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PubMed2004

Platelet morphology and plasma indices of platelet activation in essential hypertension: effects of amlodipine-based antihypertensive therapy.

BACKGROUND AND AIM: Platelet abnormalities have been described in hypertension, especially in the presence of target organ damage. Our aim was to study the differences in morphology and indices of platelet activation in treatment-naive patients with essential hypertension as compared to normotensive controls and secondly, to study the effects of amlodipine-based antihypertensive therapy on these indices. METHODS: We recruited 42 previously untreated, newly diagnosed hypertensive patients (25 men; mean age 53 years) for the cross-sectional study, where data were compared with those from 30 normotensive controls (20 men; mean age 57 years). Of the 42 untreated hypertensive patients who were recruited, 27 patients successfully completed, the six-month treatment phase with amlodipine-based antihypertensive therapy. Platelet morphology (volume and mass) was quantified, and plasma markers of platelet activation (betaTG and sPsel) measured in citrated plasma. The mass of P-selectin in each platelet (pPsel) was determined by lysing a fixed number of platelets and then determining the levels of P-selectin in the lysate. RESULTS: Hypertensive patients had significantly higher platelet volume (P = 0.01) and mass (P = 0.003), plasma betaTG and sPsel, and pPsel levels (all P < 0.001) compared to the controls. After a mean treatment time of 6 months, there was a decrease in platelet volume (P < 0.001) and mass (P = 0.02), with lower pPsel, sPsel and BTG levels (all P < 0.001) compared to the untreated state. CONCLUSION: Treatment of uncomplicated essential hypertension using amlodipine-based anti-hypertensive therapy results in a reversal of the platelet morphology abnormalities and indices of platelet activation. This may contribute to a reduction in thrombosis-related complications seen in those whose blood pressure lowering is effective.

Amlodipine↗
PubMed2005

Platelet adhesion in hypertension: application of a novel assay of platelet adhesion.

BACKGROUND: The increased risk of thromboembolism in hypertension may be related to a prothrombotic or hypercoagulable state, with abnormalities in haemostasis and platelet function. OBJECTIVE: To investigate the role of platelets in the pathogenesis of thrombosis in hypertension, we applied a novel new assay to detect and quantify the degree of platelet adhesion to a defined coagulation molecule. PATIENTS AND METHODS: Platelet-rich plasma (PRP) and citrated plasma (CP) were obtained from 50 patients with hypertension (25 treated, and 25 untreated) and 30 healthy controls. A suspension of 2 x 10(7) platelets were incubated for one hour in microtitre plates pre-coated with 5mg/mL fibrinogen. The supernatant was carefully aspirated, lysed with 5% tween and stored at -70 degrees C as supernatant platelet lysate (SPL). The wells were carefully washed with saline and bound platelets lysed as before, and stored at -70 degrees C as bound-platelet lysate (BPL). Soluble P-selectin (sP-sel) was determined in CP, SPL and BPL by enzyme-linked immunosorbent assay (ELISA). RESULTS: Patients with hypertension (both treated and previously untreated) had increased platelet adhesion, as determined by increased lysate sP-sel (P=0.002) in BPL, with no change in SPL (P=0.5) compared to healthy controls. There was no significant difference between treated and previously untreated hypertensives. CONCLUSION: Platelets from patients with hypertension display increased adhesion to an important coagulation factor (fibrinogen). This may, in part, account for the increased risk of thrombosis seen in these patients.

Biomarkers↗
PubMed1980

Membrane structure of nonactivated and activated human blood platelets as revealed by freeze-fracture: evidence for particle redistribution during platelet contraction.

The distribution of intramembrane particles of nonactivated and activated human blood platelets was studied by freeze-fracture under various experimental conditions to see whether morphological evidence for a structural coupling between the platelet actomyosin system and the fibrin network in a retracting clot could be established. Membrane particles were evenly distributed in nonactivated platelets; the total number (E + P faces) was approximately 1,500/micrometers 2 of membrane, and there were two to three times more particles present on the E face than on the P face. Transformation of discoid platelets to "spiny spheres" by cooling did not change the particle distribution. Platelet activation and aggregation by serum or ADP caused no change in membrane particle density or distribution. Particle distribution was not changed in Ca2+-activated platelets fixed immediately before fibrin formation, but after fibrin formation and during clot retraction, particles were sometimes most frequent on the P face and tended to form distinct clusters, and aggregates of E face pits were observed. Blood platelets contain contractile proteins that are distinct as filaments in platelets in retracting clots. We suggest that the redistribution of particles seen in activated platelets during clot retraction reflects the esablishment of mechanical transmembrane links between the platelet actomyosin system and the fibrin net. The P-face particle clusters may represent sites of force transmission between actin filaments bonded to the inside of the membrane and the fibrin network at the outside. Thus, whereas membrane particles may not be directly involved in the attachment of actin filaments to membranes, the transmission of the force of the contractile system to an exterior substrate apparently involves the intramembrane particles.

