinephrine, adenosine diphosphate (ADP), or A23187 also decreased phospholipid methylation under conditions in which they stimulated serotonin release. These data demonstrate that platelets are capable of synthesizing phosphatidylcholine from phosphatidylethanolamine by N-methylation and that agonists perturb this pathway as they induce platelet secretion. The precise role of phospholipid methylation in either resting or stimulated platelets remains to be established.

Adenosine Diphosphate↗