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PubMed1983

Human platelet secreted proteins and prostacyclin production by bovine aortic endothelial cells.

The effects of specific human platelet-secreted proteins on prostacyclin (PGI2) production by primary cultures of bovine aortic endothelial cells have been studied. Cells were incubated with various concentrations of highly purified preparations of platelet factor 4 (PF4), low-affinity platelet factor 4 (LA-PF4), beta-thromboglobulin (beta TG), platelet basic protein (PBP), and partially purified platelet-derived growth factor (PDGF) in the presence or absence of arachidonic acid (AA). The amount of 6-Keto-PGF1 alpha, the stable degradation product of PGI2, was determined in the cell incubation medium by means of a specific radioimmunoassay. Short-term (15 min) incubation of cell monolayers with either LA-PF4 or beta TG slightly reduced 6-keto-PGF1 alpha production. The effect was not dose-related and could not be observed after prolonged (24 hr) incubation of the cells with the same proteins. It was not seen in the cell suspensions. Moreover, 6-keto-PGF1 alpha production stimulated by AA was not affected by incubation with either of the proteins. PF4 and PBP had no significant effect on 6-keto-PGF1 alpha production by endothelial cells. Human PDGF showed a slight tendency to stimulate 6-keto-PGF1 alpha release when cells were incubated for 24 hr with the protein; however, PDGF did not potentiate the stimulatory effect of AA on 6-keto-PGF1 alpha release by the cells. We suggest that platelet-derived proteins exert only a moderate and possibly nonspecific effect on PGI2 production by endothelial cells.

6-Ketoprostaglandin F1 alpha↗
PubMed1979

Effects of prostaglandin E1 on platelet loss during in vivo and in vitro extracorporeal circulation with a bubble oxygenator.

Temporary inhibition of platelet function with prostaglandin E1 (PGE1) prevents platelets loss and functional alterations during extracorporeal circulation with a membrane oxygenator. This study evaluated the ability of PGE1 to prevent platelet injury in circuits containing a bubble oxygenator. During in vitro recirculation of human blood, the circulating platelet count, expressed as a percent of initial levels, decreased to 29%; platelets became insensitive to adenosine diphosphate (ADP) and to epinephrine; and plasma levels of low-affinity platelet factor 4 (LA-PF4) progressively rose to 7.4 microgram per milliliter. With PGE1 (1.2 micron), platelet counts remained stable at 92%; platelet reactivity remained normal for 1 hour; and plasma levels of LA-PF4 rose to only 3.3 microgram per milliliter. In rhesus monkeys that underwent cardiopulmonary bypass using a bubble oxygenator without PGE1, platelet counts, expressed as a percent of the prebypass platelet count, declined to 38%; platelets became insensitive to ADP; plasma levels of LA-PF4 progressively rose to 8.4 microgram per milliliter; and the mean postoperative bleeding time was 4.6 minutes. In monkeys that received PGE1, platelet counts declined to only 65%; platelets remained threefold more sensitive to ADP; platelets demonstrated delayed release of LA-PF4 and the mean postoperative bleeding time was 2.7 minutes. This report demonstrates that in a bubble oxygenator system, PGE1 reduces platelet loss, mitigates platelet injury, and shortens postoperative bleeding times following extracorporeal circulation.

Animals↗
PubMed2002

[Some parameters of platelet activation in patients with uremia before and after hemodialysis (HD)].