Adenosine Diphosphate↗
PubMed1990

Production of monoclonal antibodies specific for platelet activation antigens and their use in evaluating platelet function.

Monoclonal antibodies (MAb) were used to identify platelet membrane molecules that are expressed after platelet activation. Balb/C mice were immunized with fixed thrombin-activated human platelets and their spleen cells were fused with the murine myeloma cell line NS1-Ag4/1. The resulting hybridomas were screened for antibody production against fixed thrombin-activated platelets and fixed resting platelets by flow cytometry. Two MAbs 2C8 (an IgM) and 1E3 (an IgG2a) demonstrated significant binding to fixed thrombin-activated platelets while reacting minimally with fixed resting platelets. The reactivity of 2C8 and 1E3 were compared to MAb's S12 and AC1.2, both of which have known specificity for an alpha-granule membrane protein (GMP-140) expressed on the surface of activated platelets. In radioimmunoprecipitation studies, both 2C8 and 1E3 immunoprecipitated a protein of approximately 140 kDa similar to that precipitated by S12 and AC1.2. Immunodepletion studies, with S12, AC1.2, 1E3, and 2C8 confirm that they all react with the same antigen. 2C8 may recognize the same epitope as S12, whereas 1E3 appears to recognize a different epitope of the same molecule. The use of these MAbs to measure platelet activation in whole blood correlates well with the results of conventional platelet aggregometry.

Animals↗
PubMed2001

Sevoflurane inhibits unstimulated and agonist-induced platelet antigen expression and platelet function in whole blood in vitro.

BACKGROUND: Previous studies have reported conflicting results about the effect of sevoflurane on platelet aggregation. To clarify this point, we investigated the effects of sevoflurane on platelet antigen expression and function in vitro. METHODS: Human whole blood was incubated for 1 h with 0.5 and 1 minimum alveolar concentration sevoflurane, 21% O(2), and 5% CO(2). A control sample was kept at the same conditions without sevoflurane. After stimulation with adenosine diphosphate or thrombin receptor agonist peptide 6, samples were stained with fluorochrome conjugated antibodies, and the expression of platelet glycoproteins GPIIb/IIIa, GPIb, and P-selectin, as well as activated GPIIb/IIIa, were measured with two-color flow cytometry. In addition, platelet function was assessed by means of thromboelastography and using the platelet function analyzer 100. RESULTS: Already in subanesthetic concentrations, sevoflurane inhibits unstimulated and agonist-induced GPIIb/IIIa surface expression and activated GPIIb/IIIa expression on platelets in whole blood. The agonist-induced redistribution of GPIb into the open canalicular system was also impaired by sevoflurane, whereas no effect on P-selectin expression in activated platelets could be found. Sevoflurane significantly reduced the maximum thromboelastographic amplitude. Furthermore, platelet function analyzer 100 closure times were significantly prolonged. CONCLUSION: The results show that sevoflurane significantly impairs platelet antigen expression in vitro. It is especially the inhibition of GPIIb/IIIa expression and activation that impairs bleeding time as reflected in thromboelastographic measurements and platelet function analyzer 100 closure times. The exact inhibitory mechanism remains unclear.

Anesthetics, Inhalation↗
PubMed1986

A role for glycoprotein IIb-IIIa complex in the binding of IgE to human platelets and platelet IgE-dependent cytotoxic functions.

