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PubMed1982

Comparison between induced platelet aggregation and circulating platelet aggregates as platelet function tests in patients with transient ischemic attacks.

Routine blood analysis, platelet counts, number of circulating platelet aggregates (CPA) and platelet aggregation in vitro against adenosine-diphosphate (ADP), epinephrine and collagene were studied in 45 healthy controls, in 10 hospitalized patients with other neurological diseases than stroke and in 12 patients with transient ischemic attacks (TIA) before and after prophylactive treatment with anticoagulants (AC) or antiplatelet drugs (APD). Except for lower hemoglobin and hematocrit levels in women, sex, smoking, oral contraceptives of pregnancy did not significantly influence the routine blood parameter. Smoking females taking oral contraceptive had an increased number of CPA and the most easily induced aggregation in vitro. Patients with TIA had no significant differences in blood or platelet findings versus the healthy controls (except smoking females on oral contraceptives) or the non-stroke patients, even though individual patients could have high numbers of CPA and an easily induced platelet aggregation in vitro. Treatment with AC did not influence platelet function, whereas APD therapy decreased the number of CPA and inhibited the secondary platelet aggregation in vitro.

Blood Cell Count↗
PubMedDate not supplied

[Low concentrations of epinephrine can augment shear stress-induced platelet aggregation].

Platelet aggregation induced by shear stress is distinct from that induced by an agonist such as ADP or collagen. The physiological significance of shear-induced platelet aggregation was investigated by measuring the effects of the presence of physiological concentrations of epinephrine. Blood samples were taken from 10 normal volunteers who had received no drugs known to interfere with platelet functions for 1 month preceding the study. Blood was mixed with 1/10 volume of 3.1% sodium citrate solution. Platelet-rich plasma and platelet-poor plasma were prepared by centrifugation at 100 g for 15 min and 2,000 g for 15 min, respectively. The platelet count of platelet-rich plasma was adjusted to 3 x 10(5)/microliters. Shear-induced platelet aggregation in platelet-rich plasma was determined using a modified cone and plate viscometer controlled by a personal computer system. The intensity of light transmission was continuously recorded. The percent platelet aggregation was calculated according to the Lambert-Beer equation. Platelet aggregation occurred under both low (12 dyn/cm2) and high (108 dyn/cm2) shear stress. More significant aggregation was observed under high shear stress. The maximum percent platelet aggregation was 44.7 +/- 13.4%, which increased to 53.3 +/- 10.0% in the presence of 10 pg/ml epinephrine. With 100 pg/ml of epinephrine, shear-induced platelet aggregation induced by 12 dyn/cm2 shear significantly increased, but the effects on shear-induced platelet aggregation of 108 dyn/cm2 shear were not uniform. Shear-induced platelet aggregation is enhanced by physiological concentrations of epinephrine, which may be a cause of arterial thrombotic occlusion in sympathomimetic states.

Adult↗
PubMed1998

[Vertigo and dizziness related to platelet aggregability].

Platelet aggregates were measured in 82 cases with vertigo and dizziness and 60 cases with additional symptom of headache (so-called cervical vertigo). Results showed that patients with vertigo and dizziness had increased aggregability and patients with cervical vertigo were within normal range (p < 0.0001). 53 cases of these with vertigo and dizziness were administrated platelet aggregation inhibitors (mainly ticlopidine). After 1 approximately 2 weeks, most of patients became symptom free, and at this time platelet aggregates of these patients were suppressed to within normal range. Then patients were followed with chronological measurements of platelet aggregates. During this time, aggregabilities were attempted to be kept within the normal range, thus dose of platelet aggregation inhibitor was controlled depending on the result of aggregability. Also patients were encouraged to show good drug compliance by being informed of sudden increasing aggregability. One patient experienced recurrence of vertigo after ceasing the medicine. This study demonstrates that platelet aggregation may increase in most of patients with not only vertigo but also dizziness in whom administration of a platelet aggregation inhibitor is effective. It also stresses that chronological measurements of platelet aggregations are important to control the dose of medication.

