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At least 19 recordsLinked to original sources
PubMed1990

Platelets in hyperthyroidism: studies on platelet counts, mean platelet volume, 111-indium-labeled platelet kinetics, and platelet-associated immunoglobulins G and M.

We compared in 15 patients with hyperthyroidism (11 with Graves' disease, 3 with toxic adenoma, and 1 with multinodular goiter) platelet counts (PC) and mean platelet volume (MPV) before and 3 weeks after initiation of antithyroid drug therapy when the patients were euthyroid. In addition, platelet kinetic studies of autologous 111-indium-labeled platelets and platelet-associated immunoglobulins G and M (PAIgG and PAIgM, respectively) were investigated. The control group for the platelet kinetic studies consisted of 2 patients with diffuse nontoxic goiter and 86 patients who were studied for evaluation of their arteriosclerotic vascular disease. After 3 weeks of antithyroid drug therapy there was a significant increase in PC and a decrease in MPV compared with the pretreatment values (pretreatment PC median, 215 X 10(9)/L; range, 96-350 X 10(9)/L; PC median 3 weeks later, 248 X 10(9)/L; range, 157-384 X 10(9)/L; P less than 0.005; pretreatment MPV median, 10.6 fL; range, 9.1-13.2 fL; MPV 3 weeks later, 9.9 fL; range, 8.4-11.0 fL; P less than 0.005). 111-Indium platelet recovery was normal in all subjects. Platelet lifespan was significantly shortened in the patients with hyperthyroidism compared with the control group (median, 163.8 h; range, 128.5-206 h; vs. 180.0 h; range, 138.3-231.5 h; P less than 0.05). Platelet turnover averaged 45.6 (range, 25.6-71.9) X 10(9)/L.day; values above the limit of normal were found in 7 of 15 patients with hyperthyroidism. Three patients with Graves' disease had elevated levels of PAIgG; 1 of these patients had elevated levels of PAIgM and was the only patient with thrombocytopenia (PC, 96 X 10(9)/L). Various combinations of statistical correlations between the degree of hyperthyroidism, pretreatment PC and MPV, platelet kinetic studies, levels of PAIg, and serum levels of antithyroid antibodies revealed no significant differences. These findings suggest that the platelet changes observed in hyperthyroidism, such as lower PC and increased MPV, together with the shortened platelet lifespan reflect metabolically rather than immunologically mediated phenomena, although these may be involved in cases with marked thrombocytopenia.

Adolescent↗
PubMed1992

Platelet immunology. ELISA for detection of platelet antibodies, platelet-specific antigens and platelet glycoproteins.

The development of an enzyme linked immuno-sorbent assay (ELISA) for detection of platelet antibodies and platelet specific-antigens has been described. In the assay, intact platelets fixed to the bottom of microplates have been used as targets. After incubation with serum, the attached antibody has been detected by antiglobulin serum labelled with enzyme followed by assay of the enzyme reaction with its substrate. The clinical significance of platelet antibodies in alloimmune neonatal thrombocytopenia (AINT), post-transfusion purpura (PTP), and refractoriness to platelet transfusion therapy has been described. The clinical significance of autoantibodies in autoimmune thrombocytopenic purpura (AITP) and the detection of platelet surface glycoproteins by a modification of the platelet ELISA has also been described. In addition, a survey of the present state of knowledge of human platelet immunology, especially platelet-specific alloantigens and alloantibodies has been given. The studies of AINT and PTP have revealed a human immune response gene located in the MHC region: The susceptibility to anti-Zwa alloimmunization is strongly associated with the HLA-B8 and even more DR3 and DRw52a tissue types. In the studies of PTP, the first example of PTP due to anti-Zwb (only detectable in the platelet ELISA) has been described, and an association of the presence of anti-Zw antibodies of IgG3 subclasses (defined in the platelet ELISA using monoclonal mouse antibodies) and destruction of autologous platelets has been described. In an investigation of Ig classes and IgG subclasses of platelet associated Ig (PAIg) in children suffering from autoimmune thrombocytopenic purpura, no correlation was found between the immunochemical properties of the PAIg and the clinical course of the disease. However, a correlation between increased amounts of PAIgG3 and very low platelet counts was observed. A modification of the platelet ELISA using monoclonal antibodies against glycoproteins (GP) has been described. Using antibodies against GPIb and GPIIb/IIIa, it has been possible to diagnose Glanzmann's thrombasthenia (GT) and Bernard-Soulier syndrome (BSS). Especially in the diagnosis of thrombocytopenic patients suspected for BSS where platelet aggregation studies has been impossible due to low platelet counts, the detection of decreased amounts of surface GPIb in ELISA has been of great value. In conclusion, the platelet ELISA has been found simple and sensitive, and suitable for routine investigations of AINT, PTP, AITP, and refractoriness to platelet transfusion.