Patients with uremia show a tendency for hemorrhagic diathesis and thrombi formation. These disorders have been attributed to functional abnormalities of platelet and their interaction with the vascular wall. The aim of the present study was to elucidate whether and how in patients with uremia, hemodialysis affects the level of platelet activation markers, i.e.: beta-TG and PF4, and whether the changes in the examined parameters depend on creatinine level and on the type dialysis membranes used during HD. The study involved 70 patients with uremia subjected to repeated hemodialysis and 70 healthy subjects. Prior to HD, we observed a decrease in PLT, and increase in beta-TG concentration and a drop in PF4 (p = 0.000), compared to control group. Immediately after the procedure a significant increase was observed in PLT and decrease in PF4 concentration, as well as a slight rise in beta-TG level, compared to the values obtained before HD. We also found statistically significant differences in beta-TG and PF4 concentrations prior to HD, irrespective of creatinine concentration, compared to control group. Only at creatinine concentration of 10.0-15.5 mg/dL, PLT differences significantly from PLT in control group. Following HD, creatinine-dependent statistically significant changes were noted in PLT, in comparison to the values obtained before the procedure. The analysis of platelet parameters revealed no statistically significant differences associated with the type of the dialysis membrane used for HD.

Adult↗
PubMed1992

Modulation of protein C inhibitor activity by histidine-rich glycoprotein and platelet factor 4: role of zinc and calcium ions in the heparin-neutralizing ability of histidine-rich glycoprotein.

Effects of zinc and calcium ions on the heparin-neutralizing abilities of histidine-rich glycoprotein (HRG) and platelet factor 4 (PF4) were examined. Both HRG and PF4 effectively neutralized the ability of heparin to accelerate the activated protein C (APC) and the thrombin inhibitions by protein C inhibitor (PCI). the heparin-neutralizing ability of HRG in the APC inhibition by PCI, however, was decreased in a Ca(2+)-dependent manner and apparently lost at 1 mM Ca2+, while it was enhanced by Zn2+ regardless of the presence or absence of Ca2+. The heparin-neutralizing ability of HRG in the thrombin inhibition by PCI was not affected by Ca2+. In contrast to HRG, there was no significant difference in the heparin-neutralizing ability of PF4 in the presence or absence of 1 mM Ca2+. These results strongly suggest additional physiological functions of HRG and PF4 as modulators of PCI.

Calcium↗
PubMed1992

Neutralization of the antiheparin activity of platelet factor 4 by a monoclonal antibody.

We have produced a panel of monoclonal antibodies (mAbs) against rabbit platelet factor 4 (PF4). Two of these mAbs have been characterized in this study. In particular the antibody called 10B2, which also recognizes the human molecule, is able to block PF4's ability to neutralize heparin in a modified Heparin-Factor Xa chromogenic assay. The inhibition appears to be more than 95% at 1:1 mAb/PF4 molar ratio both for purified rabbit and human PF4. Similar results were obtained using supernatants from stimulated human platelets (90% of inhibition at 1:1 mAb/PF4 molar ratio) or using Fab fragments from 10B2. Studies to determine the antigenic determinant against which 10B2 is directed, show that this is an assembled epitope which involves disulfide bonds of the PF4.

Amino Acid Sequence↗
PubMed2003

Enhanced release of platelet factor 4 into the circulation in patients with atopic eczema/dermatitis syndrome.

PURPOSE: The active participation of platelet in IgE-mediated inflammatory response is well documented. Platelet factor 4 (PF4), a platelet-specific protein may play an important role in the development of the atopic eczema/dermatitis syndrome (AEDS). OBJECTIVE: The aim of the study was to evaluate the activation state of circulating platelets in patients suffering from AEDS. MATERIAL AND METHODS: In vivo platelet activity was assessed by measuring plasma level of PF4 (enzyme-linked immunoassay method) in 9 males AEDS patients and 11 healthy, nonatopic subjects. RESULTS: Plasma PF4 was significantly increased (p < 0.05) in AEDS (31.88 +/- 20.48 IU/ml) patients compared with control subjects (2.95 +/- 0.6 IU/ml). CONCLUSIONS: This result suggests that patients with AEDS may have increased in vivo platelet activation expressed by PF4 release. The aim of the study was to evaluate the activation state of circulating platelets in patients suffering from AEDS.

Adult↗
PubMed1990

Immunomodulatory properties of platelet factor 4: prevention of concanavalin A suppressor-induction in vitro and augmentation of an antigen-specific delayed-type hypersensitivity response in vivo.