A possible relationship between binding sites for Immunoglobulin E (IgE) on human platelets, involved in IgE-dependent cytotoxic functions of platelets against helminth parasites, and well-characterized platelet constituents involved in haemostasis, was investigated. We first explored the interaction with IgE of platelets from patients with rare inherited deficiencies of defined platelet constituents and functions: Glanzmann's thrombasthenia, Bernard-Soulier and grey platelet syndromes. We report that only type I and II thrombasthenic platelets, which lack the membrane glycoproteins (GP) IIb and IIIa, failed to bind IgE and to exhibit IgE-dependent effector functions. Since thrombasthenic monocytes, however, showed normal interaction with IgE, this defect appeared restricted to platelets. Polyclonal and monoclonal antibodies directed against GP IIb-IIIa complex, but not monoclonal antibody directed against GP Ib, inhibited the binding of IgE to normal platelets, and their IgE-dependent cytotoxicity. Taken together, these findings indicate a relation between the GP IIb-IIIa complex and the expression of IgE binding sites and IgE-dependent effector functions in human platelets.

Blood Platelets↗
PubMed1993

Effect of antiphospholipid antibodies on procoagulant activity of activated platelets and platelet-derived microvesicles.

We have recently described the in vitro mechanism of action of anticardiolipin (aCL) and lupus anticoagulant (LA) antibodies in patients with the antiphospholipid syndrome. LA antibodies inhibit coagulation reactions in plasma because they appear to recognize the complex of lipid-bound (human) prothrombin, whereas aCL antibodies require beta 2-glycoprotein I (beta 2-GPI) for binding to anionic phospholipids. aCL antibodies can be divided into two subgroups, according to their behaviour in lipid-dependent coagulation reactions: aCL-type A enhances the anti-coagulant effect of beta 2-GPI, whereas aCL-type B does not. In the present study we investigated the effect of purified aCL-type A and B and of LA antibodies on the procoagulant activity of both Ca-ionophore activated platelets and platelet-derived microvesicles, using an assay system with highly purified bovine coagulation factors Xa, Va, and prothrombin from human and bovine origin. In the absence of beta 2-GPI neither type of aCL was able to inhibit the prothrombinase activity of platelets or microvesicles. However, a strong and dose-dependent inhibition of the prothrombinase activity of both platelets and platelet-derived microvesicles was observed within a few minutes, when aCL-type A antibodies were added in combination with beta 2-GPI. This inhibitory effect was dependent also on the concentration of beta 2-GPI. Conversely, no inhibitory effect of aCL-type B antibodies on platelet- (or microvesicle) prothrombinase activity in the presence of beta 2-GPI could be observed. LA antibodies were able to inhibit in a dose-dependent way the procoagulant activity of activated platelets and platelet-derived microvesicles. With two LA preparations this inhibition was only apparent when human prothrombin was used as substrate, while a third preparation exhibited its inhibitory effect both in the presence of human and bovine prothrombin. The data indicate that, in the presence of their respective cofactors beta 2-GPI and prothrombin, aCL and LA antibodies interact with the membrane of activated platelets and platelet-derived microvesicles in a very similar way as previously observed for their interaction with anionic phospholipid surfaces.

Adult↗
PubMed2006

Correlation of in vitro platelet quality measurements with in vivo platelet viability in human subjects.

BACKGROUND AND OBJECTIVES: Changes in in vitro platelet quality parameters during platelet storage are associated with a decrease of in vivo platelet viability after platelet transfusion. Many attempts have been made to identify the most predictable in vitro parameters for in vivo performance. We used a riboflavin-based ultraviolet (UV) light treatment process designed to inactivate pathogens and white blood cell (WBC) contaminants in blood products as a model system in which to study the correlation of in vitro cell quality with in vivo viability. MATERIALS AND METHODS: Platelet products (n = 18) were collected by a standard Trima apheresis procedure and treated with one of three dose levels of UV light (0, 7.2 or 12.4 J/ml) in the presence of 50 microm riboflavin. Lactate production, glucose consumption and P-selectin expression, pH, pCO(2), pO(2), hypotonic shock response and swirl were measured during 5 days of platelet storage post-UV/RB treatment. Aliquots of these products were radiolabelled on day 5 of storage and were subsequently used to determine platelet recovery and survival time in autologous subjects. RESULTS: The responses of in vitro cell quality were observed to occur in a UV dose-dependent manner. Lactate production and pH were identified as the parameters most strongly correlated with platelet in vivo recovery, which ranged from 5 to 82%. The correlation coefficients (r) for lactate production and pH with in vivo recovery in human subjects were 0.9090 and 0.8831 with P-values of 0.007 and 0.031, respectively. Lactate production and pH were also found to be correlated with platelet survival time, with correlation coefficients of 0.8063 and 0.8384 (the P values were 0.01 and 0.001, respectively). CONCLUSIONS: Using conditions of riboflavin-based UV light treatment, lactate production and pH were identified as having the highest correlations with recovery and survival of radiolabelled platelets in healthy subjects.