Blood Platelets↗
PubMed1987

Platelet aggregability and platelet volume in the postoperative course: problems in the platelet aggregation test derived from the measurement of platelet volume.

Platelet count, aggregability and volume in the postoperative course of 20 patients were examined. Platelet count was decreased on the 1st postoperative d, and increased on the 7th and 14th d compared with the preoperative value. The maximal aggregation rate of platelets induced by ADP was decreased on the 3rd postoperative d, and then recovered to the preoperative level. In contrast, platelet volume was only slightly increased on the 3rd postoperative d. In this study, there was no correlation between platelet aggregability and platelet volume in PRP. We have proposed one parameter, 'platelet concentration ratio' (platelet concentration in PRP/platelet concentration in whole blood). In the postoperative course, this concentration ratio changed depending on platelet volume, and possibly on other conditions of blood such as hematocrit, viscosity and specific gravity. The concentration ratio influenced the subpopulations of platelets in PRP. Platelet aggregation tests may be performed using PRP in which platelet subpopulations differ from those in whole blood, especially in the postoperative state.

Adult↗
PubMed1990

A survey of platelet serology in UK laboratories (1987): an assessment of the efficacy of using chloroquine-treated platelets to distinguish between platelet-specific and anti-HLA antibodies. The UK Platelet and Granulocyte Serology Working Group.

This survey was designed to determine the ability of participants to distinguish between platelet specific and anti-HLA antibodies. Four well characterized reference reagents and 10 unknown samples were sent to 29 laboratories affiliated to the UK Platelet and Granulocyte Serology Working Group and to three overseas reference laboratories. Results were obtained from 27 Working Group laboratories and from 2 reference laboratories. Overall, the results indicate that the use of chloroquine-treated platelets alone, without an independent test for anti-HLA antibodies, was insufficiently reliable to elucidate mixtures of platelet specific and anti-HLA antibodies. Laboratories using chloroquine-treated platelets were no more successful in elucidating the antibody composition of sera containing platelet-specific and anti-HLA antibodies than those laboratories which did not use this technique. The results may indicate a lack of experience with the chloroquine technique and suggest that further studies into the performance of the technique are required. The survey also provided insights into other areas of platelet serology: (1) There was a decrease in the incidence of false-positive results compared to earlier UK surveys. [2) All laboratories detected potent platelet-specific antibodies but weakly reactive antibodies were less readily detected. (3) Laboratories using fluorescent antiglobulin techniques recorded fewer errors than laboratories using ELISA techniques. (4) Laboratories using paraformaldehyde (PFA)-treated platelets in fluorescent antiglobulin techniques did not perform better than laboratories using untreated platelets.

Antibody Specificity↗
PubMed1988

High affinity specific binding sites for tritiated platelet-activating factor in canine platelet membranes: counterparts of platelet-activating factor receptors mediating platelet aggregation.