The immunomodulatory properties of platelet factor 4 (PF4) have been examined in vitro and in vivo. This agent prevented the induction of concanavalin A (Con A)-induced suppressor cells in vitro in a dose-dependent manner but it did not affect the function of established Con A suppressor cells. This effect was not due to an enhanced production of interleukin-2 (IL-2) by lymphocytes exposed to PF4. The delayed-type hypersensitivity (DTH) reaction to sheep erythrocytes (SRBC) was used as a model for the generation of antigen-specific suppression in vivo. PF4 enhanced the magnitude of the swelling following SRBC challenge 10 days after sensitization by the i.p. route or following sensitization by both the s.c. and i.p. routes. These studies show that PF4 has immunomodulatory activities in well-defined models of cell-mediated immunity and suggest that this agent has a potential use in the dissection of events in antigen-specific suppression.

Animals↗
PubMed1990

The sensitivity of tests to detect in vivo platelet activation induced by the removal of arterial endothelium of the baboon (Papio ursinus).

The relative sensitivities for the various in vivo and in vitro tests for platelet activation are unknown. This was studied in a baboon model where limited and more substantial injury to the vascular endothelium was inflicted. The endothelium of a segment of the right carotid artery was removed with a balloon catheter on day 0 (limited de-endothelialisation), and that of the left carotid artery, abdominal aorta and left femoral artery on day 7 (substantial de-endothelialisation). Eight baboons (Papio ursinus) were used. Baseline tests for platelet activation (platelet volume, platelet density, platelet aggregate ratio, and platelet and plasma levels of platelet factor 4 [PF4] and beta-thromboglobulin [beta-TG]) were performed 7 days before de-endothelialisation and repeated on days 1, 9 and 16. The kinetics of indium-111-labelled platelets were measured after substantial de-endothelialisation. Sham operations were done on 3 animals exactly as in the test, except that the balloon injuries were not inflicted. No influence on the results of the platelet function tests was found. The only test capable of detecting limited injury to the endothelium was the measurement of plasma PF4. The mean platelet life-span (MPLS) shortened, mean platelet density decreased, the circulating platelet aggregate ratio decreased, and plasma levels of PF4 and beta-TG increased (P less than 0.05 in all instances) after the substantial endothelial injury. The mean platelet volume, intraplatelet PF4 and beta-TG, and the in vivo distribution and sites of sequestration of labelled platelets were poor tests for in vivo platelet activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Plasma concentrations of platelet-specific proteins in different stages of essential hypertension: interactions between platelet aggregation, blood lipids and age.

Plasma beta-thromboglobulin (beta TG) and platelet factor 4 (PF4) were significantly higher in a group of 116 hypertensive men than in a normotensive group of 142 men. They increased with the stage of hypertension but the level did not correlate with the age of the subjects. Platelet aggregation was similar in the two groups and positively correlated with the age of the subjects in the normotensive group but not in the hypertensive group. A strong positive correlation was observed between the levels of plasma beta TG and PF4 and between platelet aggregation to ADP and that to epinephrine in both the hypertensive and normotensive groups. However, there was no correlation between the level of plasma beta TG or PF4 and platelet aggregation. Plasma antithrombin III was lower in the hypertensive group than in the normotensive group. These studies suggest that plasma levels of beta TG and PF4 are closely related to the stage of hypertension and are better indicators than aggregation of in vivo platelet activation in hypertensive subjects. Enhanced platelet activation may be involved in the acceleration of hypertensive arteriovascular damage and atherosclerosis.

Adenosine Diphosphate↗
PubMed1989

Discrimination between platelet-mediated and coagulation-mediated mechanisms in a model of complex thrombus formation in vivo.