Adult↗
PubMed1995

Effects of lomefloxacin and sparfloxacin on human platelet aggregation.

Platelet aggregation is inhibited by high concentrations of most antibiotics. For this reason it is important to evaluate the effects of new antimicrobial agents on platelet aggregation. Lomefloxacin and sparfloxacin are new difluorinated quinolone antimicrobial agents. The aim of this work was to evaluate in vitro the effects of lomefloxacin and sparfloxacin on adenosinediphosphate (ADP) and collagen-induced human platelet aggregation. Our data showed that both antibiotics (lomefloxacin and sparfloxacin) at therapeutic doses did not inhibit in vitro human platelet aggregation. Lomefloxacin, only at the highest tested concentration (1 mg/ml), which is far higher than the clinically achievable one, significantly (P < 0.05) inhibited collagen-induced platelet aggregation. Sparfloxacin also caused inhibition of collagen and ADP-induced human platelet aggregation only at the highest tested concentration (0.01 mg/ml), which is higher than that reached in vivo. These findings suggest that therapeutic doses of lomefloxacin and sparfloxacin do not affect human platelet aggregation.

Adenosine Diphosphate↗
PubMed1988

Diltiazem potentiates the inhibitory effect of aspirin on platelet aggregation.

Platelet aggregation in vivo occurs through the combined effects of many agonists. Aspirin inhibits platelet aggregation but its antiaggregate effects can be overcome by the synergistic action of sodium arachidonate (AA) plus platelet activating factor (PAF). We tested the effect of a calcium entry-blocking agent, diltiazem, on AA-PAF-induced platelet aggregation in platelet-rich plasma from seven healthy volunteers. The studies were done before and after aspirin (100 mg/day) administration for 7 to 10 days. Stimulation of platelet was done in vitro by AA, PAF, or both. Before aspirin treatment, diltiazem (2 micrograms/ml) added in vitro to the platelet-rich plasma inhibited platelet aggregation induced by AA (0.75 mmol/L) by 50%. When PAF was used the inhibition of aggregation was obtained at a lower concentration of diltiazem (0.4 to 1 microgram/ml). After aspirin treatment, AA-induced aggregation was inhibited, and PAF alone (30 nmol/L) produced a first-wave aggregation followed by complete disaggregation. When AA and PAF were added together a full aggregation of postaspirin treatment platelets was obtained. Diltiazem added in vitro at the clinically attainable concentration of 0.1 microgram/ml produced a complete inhibition of this AA-PAF synergism on platelet aggregation. These results suggest that administration of a combination of low-dose aspirin and diltiazem may be of greater benefit than aspirin alone for prophylaxis of cardiovascular diseases where platelets are involved in the pathogenesis.

Arachidonic Acids↗
PubMed1987

Effect of omega-3 fatty acid supplementation on platelet aggregability and platelet produced thromboxane.

We investigated the sustained effect of 12-week supplementation of 2.880 g/day of omega-3 fatty acids on platelet aggregability, platelet produced thromboxane B2 concentration and serum fatty acid composition in a double-blind controlled trial in 44 healthy mildly overweight eastern Finnish men recruited from a representative population sample. The supplementation was discontinued seven days before the biochemical measurements. Body weight, alcohol consumption and dietary composition remained constant during the study. Even though the percentage of eicosapentaenoic acid (20:5 omega 3) in total serum lipids increased by 37% (p less than 0.01) and that of dihomo-gamma-linolenic acid (20:3 omega 6) decreased by 18% (p less than 0.01) more in the omega-3 supplemented than placebo group during supplementation, there were no significant differences in the changes in either the ADP induced platelet aggregation or in vitro platelet produced thromboxane B2 concentration between the groups. These data suggest that omega-3 fatty acids have no detectable sustained effect either on ADP induced platelet aggregation or on thromboxane produced by the platelets in vitro.