In canine platelet membranes, tritiated platelet activating factor (PAF) labels in a saturable and reversible manner a single population (nH = 0.97) of binding sites. The affinity of this binding was high (Kd = 0.23 +/- 0.02 nM, n = 4, and 0.21 +/- 0.05, n = 8, determined by kinetics or saturation experiments, respectively), and the density of binding sites (Bmax) was 911 +/- 31 fmol/mg of protein (n = 8). [3H]PAF binding was entirely reversed by unlabeled PAF (10 microM). [3H]PAF exhibited stereoselective discrimination inasmuch as it was poorly displaced by enantio-PAF, the PAF enantiomer that does not occur naturally. Furthermore, the displacing potency of the (+)-enantiomer of the PAF antagonist 52770 RP against [3H]PAF was 45 times higher than that of the (-)-enantiomer. [3H]PAF binding displayed a remarkable specificity in that it was not affected by a variety of classical pharmacological agents. However, this binding was displaced by several PAF receptor antagonists such as 59227 RP, CV-6209, Ro 19-3704, 52770 RP, brotizolam, WEB 2086, SRI 63-441, L-652,731, alprazolam, triazolam, and BN 52021. The Ki of the 16 studied antagonists ranged from 7.9 nM (59227 RP, most potent) to 16.8 microM (BN 52021, least potent). The possible biological significance of our binding procedure was assessed by correlating the potencies of 16 PAF antagonists as [3H]PAF displacers in dog platelet membranes and as inhibitors of PAF-induced platelet aggregation in washed canine platelets. This analysis revealed the existence of a highly significant correlation (r = 0.82, p less than 0.001) between biochemical and functional tests. However, two compounds (Ro 19-3704 and BN 52021) were found to be located outside the confidence limits when the probability level of belonging to the regression line was set at 0.01. In conclusion, this study provides evidence that [3H]PAF binding in canine platelet membranes exhibits the required properties for a valid binding procedure. Furthermore, the labeled sites are likely to be the counterparts of platelet receptors that, when activated by PAF, induce aggregation.

Animals↗
PubMed1986

Storage of platelets for tests of platelet function: effects of temperature on platelet aggregation, platelet morphology and liberation of beta-thromboglobulin.

We have studied the effect of temperature on platelets during storage for tests of platelet function. Aliquots of PRP were stored at constant pH at 37 degrees C, room temperature and 4 degrees C. At intervals up to five hours, samples were taken for estimation of platelet shape, plasma levels of beta-thromboglobulin and 14C-serotonin, and assessment of platelet aggregation in response to a range of concentrations of ADP and collagen. When PRP was stored at 37 degrees C there was a gradual decrease in the aggregation response during the period of storage. At room temperature the decrease was slower but the response to ADP often increased dramatically before decreasing; at this temperature there was pronounced liberation of beta TG while there was none at 37 degrees C. Platelets stored at 37 degrees C were smooth and elliptical when examined by electron microscopy, but those stored at room temperature showed partial loss of discoid shape and formation of some pseudopodia. Storage at 4 degrees C was associated with total loss of discoid shape and formation of many large pseudopodia. Light transmission studies also showed loss of discoid shape at room temperature and 4 degrees C. We conclude that storage at 4 degrees C or at room temperature causes platelet activation. To avoid this PRP should be stored at 37 degrees C prior to tests of platelet function.

Blood Platelets↗
PubMed1988

Increased proportion of giant platelets and platelet distribution width are better indicators of altered platelet homeostasis than mean platelet volume in liver cirrhosis.

Platelet count, mean platelet volume (MPV), giant platelet percentage, expressed by us as megathrombocytic index (MTI) and platelet distribution width (PDW) have been evaluated in 32 control subjects and in 27 patients suffering from liver cirrhosis (LC) and thrombocytopenia. MTI and PDW were linearly and inversely correlated to platelet count both in controls and patients. MTI and PDW were markedly increased in LC as compared to controls, while MPV was not significantly different. It is concluded that MTI and PDW are good indices of thrombopoietic stimulus both in controls and in CL and better indicators of altered platelet homeostasis than MPV in LC.

Adolescent↗
PubMed1991

Wheat germ agglutinin potentiates specific binding of platelet-activating factor to human platelet membranes and induces platelet-activating factor synthesis in intact platelets.