To study mechanisms of complex thrombus formation in vivo, and to compare the relative antithrombotic effects of anticoagulants and antiplatelet agents, a model was developed in baboons. Segments of collagen-coated tubing followed by two sequentially placed expansion chambers exhibiting disturbed flow patterns were exposed to native blood under laminar flow conditions. The device was incorporated for 1 hour into an exteriorized arteriovenous shunt in baboons under controlled blood flow (20 ml/min). Morphologic evaluation by scanning electron microscopy showed that thrombi associated with collagen were relatively rich in platelets but thrombi in the chambers were rich in fibrin and red cells. Deposition of indium 111-labeled platelets was continuously measured with a scintillation camera. Platelet deposition increased in a linear (collagen-coated segment) or exponential (chambers 1 and 2) fashion over time, with values after 40 minutes averaging 24.1 +/- 3.3 x 10(8) platelets (collagen segment), 16.7 +/- 3.4 x 10(8) platelets (chamber 1), and 8.4 +/- 2.4 x 10(8) platelets (chamber 2). Total fibrinogen deposition after 40 minutes was determined by using iodine 125-labeled baboon fibrinogen and averaged 0.58 +/- 0.14 mg in the collagen segment, 1.51 +/- 0.27 mg in chamber 1, and 0.95 +/- 0.25 mg in chamber 2. Plasma levels of beta-thromboglobulin (beta TG), platelet-factor 4 (PF4), and fibrinopeptide A (FPA) increased fourfold to fivefold after 60 minutes of blood exposure to the thrombotic device. Platelet deposition onto the collagen segment, chamber 1, and chamber 2 was linearly dependent on the circulating platelet count. Platelet accumulation in chamber 1 and chamber 2 was also dependent on the presence of the proximal collagen segment. An anticoagulating dose of standard heparin decreased platelet deposition in the chambers (p less than 0.05) but did not decrease deposition onto the collagen segment. Although beta TG and PF4 levels remained elevated after the administration of standard heparin, the elevation in plasma FPA was interrupted. Further evidence that the thrombotic process was dependent on platelets was provided by the finding that prostaglandin I2 at high concentration (35 ng/ml) decreased platelet deposition onto the collagen segment and in chambers 1 and 2, decreased beta TG and PF4 release, and reduced FPA formation. The combination of standard heparin and PGI2 produced the most potent inhibition of platelet thrombus formation and prevented the increases in plasma PF4, beta TG and FPA.

Animals↗
PubMed1989

[Antiplatelet effects of combination therapy with low-dose aspirin and ticlopidine in cerebral ischemia].

Antiplatelet effects of combination therapy with aspirin and ticlopidine were investigated in comparison with single aspirin or ticlopidine therapy in 62 patients with cerebral thrombosis or transient ischemic attack. The 14, 21 and 27 patients were given orally daily aspirin 300mg, ticlopidine 200mg and aspirin 81mg with ticlopidine 100mg, respectively. Various platelet function tests were performed before and a week after medication. They included platelet aggregation (PA) to adenosine diphosphate (ADP), arachidonic acid (AA) and platelet activating factor (PAF) with turbidimetry, plasma beta-thromboglobulin (beta TG), platelet factor 4(PF4), thromboxane B2(TXB2) and 6keto-prostaglandin-F1 alpha(6keto PGF1 alpha) with radioimmunoassay, bleeding time with Simplate device, and platelet survival and lysis with Indium-111-tropolone-labelled platelets. Aspirin inhibited PA to ADP and AA but not to PAF, while ticlopidine inhibited PA to ADP and PAF but not to AA. In contrast, aspirin with ticlopidine inhibited PA to all of these agonists despite their smaller doses used. Aspirin reduced plasma TXB2 but not beta TG or PF4, while ticlopidine reduced beta TG and PF4 but not TXB2. On the contrary, aspirin with ticlopidine reduced TXB2 as well as beta TG and PF4. 6keto PGF1 alpha tended to be reduced by aspirin 300mg alone but not by ticlopidine with or without aspirin 81mg. Bleeding time was significantly prolonged by aspirin or ticlopidine alone, although most prolongation was produced by combination of aspirin and ticlopidine. Platelet survival and lysis remained unaltered in 4 patients treated with aspirin or ticlopidine alone, whereas platelet survival was prolonged and platelet lysis was reduced in 4 patients treated with both aspirin and ticlopidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Multiple and alternative adhesive responses on defined substrata of an immortalized dorsal root neuron hybrid cell line.