Blood Platelets↗
PubMed1995

Diacylglycerol elevations in control platelets are unaccompanied by pleckstrin phosphorylation. Implications for the role of diacylglycerol in platelet activation.

Several laboratories have reported that diacylglycerol levels in human platelets (approximately 100 pmol/10(9) platelets) increased severalfold in response to 0.5-1 U/ml thrombin. We report here fluctuations in diacylglycerol mass in control platelets, the magnitude of which were 60-90% of that measured in platelets treated with 0.2-0.5 U/ml of thrombin. These control platelets were not activated by such criteria as absence of aggregation, secretion, phosphatidic acid production and phosphorylation of the protein kinase C substrate, pleckstrin. Thrombin treatment evoked all of the above responses. Analysis of the diacylglycerol molecular species by reverse-phase HPLC of the dimethylated, phosphorylated derivatives showed that all of the molecular species that were present in control platelets were also present in thrombin-treated platelets. Most of the species appeared to fluctuate at random in control platelets with the exception of 1-stearoyl-2-arachidonoyl-sn-glycerol which was more or less stable and increased severalfold over control values only upon thrombin treatment. Furthermore, only this species accumulated as [32P]phosphorylated PtdOH in thrombin-treated platelets prelabelled with [32P]Pi. Our findings show that, in platelets, elevation of diacylglycerol molecular species other than the 1-stearoyl-2-arachidonoyl species occurs, but these changes are not necessarily linked to activation of protein kinase C as measured by pleckstrin phosphorylation which was observed only upon elevation of 1-stearoyl-2-arachidonoyl-sn-glycerol.

Blood Platelets↗
PubMed2005

Platelet activation and platelet-leucocyte interaction in patients with migraine. Subtype differences and influence of triptans.

As migraine is the result of an inflammatory mechanism with serotonergic signalling, leucocyte function, platelet function and intercellular communication between those cells is likely to be connected to the final pathway of the disease. We examined P-selectin expression on platelets (platelet activation) and leucocyte-platelet aggregate formation in 72 migraine patients during their attack-free interval and controls using a flow cytometric assay. Patients suffering from migraine without aura had a significantly increased platelet activation and leucocyte-platelet aggregation compared with the control group, unlike the migraine patients with aura. Patients who had taken a triptan within 3 days prior to the investigation showed platelet activation values similar to the control group. The variations in platelet activation patterns of migraine subgroups could indicate different pathomechanisms. Even outside an attack, migraine patients, particularly those without aura, show an increased level of platelet activation which seems to be down-regulated by triptans. This mechanism may account for the triptan-induced increases in headache frequency. The involvement of proinflammatory platelet-leucocyte cross-talk suggests a possible therapeutic strategy using anti-inflammatory drugs.

Female↗
PubMed1990

Labelling autologous platelets with 111In tropolonate for platelet kinetic studies: limitations imposed by thrombocytopenia.

An in vitro method of radiolabelling platelets with 111In tropolonate in plasma has been devised enabling imaging and cell kinetic studies to be performed in patients with thrombocytopenia (TP) using autologous, rather than donor, platelets. Platelets from 10 TP patients, with platelet counts ranging from 4-91 x 10(9)/l, were labelled in 50% plasma with 111In tropolonate, containing the optimum tropolone concentration of 2 x 10(-4) mol/l, at platelet concentrations ranging from 0.08-4.5 x 10(9)/ml resulting in labelling efficiencies (LE) between 51 and 86%. In 4 patients, red cells contaminated the platelets but this was corrected for by measuring the proportion of 111In on the platelets prior to injection and in the post-injection blood samples. Platelet recovery (PR), mean platelet life-span (MPLS) and platelet production rate (PPR) were calculated and splenic and hepatic images were taken. The results clearly show that useful clinical data can be obtained by this method even in patients with severe TP.