Specific binding of tritium-labeled platelet-activating factor (PAF) and a nonmetabolizable bioactive analog of PAF, 1-O-alkyl-2-N-methylcarbamyl-sn-glyceryl-3-phosphorylcholine, to human platelet membranes was found to be potentiated by wheat germ agglutinin (WGA) and erythroagglutinin. As demonstrated in Scatchard plots, the potentiation effect is due to an increase in the maximal number of receptor sites, with no alteration in the equilibrium dissociation constant. The WGA-potentiated specific binding can be specifically inhibited by N-acetylglucosamine, shows identical affinity for PAF agonists and a receptor antagonist, L-659,989, and has an identical Na+ inhibition pattern to non-treated membranes in the absence of WGA. The WGA-induced potentiation is preferential in the plasma membrane-enriched fraction. The maximal number of receptor sites increases in membranes pretreated with neuraminidase and beta-N-acetylglucosaminidase. Therefore, WGA may bind to an endogenous PAF receptor modulator, which then either dissociates from or associates with the PAF receptor and regulates the receptor conformation. The membrane fraction enriched with intracellular membranes is also enriched with PAF receptors. WGA was also found to increase the maximal aggregation of rabbit and human platelets induced by PAF and to induce the synthesis of PAF, which preceded aggregation in human platelets. An intracellular PAF receptor may also exist, and it could modulate the function of PAF retained inside of the stimulated cells.

Acetylglucosaminidase↗
PubMed1986

The relation of platelet density to platelet age: survival of low- and high-density 111indium-labeled platelets in baboons.

The relationship between platelet density and platelet age has been studied using continuous linear Percoll density gradients and 111In-labeling of autologous platelets in baboons. To investigate changes in platelet density during senescence in the circulation, baboons were infused with 111In-labeled autologous platelets, and blood was collected at one hour postinfusion and twice daily thereafter for six days. Platelets were isolated from these samples in high yield (greater than 95%) and separated in continuous linear Percoll density gradients following density equilibrium centrifugation. Although at one hour postinfusion the density distribution of radiolabeled platelets coincided closely with the distribution of the total platelet population, a detectable symmetrical shift toward higher densities was observed after five days. The relative specific radioactivity (RSR) of high-density platelets (1.064 to 1.067 g/mL) decreased at a slower rate than that of the total platelet population (platelets of all densities), whereas the RSR of low-density platelets (1.053 to 1.056 g/mL) showed a more immediate and rapid decrease. These results give rise to one of two interpretations: (1) low-density platelets have a shorter survival time than more dense platelets and are therefore cleared from the circulation at a faster rate, or (2) platelets of all densities increase in density upon aging in the circulation. To determine the explanation for changing RSR of different density fractions we studied the in vivo disappearance characteristics of low- and high-density 111In-labeled platelets. There were no significant differences between the mean survival times of low-density platelets (5.0 +/- 0.49 days, +/- 1 SD, n = 6), high-density platelets (4.9 +/- 0.56 days, n = 6), or control platelets representing platelets of all densities (4.9 +/- 0.38 days, n = 6). Although a slight increase in the density of all platelets during platelet senescence is indicated by these studies, we conclude that platelet density heterogeneity is not primarily a consequence of age-related changes in platelet density.

Animals↗
PubMed1987

Platelet enhancement of tumor cell adhesion to subendothelial matrix: role of platelet cytoskeleton and platelet membrane.

Platelet involvement during tumor cell adhesion to subendothelial matrix was examined in vitro. Platelets were subjected to thrombin stimulation and mechanical lysis and examined for their effects on tumor cell adhesion. These treatments altered the platelet ultrastructure and cytoskeletal integrity. Untreated washed rat platelets (WRP) exhibited extensive adhesion to and spreading on substrates and substantially enhanced tumor cell adhesion to the same substrates (i.e., 250% greater than tumor cells without platelets). Thrombin prestimulation of platelets limited platelet adhesion and spreading and platelet facilitation of tumor cell adhesion. Complete mechanical lysis disrupted both the platelet membrane and the cytoskeleton and eliminated the ability of platelets to adhere or to enhance tumor cell adhesion. Partially lysed platelets resembled membrane ghosts and facilitated tumor cell adhesion by a mechanism independent of spreading and cytoskeletal rearrangement. Fractionation studies indicated that platelet cytoskeletal components played a role in the adhesion process. Pretreatment of WRP with cytochalasin A or B dose dependently inhibited microfilament-mediated platelet spreading and platelet-enhanced tumor cell adhesion. Colchicine and vinblastine induced microtubule depolymerization, but they had no observable effect on platelet spreading or platelet-enhanced tumor cell adhesion. It was concluded that platelet-enhanced tumor cell adhesion to subendothelial matrix depends on an intact platelet cytoskeleton and on a platelet membrane component(s) and is mediated by surface contact between platelets and tumor cells. Furthermore, platelet-mediated tumor cell adhesion to subendothelial matrix may involve two mechanisms: one dependent on, and one independent of, platelet spreading and cytoskeletal rearrangement.