Attachment and neurite extension processes have been evaluated for an immortalized derivative cell of a rat dorsal root neuron after fusion with a mouse neuroblastoma cell (the clonal F11 hybrid cell line) and these processes compared with previous studies of neuroblastoma cells, since both cell types may be derived from the neural crest of the developing embryo. Biochemically defined substrata were provided by human plasma fibronectin (pFN), the heparan sulfate-binding protein platelet factor-4 (PF4), and the ganglioside GM1-binding protein cholera toxin B subunit (CTB). While some attachment of unsupplemented cells was noted on CTB substrata, GM1 supplementation permitted F11 cells to attach as well on CTB as on pFN or PF4. On PF4, very few neurite processes were observed while on pFN two morphologically distinct types of neurites could be identified: short, linear processes in a low percentage of cells resembling those of neuroblastoma cells and long, irregular and narrow processes in a higher percentage of cells resembling those of dorsal root neurons. On CTB, neurites of the latter class were even more prominent; however, cell bodies on CTB failed to spread by cytoplasmic extension as commonly observed in F11 cells on pFN and, to some extent, on PF4. The formation of both neurite classes on either pFN or CTB was completely inhibited by low concentrations of an RGDS (Arg-Gly-Asp-Ser) peptide in the medium of cultures, indicating the significance of pFN's binding to cell surface integrin or ganglioside GM1's possible interaction with integrin for mediating the differentiative process. In contrast, neurite formation of neuroblastoma cells is refractile to the soluble peptide as reported previously. Neurite extensions of F11 cells on either pFN or CTB were comparably sensitive to low concentrations of cytochalasin D, revealing the mediation of microfilament reorganization in these processes. Treatment of F11 cells with cycloheximide failed to inhibit neurite extension on pFN but did partially inhibit extension on CTB; this contrasts with the very high sensitivity of neurite formation by neuroblastoma cells on CTB substrata reported previously.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1980

[Clinical applications of beta-thromboglobulin and platelet factor 4 radioimmune assays (author's transl)].

beta-Thromboglobulin (beta-TG) and the anti-heparin activity platelet factor 4 (PF4) were simultaneously assayed by a radioimmune method in 108 subjects, most of whom had already be studied for platelet kinetics. The following data were obtained : while there was no technical cross-reaction, the two assays correlated closely, which indicates that they explore the same physiological phenomena : when controls were chosen at random in a population of wide age range, considerable differences were observed in the results, the values that could be considered excessive in a large percentage of cases, particularly among old, "normal" individuals ; there was no correlation between beta-TG and PF4 values on the one hand platelet destruction rate on the other ; plasma levels of beta-TG and PF4 were significantly higher in patients with vascular diseases and polycythaemia vera than in control but clearly overlapped with the values observed in controls of the same age group. The clinical significance of these data requires, to be assessed, a long-term prospective study aimed at determining whether patients with high beta-TG and PF4 levels present a high risk of thromboembolic complications and whether this risk can be reduced by correcting the biological abnormality with agents altering platelet function.

Adult↗
PubMed1982

Release of lysosomal hydrolases during simulated extracorporeal circulation.