Adult↗
PubMed1991

Relationship between platelet volume and anti-platelet autoantibodies in idiopathic thrombocytopenic purpura.

We used flow cytometry to explore the relationship between platelet volume and anti-platelet autoantibodies in 71 patients with idiopathic thrombocytopenic purpura (ITP). An increase in platelet volume was found more frequently in patients with a platelet count of less than 20,000/microliters. Platelet volume was larger in patients without anti-GPIIb/IIIa autoantibodies than in patients with these autoantibodies. Furthermore, the platelet count was significantly lower in patients without anti-GIIb/IIIa autoantibodies than in the patients with these autoantibodies. There was a positive correlation between a large platelet volume in patients with a platelet count of less than 30,000/microliters and high platelet-associated IgM levels. These results suggest that the platelet volume is related to the severity of thrombocytopenia in ITP.

Autoantibodies↗
PubMed1998

Platelet activation in the Dutch haemocytometry quality assessment programme: correlation between P-selectin expression and variation in platelet count.

Since 1990, our laboratory has prepared a set of 8 fresh whole blood samples for use in a countrywide quality assessment (QA) programme. The samples are intended as external controls for haemocytometry analysers. These samples are of 8 different haematocrit levels and each one is prepared from a single donor. About 210 laboratories participate in this QA programme. From the start of this programme large interlaboratory variations in platelet counts were encountered in some of the samples. This variability was much higher than would be expected and was independent of the platelet count of the samples. The main cause was thought to be formation of platelet aggregates. The aim of the present study was to find a parameter that can predict a high interlaboratory variation in the QA programme. Therefore we investigated the initial platelet activation status in the donors and the activation status of platelets in the prepared QA blood. As a marker for platelet activation P-selectin expression on the platelets was measured using flow cytometry. During 5 rounds of the QA programme we found a good correlation of r = 0.53 (p < 0.001) between P-selectin expression on platelets in the reconstituted QA blood and the interlaboratory platelet count variability. We conclude that P-selectin expression in the prepared QA blood is an important parameter to exclude samples that lead to high CVs of platelet counts in the QA programme.

Blood Specimen Collection↗
PubMed1997

Platelet-associated IgM elevated in patients with chronic hepatitis C contains no anti-platelet autoantibodies.

We investigated whether thrombocytopenia in patients with chronic hepatitis C is due to anti-platelet autoantibodies. Platelet-associated IgG (PAIgG) and platelet-associated IgM (PAIgM) were measured by direct immunofluorescent flow cytometric analysis. Elevation of PAIgM level was detected in 70% of chronic hepatitis C patients, while only a mild elevation of PAIgG level was detected in 32% of the cases. The elevation of PAIgM values in these patients was comparable to that in patients with chronic immune thrombocytopenic purpura (ITP). However, elevated PAIgM was also found in both patients with and without thrombocytopenia, and no correlation was found between PAIgM and platelet count. Eluted PAIgM did not react with normal platelets in all cases with a positive PAIgM value, indicating that eluted PAIgM contained no detectable anti-platelet antibodies. During alpha-interferon therapy, the level of PAIgM increased in association with the decrease in platelet counts in 75% of the cases; however, eluted PAIgM at any day point never reacted with platelets from normal donors. PAIgM was elevated in patients with chronic hepatitis C, but contained no detectable anti-platelet autoantibodies. Thrombocytopenia in these patients is not due to anti-platelet autoantibodies.

Autoantibodies↗
PubMed2003

Serial measurement of surface expressions of CD63, P-selectin and CD40 ligand on platelets in atherosclerotic ischemic stroke. A possible role of CD40 ligand on platelets in atherosclerotic ischemic stroke.

BACKGROUND: Platelet activation is a key step in the progression of atherosclerosis. The CD40 ligand (CD40L) on platelets may be a critical factor to develop the acute vascular events from atheroma. METHODS: To determine the role of CD40L on platelets in atherosclerotic ischemic stroke, we serially measured the expressions of CD63, P-selectin and CD40L on platelets in patients with atherosclerotic ischemic stroke (n = 25) and compared them with those in patients with asymptomatic carotid stenosis (n = 20) and in normal subjects (n = 24). RESULTS: The expressions of CD63 and P-selectin on platelets were significantly higher in patients with atherosclerotic ischemic stroke (n = 25) than in normal subjects (n = 24). The extents of surface expressions of CD63 and P-selectin on platelets showed no significant differences between atherosclerotic ischemic stroke and asymptomatic carotid stenosis. However, the CD40L expression on platelets was significantly higher in atherosclerotic ischemic stroke when compared to that in asymptomatic carotid stenosis. CONCLUSIONS: In our data, among the population with large artery atherosclerosis, the patients with symptomatic ischemic events showed a significantly elevated expression of CD40L on platelets compared to those without ischemic events. Therefore, the upregulation of CD40L on platelets may be a specific marker of platelet activation to provoke ischemic stroke from large artery atherosclerosis.