Animals↗
PubMed1990

The platelet extinction coefficient measured by aggregometry is dependent on platelet composition rather than size: implications for studies of platelet heterogeneity and abnormalities.

Extinction (E) or light transmission measurements of platelet suspensions have been widely used to evaluate platelet structure and aggregation for platelet populations of varying mean platelet size (V). However, useful comparisons of platelet suspensions from donors having abnormally-sized platelets with those from healthy controls require a knowledge of the dependence of E on V. We have analyzed the extinction per platelet (e) as a function of the geometric scattering cross-section of equivalent spheres, V2/3, related to the apparent mean platelet optical efficiency, k. Such an analysis using data previously reported by Holme et al., for healthy controls and a variety of platelet-associated disorders showed e/V2/3 or k to be constant over an eight-fold variation in V. The outstanding exception was platelet suspensions from myeloproliferative disorder patients (MPD) which showed approximately 25% reduction in k values. When we analyzed e/V2/3 data for different-sized platelet subpopulations which were isolated by elutriation from healthy donors, we found that k doubled with a doubling in V from small to large platelets. It appears that the use of aggregometry devices with wide light acceptance angles yields k values for platelets which are insensitive to variations in V, but rather are sensitive to the expected variations in refractive index associated with distinct platelet internal composition and organization expected for different-sized normal subpopulations and "diseased" platelets as found in MPD. We relate these observations to photometric studies of platelet heterogeneity and of aggregation of platelets with different V and k values.

Adult↗
PubMed1987

Platelet-collagen adhesion enhances platelet aggregation induced by binding of VWF to platelets.

Ristocetin-induced platelet aggregation (RIPA) was evaluated in the presence of platelet-collagen adhesion. RIPA of normal donor platelet-rich plasma (PRP) demonstrated a primary wave of aggregation mediated by the binding of von Willebrand factor (VWF) to platelets and a secondary aggregation wave, due to a platelet-release reaction, initiated by VWF-platelet binding and inhibitable by acetylsalicylic acid (ASA). An enhanced RIPA was observed in PRP samples to which collagen had been previously added. These subthreshold concentrations of collagen, which by themselves were insufficient to induce aggregation, caused measurable platelet-collagen adhesion. Subthreshold collagen did not cause microplatelet aggregation, platelet release of [3H]serotonin, or alter the dose-responsive binding of 125I-labeled VWF to platelets, which occurred with increasing ristocetin concentrations. However, ASA inhibition of the platelet release reaction prevented collagen-enhanced RIPA. These results demonstrate that platelet-collagen adhesion altered the platelet-release reaction induced by the binding of VWF to platelets causing a platelet-release reaction at a level of VWF-platelet binding not normally initiating a secondary aggregation. These findings suggest that platelet-collagen adhesion enhances platelet function mediated by VWF.

Blood Platelets↗
PubMed1987

Binding of aggregated immunoglobulins to the human platelet Fc receptors: a mechanism of platelet to platelet bridging.