Contact with surfaces results in activation of formed blood elements. This study demonstrates that during extracorporeal circulation, release of lysosomal enzymes occurs concomitantly with platelet granule secretion. Fresh, heparinized human blood was recirculated for 2 hours at 1,000 ml/min at 37 degrees C in silicone rubber circuits containing a membrane oxygenator (0.85 m2). The plasma levels of a platelet-specific protein, low affinity platelet factor 4 (LA-PF4), rose from less than 0.5 to 16 +/- 3 SEM microgram/ml plasma, indicating extensive release of platelet alpha granule contents. Concurrently, plasma activity of acid phosphatase and N-acetyl-beta-glucosaminidase increased nearly fivefold. Platelet inhibition prevented release of LA-PF4 and reduced acid phosphatase levels, but failed to alter the levels of N-acetyl-beta-glucosaminidase. Lidocaine (10 to 20 microgram/ml), however, prevented the rise in N-acetyl-beta-glucosaminidase activity and diminished acid phosphatase levels without altering secretion of LA-PF4. The failure of platelet inhibitors to block the increase in N-acetyl-beta-glucosaminidase, and the efficacy of lidocaine to do so without altering LA-PF4 secretion, suggest that leukocytes, not platelets, are the primary source of this lysosomal enzyme. Although acid phosphatase activity measured in plasma my be derived from leukocytes, platelet membranes, and not lysosomes, appear to be a more likely source. Release of hydrolytic enzymes from formed blood elements during cardiopulmonary bypass may cause endothelial cell injury and thus contribute to the increased vascular permeability associated with extracorporeal circulation.

Acetylglucosaminidase↗
PubMed1982

Proteoglycan carrier of human platelet factor 4. Isolation and characterization.

A large scale purification procedure for the human platelet factor 4 proteoglycan carrier molecule has been developed. A yield of 46% and a 33,000-fold purification have been achieved, using poly-L-lysine-Sepharose affinity column chromatography, PF4-agarose affinity column chromatography, and Bio-Gel A-0.5m gel filtration. The purified proteoglycan migrates as a single band during electrophoresis on cellulose acetate strips. A single symmetric peak was observed in sedimentation velocity analysis with an s value of 2.85. The molecular weight of the proteoglycan was determined to be 53,000 by sedimentation equilibrium. The purified proteoglycan contains 32% uronic acid, 31% galactosamine, 6.1% sulfate, and 9.9% protein. Aspartic acid, glutamic acid, leucine, glycine, and serine account for 55% of the total amino acids. The chondroitinase AC digest of the proteoglycan is sensitive to hydrolysis by chondro-4-sulfatase but not by chondro-6-sulfatase, indicating the presence of chondroitin 4-sulfate but not chondroitin 6-sulfate in the proteoglycan molecule. The interaction between this proteoglycan carrier of human PF4 and PF4 is strongly ionic strength-dependent. 0.3 M NaCl is required to dissociate the proteoglycan PF4 complex.

Amino Acids↗
PubMed1993

Comparative analysis of the human macrophage inflammatory protein family of cytokines (chemokines) on proliferation of human myeloid progenitor cells. Interacting effects involving suppression, synergistic suppression, and blocking of suppression.

Macrophage inflammatory protein (MIP)-1 alpha, part of a family termed chemokines, has been implicated in suppression of hemopoietic stem and progenitor cell proliferation. The chemokine family has been organized into two subgroups with MIP-1 alpha, MIP-1 beta, macrophage chemotactic and activating factor (MCAF) and RANTES belonging to one subgroup, and GRO-alpha, MIP-2 alpha (GRO-beta), MIP-2 beta (GRO-gamma), platelet factor 4 (PF4), IL-8, and neutrophil activating peptide (NAP)-2 belonging to the other. These molecules were evaluated for effects on colony formation by human bone marrow multipotential (CFU-GEMM), erythroid (BFU-E) and granulocyte-macrophage (CFU-GM) progenitor cells. None of the chemokines stimulated colony formation in the absence of CSF, or influenced colony formation stimulated by a single growth factor such as granulocyte-macrophage-CSF or erythropoietin. However, MIP-1 alpha, MIP-2 alpha, PF4, IL-8, and MCAF suppressed in dose-response fashion colony formation of immature subsets of myeloid progenitor cells stimulated by GM-CSF plus steel factor. Effects were apparent on low density and CD34 HLA-DR(+)-sorted marrow cells in which up to 88.4% of the cells were composed of progenitor cells, suggesting direct effects on the progenitors themselves. Up to 2500-fold less of each chemokine could be used to demonstrate synergistic suppression when any two of these five chemokines were used together at low concentrations, effects also apparently directly on the progenitors. In contrast, MIP-1 beta, MIP-2 beta, GRO-alpha, NAP-2, and RANTES were not suppressive nor did they synergize with MIP-1 alpha, MIP-2 alpha, PF4, IL-8, or MCAF to suppress. However, a fivefold excess of MIP-1 beta blocked the suppressive effects of MIP-1 alpha. Similarly, a fivefold excess of either MIP-2 beta or GRO-alpha blocked the suppressive effects of IL-8 and PF4. These suppressing, synergizing and blocking effects may be of relevance to blood cell regulation.

