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PubMed1981

Choline magnesium trisalicylate does not impair platelet aggregation.

Blood platelet aggregation in response to adenosine diphosphate (ADP), epinephrine or collagen stimulation was measured in 9 mainly arthritic patients continually treated with choline magnesium trisalicylate for an average of 11 months. Aggregation was entirely normal in 5 of the subjects and only minimally reduced in 3 who showed suppression, in 2 cases borderline or minimal, of ADP-induced aggregation only; the reasons were unclear and the possibility of pre-treatment subnormal responses to ADP, in this group, could not be ruled out. The ninth subject showed no secondary wave of aggregation with ADP or epinephrine and only 21% aggregation with collagen, findings typical of aspirin use. She was thought to have ingested this drug unknowingly and to warrant exclusion from the evaluation. It is concluded that protracted use of choline magnesium trisalicylate does not interfere with platelet aggregation under the conditions of this study. The results obtained were consistent with the reported failure of this drug to cause significant faecal blood loss in clinical trials.

Adenosine Diphosphate↗
PubMed1990

Platelet aggregating IgG antibody to platelet surface glycoproteins associated with thrombosis and thrombocytopenia.

Previously described platelet-aggregating antibodies associated with thrombosis and thrombocytopenia required heparin for their in vivo and in vitro expression. We have observed a patient with thrombosis who became thrombocytopenic during heparin treatment, but who suffered further thrombotic events and continued thrombocytopenia for 3 months after heparin withdrawal. The patient's plasma contained a potent platelet aggregating factor reactive with both his own and normal platelets in the absence of heparin. It also caused [14C]serotonin secretion from labelled platelets from normal donors and patients with either Glanzmann's thrombasthenia or Bernard-Soulier syndrome. This factor was an IgG and was neutralized by antibody specific for IgG lambda light chains. While the patient was thrombocytopenic an IgG paraprotein with lambda light chains was detected by isoelectrofocussing. After corticosteroid treatment it disappeared and the patient recovered. The active, but not the recovery serum contained IgG which immunoprecipitated a glycoprotein with characteristics of Glycoprotein IV from platelets labelled with Na[3H]BH4/periodate. Thus platelet-aggregating IgG antibodies with direct specificity for platelet surface glycoproteins may be associated with thrombosis/thrombocytopenia.

Humans↗
PubMed1977

Photometric platelet aggregation test III: a new tool for the detection of enhancet platelet aggregation.

In clinical investigation on ehnanced platelet aggregation the changes of the various tests with time after blood sampling must be considered. The photometric PAT III for the evaluation of spontaneous aggregation showed enhanced aggregation in a high percentage of patients with vascular disease, and prospective data obtained so far make it likely that enhanced aggregation is a risk factor for thrombosis. More prospective studies are necessary to prove whether continuously enhanced spontaneous platelet aggregation is indicating progressive atherosclerosis.

Coronary Disease↗
PubMed1993

The effect of MCI-9042 on serotonin-induced platelet aggregation in type 2 diabetes mellitus.

MCI-9042, a potent inhibitor of 5HT2 receptor, was used to examine its effects on serotonin induced-aggregation of platelets obtained from patients with type 2 diabetes mellitus (DM). The extent of platelet aggregation induced by serotonin increased in DM patients without retinopathy, but the increase was further significant in DM patients with retinopathy. MCI-9042 as well as ketanserin, inhibited significantly serotonin induced-aggregation of platelets obtained from DM patients with retinopathy. MCI-9042 dose dependently inhibited platelet aggregation induced by serotonin and collagen. These results suggest that serotonin which may be released from platelets of DM patients may activate platelets together with collagen exposed on atherosclerotic endothelium and that MCI-9042 may be inhibitory to enhanced platelet aggregability under these conditions.

Adult↗
PubMed1972

The mechanism of adenosine diphosphate induced platelet aggregation: binding to platelet receptors and inhibition of binding and aggregation by prostaglandin E 1 .

1. Normal human blood platelets in stirred plasma were incubated with [(14)C]ADP for 10-360 sec and the aggregation responses were correlated with platelet bound radioactivity, the platelets being separated from the plasma within 25 sec of the end of the experiment.2. The platelet aggregation response, measured as a change in light transmittance through platelet-rich plasma, was related to the plasma [(14)C]ADP concentration and linearly related to the log platelet bound [(14)C]ADP 60-120 sec after addition of nucleotide to plasma.3. Thin layer chromatography of the platelet bound radioactivity showed that 78-90% was unmetabolized ADP, the remainder being AMP. Plasma radioactivity consisted of ADP, AMP and adenosine. There was no detectable radioactive cyclic AMP in either platelets or plasma.4. Further accumulation of radioactivity occurred after 180 sec but was not related to the aggregation response.5. Prostaglandin E(1) inhibited aggregation and platelet [(14)C]ADP accumulation when added to platelet-rich plasma 60 sec before [(14)C]ADP. There was a significant correlation between inhibition of aggregation and inhibition of [(14)C]ADP accumulation.6. Prostaglandin E(1) also reversed ADP aggregation when added to platelet-rich plasma after the nucleotide, with an accompanying decrease in platelet bound [(14)C]ADP.7. It is concluded that ADP induces platelet aggregation by binding to specific receptors probably located on the plasma membrane, and that prostaglandin E(1) inhibits this effect by interfering with the ADP binding.