Aggregated immunoglobulins react with human platelets by occupying the Fc receptors present on their surface, inducing aggregation and the release reaction. We studied the effect of heat aggregated gammaglobulins (HAGG) on ADP-induced aggregation of platelets. We used the minimum concentration of ADP required to induce a reversible aggregation of platelets without any substantial amount of serotonin (14C-5HT) release. EDTA (5 mM) added at the peak of platelet aggregation resulted in rapid deaggregation of these platelets. However, incubation of platelets with HAGG at a dose that did not by itself induce any aggregation or release reaction, followed by ADP addition resulted in an irreversible platelet aggregation of greater magnitude accompanied by a substantial release of 14C-5HT. The addition of EDTA at the peak of platelet aggregation failed to deaggregate these platelets. To determine whether the augmented aggregation response and the inhibition of deaggregation was due to HAGG or a consequence of platelet release products, we used thrombin-degranulated platelets. The augmented aggregation response and the inhibition of deaggregation due to HAGG and ADP could be demonstrated using these platelets. To confirm that the binding of HAGG to the platelet Fc receptors was responsible for these observations, we incubated platelets with an excess of Fc fragments of IgG prior to the addition of HAGG and ADP. This abolished the aggregation response observed previously. From this study we conclude that interplatelet bridging by HAGG renders the platelets hyperaggregable and appears to be a mechanism involved in maintaining platelet aggregates.

Adenosine Diphosphate↗
PubMed1990

The association of platelet and red cell count with platelet impedance changes in whole blood and light-scattering changes in platelet rich plasma: evidence from the Caerphilly Collaborative Heart Disease Study.

This epidemiological study was undertaken to explore possible relationships among various haematological indices, prevalent ischaemic heart disease and platelet "function" as measured by two rather different methods. ADP-induced platelet impedance changes in whole blood were strongly associated with prevalent ischaemic heart disease in a general population of 49-66 year men at increased risk. Adenosine diphosphate (ADP) induced platelet aggregation in platelet rich plasma (PRP) at a constant platelet count and also the whole blood platelet count and red cell (RBC) count were strongly and independently related to ADP-induced platelet impedance changes. Both platelet count and platelet aggregation in PRP assessed by changes in optical density were directly related to increasing platelet "sensitivity" as measured by impedance changes in whole blood but RBC count was inversely related. Positive independent relationships between platelet impedance changes and plasma viscosity and fibrinogen were markedly attenuated when platelet count was taken into account, but this finding does not discount a role for these factors in platelet aggregation. No relationship was noted between white blood cell (WBC) count and platelet impedance changes; however, a significant inverse relationship was noted with platelet aggregation in PRP. These findings indicate that laboratory-based experimental findings can be observed in population based studies, and that these haematological factors may be important indicators of ischaemic disease in the population.

Adenosine Diphosphate↗
PubMed1986

Relationship of platelet-associated immunoglobulin G and platelet protein to platelet size and density in normal individuals and patients with thrombocytopenia.

Total platelet-associated immunoglobulin G (PA-IgG) and platelet volume and protein content in normal individuals and in patients with idiopathic thrombocytopenic purpura (ITP) and other thrombocytopenias of presumed nonimmune origin have been measured on platelets separated into subpopulations on the basis of density on continuous polyvinylpyrrolidone (Percoll) gradients. In all subjects PA-IgG per platelet was primarily found in the lightest platelets at levels up to sevenfold greater than in the heavier platelets. PA-IgG level per platelet was raised in light platelets in 29% of patients with thrombocytopenia and in heavy platelets in 60%. In almost half of these instances the PA-IgG level fell to within the normal range when considered in relation to either platelet volume or protein content. PA-IgG levels of patients with untreated ITP did not differ significantly from those with treated ITP or thrombocytopenia of other causes. Mean platelet volume and protein content of the total platelet population of all subjects showed significant linear correlation (P less than 0.01). Thus PA-IgG of both controls and patients with thrombocytopenia of all causes is preferentially located in the lightest platelets, but increases in PA-IgG in immune thrombocytopenias occur more frequently in the heavier platelets. These findings suggest that part of the process of IgG accumulation by platelets is the same in normal individuals as in patients with thrombocytopenia.

Adolescent↗
PubMed1985

Platelet interaction with subendothelial extracellular matrix: platelet-fibrinogen interactions are essential for platelet aggregation but not for the matrix-induced release reaction.