Adult↗
PubMed2006

Disabled-2 is a novel alphaIIb-integrin-binding protein that negatively regulates platelet-fibrinogen interactions and platelet aggregation.

Platelet aggregation plays a pivotal role in the haemostatic process and is involved in the pathological counterpart of arterial thrombosis. We have shown that the adapter protein disabled-2 (DAB2) is expressed abundantly in platelets. In this study, DAB2 was found to distribute in the platelet alpha-granules and was released from the granular compartment upon platelet activation. The secreted DAB2 binds to the extracellular region of alphaIIbbeta3 integrin on the platelet surface through the phosphotyrosine-binding domain. The DAB2-platelet interactions result in the inhibition of agonist-induced platelet aggregation with the exception of thrombin, a DAB2 protease that renders DAB2 inactive. Biochemical and mutational analysis revealed that the DAB2 cell-adhesion Arg-Gly-Asp (RGD) motif (amino acid residues 64-66) and the alphaIIb-integrin-fibrinogen-binding region (amino acid residues 171-464) are important for the DAB2-platelet interactions. Such interactions compete for the binding of alphaIIb integrin with fibrinogen and provide a mechanism for DAB2 to inhibit platelet aggregation. Accordingly, the synthetic RGD-motif-containing DAB2 peptide PDARGDKM also elicited anti-platelet aggregation activity. These findings demonstrate for the first time that DAB2 is an alphaIIb-integrin-binding protein that plays a novel role in the control of platelet-fibrinogen interactions and platelet aggregation.

Adaptor Proteins, Signal Transducing↗
PubMed1993

Studies on the role of platelet eicosanoid metabolism and integrin alpha IIb beta 3 in tumor-cell-induced platelet aggregation.

Platelet eicosanoid metabolism resulting from tumor-cell-induced platelet aggregation (TCIPA) was examined in a homologous in vitro system. Rat Walker 256 carcinosarcoma cells induced the aggregation of rat platelets via a thrombin-dependent mechanism with concomitant production of eicosanoid metabolites (e.g., 12-HETE, TXA2). TCIPA was dependent on the concentration of tumor cells inducing aggregation, as well as cyclooxygenase and lipoxygenase products. Cyclooxygenase inhibitors, but not lipoxygenase inhibitors, blocked platelet aggregation induced in vitro by a low concentration of agonist. At a high agonist concentration, neither cyclooxygenase nor lipoxygenase inhibitors alone affected platelet aggregation; however, the combined inhibition of both the cyclooxygenase and lipoxygenase pathways resulted in subsequent inhibition of platelet aggregation regardless of agonist concentration. The extent of platelet TXA2 and 12-HETE biosynthesis was likewise dependent on and correlated with agonist concentration. The inhibitors used in this study did not significantly inhibit protein kinase C activity at the doses tested. Platelet surface glycoprotein alpha IIb beta 3 play an important role in platelet aggregation. The effect of platelet cyclooxygenase and lipoxygenase inhibition in regulating alpha IIb beta 3 surface expression was examined by flow cytometric analysis. Thrombin stimulation of washed rat platelets resulted in significantly increased surface expression of platelet alpha IIb beta 3 integrin complex. The enhanced surface expression was not inhibited by a cyclooxygenase inhibitor (aspirin), a thromboxane synthase inhibitor (CGS-14854) or a thromboxane receptor antagonist (SQ 29,548), nor was it stimulated by a thromboxane A2 mimic (pinane-thromboxane A2). However, alpha IIb beta 3 expression was blocked by lipoxygenase inhibition and stereospecifically increased by the platelet lipoxygenase metabolite 12(S)-HETE. These results suggest that both the platelet lipoxygenase and cyclooxygenase pathways are important for TCIPA but that different mechanisms of action are involved.

Animals↗
PubMed1996

Polyunsaturated fatty acids and platelet aggregation.