Animals↗
PubMed1993

Studies of thromboxane B2, platelet factor 4, and fibrinopeptide A in bleeding-time blood of patients deficient in von Willebrand factor, platelet glycoproteins Ib and IIb-IIIa, and storage granules.

The blood volumes and concentrations of thromboxane B2 (TxB2), platelet factor 4 (PF4), and fibrinopeptide A (FPA) were measured every 30 seconds in bleeding-time blood in normal subjects and in patients with idiopathic thrombocytopenic purpura (ITP), delta and alpha delta storage pool deficiency (SPD), Bernard-Soulier Syndrome (BSS), thrombasthenia (TSA), and von Willebrand's disease (vWD). Data were fitted to second-order (TxB2, PF4, and FPA) or third-order (volumes) polynomials. Average values for various parameters over fixed-time intervals were determined by numerical methods. The bleeding time was greater than 15 minutes in all patient groups and the initial bleeding, as reflected by the initial slope of the fitted blood volume curves, was increased in ITP, BSS, and SPD (delta-SPD in particular), but not in vWD and TSA. The increased values for both the initial slope and the volume of blood collected after 2 minutes in SPD suggest that vascular tone may be modulated, in part, by dense granule substances such as adenosine triphosphate (ATP) or serotonin. In TSA, uniquely, both platelet (TxB2 and PF4) and coagulation (FPA) values were increased in early bleeding samples (initial slope). In vitro studies of TxB2 production, together with previous flow studies of fibrin formation, also suggest enhanced activation and coagulant properties of thrombasthenic platelets. In other patients, reduced values of all substances at later times may reflect impaired platelet-fibrin plug formation in the high-shear regions at the ends of transected blood vessels. However, the initial slopes of the fitted curves for both TxB2 and PF4 were normal in vWD, suggesting that the early appearance of these substances may typically be from platelets that are adherent to collagen within the lower shear environment of the wound surface. The finding that FPA values were not decreased initially in any patient group, including ITP, but were decreased at later times (except for TSA), suggests that early fibrin formation occurs independently of platelets in the low-shear environment of the wound surface, whereas at later times fibrin is formed in a platelet-dependent manner in the high-shear regions at the ends of transected vessels.

Adult↗
PubMed1979

[Clinical significance of the radioimmunological determination of beta-thromboglobulin and platelet factor 4].

Recently new radioimmunoassay methods have been established to measure plasma concentrations of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), platelet release products which are set free when platelets aggregate. Plasma concentrations of beta-TG and PF4 were investigated in disorders with increased thromboembolic risk. Extremely high concentrations of these platelet proteins were found in patients with venous thrombosis, pulmonary embolism, polycythemia vera, and chronic renal failure. Moderately increased beta-TG and PF4 levels were observed in patients with peripheral vascular disease, coronary artery disease, chronic rheumatoid arthritis, multiple myeloma, and diabetes mellitus. These data indicate, that plasma concentrations of beta-TG and PF4 are useful parameters for the evaluation of the "in vivo" platelet activity. By using these new methods for clinical applications special blood sampling conditions have been taken into account; moreover one has to consider that the plasma levels of the platelet "release products" are dependent from renal function.

Arthritis, Rheumatoid↗