Cultured endothelial cells produce an extracellular matrix (ECM) to which platelets adhere and spread, ultimately resulting in platelet aggregation, thromboxane B2 production, and serotonin release. We have investigated the role of fibrinogen binding to the platelet GPIIb/IIIa complex in these reactions by comparing normal platelet-rich plasma (PRP), PRP from patients with Glanzman's thrombasthenia (whose platelets lack the GPIIb/IIIa complex), PRP in the presence of a monoclonal antibody that blocks the binding of fibrinogen to the GPIIb/IIIa complex, platelets washed free of fibrinogen, and washed platelets to which fibrinogen was added. Although platelet aggregation was virtually completely inhibited in the samples in which the normal interaction between fibrinogen and GPIIb/IIIa was impaired, adhesion of platelets to the matrix, spreading, and release of [14C]-serotonin were not affected. All of the platelet preparations released significant amounts of T X B2 with time, but there was a decrease in the amount produced by both the thrombasthenic and antibody-treated platelets. We conclude that the interaction of fibrinogen with platelet GPIIb/IIIa is not required for platelet adhesion to ECM or for adhesion-induced shape change or serotonin release. On the other hand, the platelet-fibrinogen interaction may play some role in augmenting adhesion-induced T X B2 production, and it is absolutely required for adhesion-induced platelet aggregation.

Animals↗
PubMed1989

Platelet aggregability and in vivo platelet deposition in patients with ischemic cerebrovascular disease--evaluation by indium-111-platelet scintigraphy.

In ischemic cerebrovascular disease, it is not clear whether platelet function in vitro actually reflects the situation in vivo. Using indium-111 platelet scintigraphy as a method for detecting platelet activation in vivo, we tried to elucidate this problem. Twenty eight patients with chronic stage of ischemic cerebrovascular disease (CVD) and 17 control subjects were examined. Platelet scintigrams were positive in 9 of 28 patients in CVD, while all were negative in control. A comparison of the results obtained from qualitative platelet imaging and platelet aggregability was performed to evaluate whether threshold aggregation concentration (TAC) grade differed across the three groups (control, CVD patients without platelet deposition and CVD patients with platelet deposition). CVD patients with platelet deposition showed a higher TAC than those patients who did not show platelet deposition (P less than 0.05) or control subjects without platelet deposition (P less than 0.05). These results suggest that some patients in chronic stages of CVD may have active platelet deposition on carotid atheromatous lesions, and presence of platelet deposition in vivo could contribute to reduce platelet reactivity in peripheral blood.

Adult↗
PubMed1986

Platelet surface glycoproteins. Studies on resting and activated platelets and platelet membrane microparticles in normal subjects, and observations in patients during adult respiratory distress syndrome and cardiac surgery.

The accurate definition of surface glycoprotein abnormalities in circulating platelets may provide better understanding of bleeding and thrombotic disorders. Platelet surface glycoproteins were measured on intact platelets in whole blood and platelet membrane microparticles were assayed in cell-free plasma using 125I-monoclonal antibodies. The glycoproteins (GP) studied were: GP Ib and GP IIb-IIIa, two of the major intrinsic plasma membrane glycoproteins; GMP-140, an alpha-granule membrane glycoprotein that becomes exposed on the platelet surface following secretion; and thrombospondin (TSP), an alpha-granule secreted glycoprotein that rebinds to the platelet surface. Thrombin-induced secretion in normal platelets caused the appearance of GMP-140 and TSP on the platelet surface, increased exposure of GP IIb-IIIa, and decreased antibody binding to GP Ib. Patients with adult respiratory distress syndrome had an increased concentration of GMP-140 and TSP on the surface of their platelets, demonstrating in vivo platelet secretion, but had no increase of platelet microparticles in their plasma. In contrast, patients after cardiac surgery with cardiopulmonary bypass demonstrated changes consistent with membrane fragmentation without secretion: a decreased platelet surface concentration of GP Ib and GP IIb with no increase of GMP-140 and TSP, and an increased plasma concentration of platelet membrane microparticles. These methods will help to define acquired abnormalities of platelet surface glycoproteins.

Antibody Specificity↗