Platelets take part in haemostasis and thrombosis, and studies have been carried out to try to understand how dietary fatty acids could reduce platelet activation and thus the risk of cardiovascular disease. Unfortunately, many of these studies had serious methodological flaws, and the shortcomings in their study designs are probably the main reason for contradictory results in humans. The evidence concerning linoleic acid is not consistent, but intervention studies show increased platelet aggregation to various agonists after high-linoleic-acid diets. On the other hand, intake of alpha-linoleic acid either has no effect or leads to decreased platelet aggregation when compared with linoleic acid. High intake of long-chain n-3 fatty acids of fish or fish oils seems to usually decrease platelet aggregation. To date, there have not been many studies on the effect of platelet aggregation of small or reasonable amounts of n-3 fatty acids.

Coronary Disease↗
PubMed1984

The effects of antiallergic and bronchodilator drugs on platelet-activating factor (PAF-acether) induced bronchospasm and platelet aggregation.

Platelet activating factor (PAF-acether) is a potential mediator of asthma and inflammation. Recently, the suggestion was made that inhibition of PAF-acether by disodium cromoglycate (DSCG) might be partly responsible for the effectiveness of DSCG in asthma. We have extended these studies and examined the effects of antiallergic and bronchodilator drugs on PAF-acether induced bronchospasm after i.v. administration in guinea pigs and in vitro platelet aggregation in rabbits. Neither DSCG nor Wy-41,195, a potent orally effective antiallergic, altered either of the PAF-acether responses. Furthermore, aerosolized ipratropium, promethazine, ketotifen and FPL 55712 failed to affect the PAF-acether-induced bronchospasm. The same drugs were also ineffective against platelet aggregation induced by PAF-acether. In contrast, aerosolized thiazinamium chloride inhibited the bronchospasm and also inhibited PAF-acether-induced platelet aggregation. Thiazinamium chloride possessed weak antiaggregatory effects against ADP and was without effect against arachidonic acid-induced platelet aggregation. Both lipoxygenase and cyclooxygenase products of arachidonic acid metabolism appear to be involved in PAF-acether bronchospasm since i.v. administered lipoxygenase inhibitors (phenidone, BW755c and NDGA) and indomethacin independently inhibited this in vivo response. However, these drugs failed to alter platelet aggregation to PAF-acether. Thiazinamium chloride may be capable of directly antagonizing the PAF-acether-induced platelet aggregatory response and, in addition, inhibiting the synthesis and/or effects of bronchoconstrictor amines and endogenously generated arachidonic acid metabolites.

Animals↗
PubMed1987

Increased surface expression of the membrane glycoprotein IIb/IIIa complex induced by platelet activation. Relationship to the binding of fibrinogen and platelet aggregation.

Platelet activation altered the binding of three monoclonal antibodies (monovalent Fab' fragment) directed against the glycoprotein (GP) IIb/IIIa complex. An increased binding of two- to threefold occurred after stimulation with thrombin or phorbol myristate acetate (PMA), with slight but significant increase in the dissociation constants (Kd) of two antibodies (LJ-CP8 and LJ-P9). In contrast, no statistically significant changes were observed with ADP-stimulated platelets. The increased binding of LJ-CP3, but not of the other two antibodies, to activated platelets decreased by 30% to 40% in the presence of EDTA at 22 to 25 degrees C. Platelets stimulated by thrombin or PMA bound more fibrinogen than did those stimulated by ADP, and significant differences in the extent but not in the affinity of fibrinogen binding were observed with various platelet agonists. When the pool of GP IIb/IIIa molecules exposed on the surface of unstimulated platelets was reacted with the monoclonal antibody LJ-CP3 to block ADP-induced fibrinogen binding and platelet aggregation, stimulation with thrombin or PMA still induced substantial binding of antibody and fibrinogen, and aggregation ensued. Therefore, platelets exposed to "strong" agonists exhibit an increased number of surface-oriented epitopes associated with GP IIb/IIIa. The GP IIb/IIIa molecules bearing these newly exposed epitopes are functional in that they can bind fibrinogen and mediate platelet aggregation.