Adult↗
PubMedDate not supplied

Platelet adhesion to vascular cells. The role of exogenous von Willebrand factor in platelet adhesion.

Platelet deposition on cultured fibroblasts and on their extracellular matrix (FBM) was investigated in a flow system with citrated blood and was compared with platelet deposition on cultured endothelial cells, smooth muscle cells, and their extracellular matrices. Platelet deposition was present at all surfaces except on intact endothelial cells. Deposition on FBM consisted of contact platelets, spread platelets, and a few small aggregates. On intact fibroblasts cells, the surface coverage was lower, and platelets formed aggregates. Factors involved in primary hemostasis, particularly the wall shear rate, von Willebrand factor (vWF), and fibronectin, were investigated on FBM. The reactivity of FBM was determined by the passage number of the cultured cells. The vWF was involved in platelet adhesion on FBM at only the high shear rate (greater than 800 s-1). Platelet deposition was independent of plasma fibronectin at all shear rates tested. Matrix-associated fibronectin was involved in adhesion at low and high wall shear rates. We conclude that FBM can be used as a platelet adhesive surface especially to study the contribution of exogenous vWF to platelet adhesion because FBM does not contain vWF.

Blood Platelets↗
PubMed2006

Course of platelet activation and platelet-leukocyte interaction in cerebrovascular ischemia.

BACKGROUND AND PURPOSE: Platelet activation plays a crucial role in the pathophysiology of cerebral ischemia. The aim of this study was to investigate the contribution of platelet activation and leukocyte-platelet interactions to the disease. METHODS: One hundred thirty-five patients with transient ischemic attack (TIA) or stroke were enrolled in this single-center study. They underwent cranial computer tomography within 24 hours of clinical onset and after 3 months, and systemic venous blood samples were drawn. Platelet activation (CD62P expression), leukocyte activation (L-selectin expression), and the appearance of platelet-specific antigens on leukocytes as an index of platelet-leukocyte aggregation were measured by flow cytometric techniques in the acute state and at 3-month follow-up. RESULTS: Patients with a completed stroke or TIA had significantly increased circulating platelet-leukocyte aggregates, increased P-selectin expression on platelets, and decreased L-selectin expression in the acute state compared with the control group (healthy volunteers). No differences in regard to the tested activation markers could be detected between patients with stroke or TIA in the acute phase of the disease. However, platelet and leukocyte activations were normalized after 3 months in patients with TIA, whereas leukocyte activation (reduced L-selectin expression) remained in stroke patients. CONCLUSIONS: In patients with TIA and completed stroke, platelet and leukocyte activation is substantially enhanced in the acute phase of the disease. The sustained leukocyte activation observed in stroke but not in TIA patients at 3-month follow up might play a pathophysiological role in the course of the disease.

Aged↗
PubMed1983

Immunoelectron microscopic localization of platelet factor 4 and fibrinogen in the granules of human platelets.

To determine the storage site of platelet fibrinogen and of platelet factor 4 (PF4) in human platelets by immunoelectron microscopic techniques, washed human platelets were briefly exposed to Karnovsky's fixative and embedded in water-soluble Durcupan. Thin sections of platelets were exposed to Fab fragments of rabbit anti-human fibrinogen or of goat anti-human PF4, followed by a peroxidase conjugate of Fab fragments of antibodies to rabbit immunoglobulin (Ig) G or to goat IgG. The technique enabled preservation of the antigenic determinants of the platelet proteins, accessibility of Fab fragments to the platelet proteins, and maintenance of the ultrastructural integrity of the platelets. Using this approach, it was directly demonstrated that platelet fibrinogen and PF4 are stored in the alpha-granules of human platelets.

Animals↗