Antibodies, Monoclonal↗
PubMed2004

Effects of trace element levels on platelet aggregation.

Platelet aggregation was measured by an optical method in 32 patients with iron-deficiency anemia at the time of diagnosis and after a period of supplementation with iron. Epinephrine- and adenosine diphosphate-induced platelet aggregation were lower in anemic patients than in the controls (p<0.05). After iron-supplementation therapy, these values showed no significant differences. If induced by collagen or ristocetin, platelet aggregation was the same for patients and controls, but increased after treatment of patients (p<0.05). The plasma zinc values did not show significant differences among the subjects included in this study. These results show that iron is involved in the enzymatic systems that regulate platelet aggregation. The exact nature of this interaction is still to be determined.

Anemia, Iron-Deficiency↗
PubMed2004

Direct demonstration of involvement of the adaptor protein ShcA in the regulation of Ca2+-induced platelet aggregation.

Platelet aggregation is mediated by conformational change of integrin alpha(IIb)beta(3). Tyrosine-phosphorylation of cytoplasmic domain of beta(3) upon platelet activation has been demonstrated to play a critical role in this process. Recently, the adaptor protein ShcA has been shown to bind to the tyrosine-phosphorylated beta(3), while it remains open whether ShcA plays any role in platelet aggregation. Here, we show that ShcA bound to tyrosine-phosphorylated beta(3)-tail peptide through its phosphotyrosine-binding domain in vitro. Then, we examined the involvement of ShcA in platelet aggregation by a previously established in vitro assay using platelets permeabilized with streptolysin-O, where exogenous addition of platelet cytosol is required for reconstitution of the Ca(2+)-induced aggregation. When ShcA was specifically depleted with anti-ShcA antibody from the cytosol, this ShcA-depleted cytosol lost the aggregation-supporting activity, which was rescued by addition of purified recombinant ShcA. Thus, ShcA is essential for the Ca(2+)-induced platelet aggregation.

Adaptor Proteins, Signal Transducing↗
PubMed2003

Abciximab, eptifibatide, and tirofiban exhibit dose-dependent potencies to dissolve platelet aggregates.

Platelet GPIIb/IIIa antagonists are not only used to prevent platelet aggregation, but also in combination with thrombolytic agents for the treatment of coronary thrombi. Recent data indicate a potential of abciximab alone to dissolve thrombi in vivo. We investigated the potential of abciximab, eptifibatide, and tirofiban to dissolve platelet aggregates in vitro. Adenosine diphosphate (ADP)-induced platelet aggregation could be reversed in a concentration-dependent manner by all three GPIIb/IIIa antagonists when added after the aggregation curve reached half-maximal aggregation. The concentrations chosen are comparable with in vivo plasma concentrations in clinical applications. Disaggregation reached a maximum degree of 72.4% using 0.5 microg/ml tirofiban, 91.5% using 3.75 microg/ml eptifibatide, and 48.4% using 50 microg/ml abciximab (P < 0.05, respectively). A potential fibrinolytic activity of the GPIIb/IIIa antagonists was ruled out by preincubation with aprotinin or by a plasma clot assay. A stable model Chinese hamster ovary (CHO) cell line expressing the activated form of GPIIb/IIIa was used to confirm the disaggregation capacity of GPIIb/IIIa antagonists found in platelets. Not only abciximab, but also eptifibatide and tirofiban have the potential to disaggregate newly formed platelet clusters in vitro. Because enzyme-dependent fibrinolysis does not appear to be involved, competitive removal of fibrinogen by the receptor antagonists is the most likely mechanism.

Abciximab↗
PubMed1969

Coumarin therapy and platelet aggregation.

Platelet aggregation has been related to blood coagulation studies in patients on nicoumalone, a coumarin anticoagulant. Aggregation studies were performed by means of Chandler's tube and the adenosine diphosphate (A.D.P.)-induced optical density method. Platelet aggregation in Chandler's tube has been shown to be quite different from A.D.P. aggregation and to be dependent on the "intrinsic" (blood) clotting system. When the intrinsic system was depressed by coumarin anticoagulant, aggregation was delayed in Chandler's tube, but patients with a predominantly "extrinsic" (tissue) system defect gave normal results even when their prothrombin time was excessively prolonged. In contrast there was an increased response to A.D.P. in the anticoagulated patients.The study emphasizes the different mechanisms of platelet aggregation, which we have referred to as coagulation-induced and A.D.P.-induced aggregation. It also shows the limitations of routine control of oral anticoagulants by prothrombin time alone, as the coagulation-induced platelet aggregation appears to be quantitatively related to the overall level of clotting factors in the intrinsic system and independent of the extrinsic system.

Adenine Nucleotides↗
PubMed2002

Short-term diets enriched in stearic or palmitic acids do not alter plasma lipids, platelet aggregation or platelet activation status.

OBJECTIVE: To determine whether healthy males who consumed increased amounts of dietary stearic acid compared with increased dietary palmitic acid through the consumption of commercially available foods, exhibited any changes in plasma lipids, platelet aggregation or platelet activation status. DESIGN: A randomised cross-over dietary intervention. SUBJECTS AND INTERVENTIONS: Nine free-living healthy males consumed two experimental diets (stearic acid enriched, diet S, and palmitic acid enriched, diet P) for 3 weeks in a randomised cross-over design separated by a 3 week washout phase. The diets consisted of approximately 30% of energy as fat (30% of which was derived from the treatment diets) providing approximately 13 g/day as stearic acid and 17 g/day as palmitic acid on diet S and approximately 7 g/day as stearic acid and 22 g/day as palmitic acid on diet P. The dietary ratio of stearic to palmitic acids was 0.76 on diet S compared with 0.31 on diet P. Blood samples were collected on days 0 and 21 of each dietary period. RESULTS: LDL cholesterol levels and platelet aggregation response to the agonist ADP were significantly decreased (P<0.025) in subjects on diet S compared with day 0. Apart from that, there were no significant changes in plasma lipids, platelet aggregation, mean platelet volume and platelet reactivity between diets. There were no significant changes in stearic or palmitic acid levels in plasma phospholipid or triacylglycerol. There was a significant difference in palmitic acid levels in platelet phospholipids between the two diets. CONCLUSIONS: Use of commonly available foods led to a 27% increase in stearic acid (diet S) and a 19% increase in palmitic acid (diet P), on diets S and P respectively, and no significant differences between the two diets in plasma lipoprotein concentrations, platelet aggregation or platelet activation status.

Adult↗
PubMed1997

Circulating aggregated platelets, number of platelets per aggregate and platelet size in chronic dialysis patients.

The accelerated arteriosclerosis of chronic dialysis patients is multifactorial. Both non-uremic patients with atherosclerosis and uremic patients have functional platelet abnormalities. Our aim was to study platelet function in chronic dialysis patients and to correlate the findings with the presence of cardiovascular morbidity. Fifty-three chronic dialysis patients were examined. The presence of risk factors for cardiovascular disease (CVD) was recorded, and the patients were examined for the presence of ischemic heart disease, peripheral vascular disease and cerebrovascular accident. The parameters of platelet function, which were examined with the modified Wu and Hoak method, included platelet number, percentage of totally, reversibly and irreversibly aggregated platelets, average number of platelets per aggregate and percentage of large platelets. Significant differences were found between totally aggregated platelets, reversibly and irreversibly aggregated platelets, the percentage of large platelets (p < 0.0001) and the average number of platelets per aggregate (p < 0.001) in dialysis patients compared with control persons. There was no difference between the 2 groups in platelet count. No differences were found between hemodialysis and peritoneal dialysis groups, and the duration of dialysis treatment had no effect. We conclude that platelet abnormalities evident in chronic dialysis patients are a part of the multifactorial etiology of advanced CVD and may predispose dialysis patients to CVD.

Arteriosclerosis↗