Adenine Nucleotides↗
PubMed1991

The effect of the menstrual cycle and of decompression stress on arachidonic acid-induced platelet aggregation and on intrinsic platelet thromboxane production in women compared with men.

Menstrual cycle variations in platelet aggregation and thromboxane production in association with sex steroids have been reported. External stimuli such as decompression sickness have been associated with clotting activity changes, specifically, increased platelet aggregation. Differences in response of platelets from women and men, when subjected to such a stress, have been observed. This study evaluated the ability of washed platelets from women in the proliferative and secretory phases of the menstrual cycle to aggregate in response to arachidonic acid and the aggregation difference between washed platelets from women and men in response to decompression stress and arachidonic acid. Additionally, platelet thromboxane production differences between the assessed platelet populations were compared. Our results indicate no difference in platelet aggregability between phases of the menstrual cycle. A significant aggregation difference between platelets from women and men was noted. Platelets from women were more sensitive to arachidonic acid aggregation. These differences were not affected by decompression stress. No difference in thromboxane B2 production was noted between the platelet populations evaluated.

Adult↗
PubMed1989

Human endothelial cells inhibit platelet aggregation by separately stimulating platelet cyclic AMP and cyclic GMP.

Thrombin-induced platelet aggregation was monitored in a mixture of washed human platelets and cultured human endothelial cells on microcarrier beads. Endothelial cells completely inhibited platelet aggregation and enhanced the content of both cyclic AMP and cyclic GMP in the platelets. Inhibition of endothelial prostacyclin synthesis with indomethacin abolished the cyclic AMP increase in the platelets, whereas the cyclic GMP increase was unimpaired. A significant component of the endothelial anti-aggregatory effect persisted in the presence of indomethacin. This anti-aggregatory component and the elevation of cyclic GMP were blocked by the inhibitors of endothelium-derived relaxing factor (EDRF), gossypol, haemoglobin and methylene blue. These inhibitors did not affect the endothelium-induced increases in cyclic AMP or the cyclic AMP-mediated anti-aggregatory effects. Exogenous prostacyclin stimulated only platelet cyclic AMP, whereas sodium nitroprusside selectively enhanced cyclic GMP. These data suggest that the endothelium can inhibit platelet aggregation by two completely separate mechanisms, one mediated by prostacyclin and cyclic AMP, and the other by EDRF and cyclic GMP.

Biological Factors↗
PubMed1981

Two platelet aggregation inhibitors in tsetse (Glossina) saliva with studies of roles of thrombin and citrate in in vitro platelet aggregation.

Two inhibitors of platelet aggregation have been identified in saline extracts of Glossina morsitans (tsetse) salivary glands. A protein fraction (MW greater than 30 000) inhibited primary and secondary aggregation to ADP, secondary aggregation to adrenalin, and aggregation to collagen. It also caused disaggregation of platelets stimulated by ADP and adrenalin. These properties could be explained by ADP hydrolytic activity. A previously identified antithrombin fraction (MW 11 000-13 000) abolished thrombin-induced aggregation. It did not affect platelet aggregation to ADP, adrenalin or collagen, as compared to aggregation in citrate, when used as sole anticoagulant for platelet rich plasma or when added to citrated platelet rich plasma. These results fail to support hypotheses (i) that thrombin plays an important role in platelet aggregation by other agonists and (ii) that secondary platelet aggregation is an artefact induced by citrate. It is proposed that these inhibitors may be important in maintaining mouthpart and crop patency during feeding. Their discovery suggests that other arthropods may also have antiplatelet agents in their saliva which might be entomologically important, provide useful tools for platelet studies, and be of potential therapeutic interest.

Animals↗
PubMed1992

Xanthines inhibit human platelet aggregation induced by platelet-activating factor.

1. Platelet-activating factor (PAF) may be involved in the pathogenesis of asthma, and therefore the effects of the anti-asthma drugs theophylline and enprofylline on human platelet aggregation and adenosine triphosphate (ATP) release induced by PAF and adenosine diphosphate (ADP) were studied. 2. Enprofylline (50% inhibitory concentration [IC50] = 94.8 +/- 13.2 mumol/L) was more potent than theophylline (IC50 = 934.1 +/- 40.1 mumol/L) as an inhibitor of PAF-induced aggregation, and the xanthines were twice as potent as inhibitors of PAF-induced aggregation when compared with ADP-induced aggregation. ATP release was 1.4 times more sensitive to inhibition by the xanthines than aggregation. 3. Although high concentrations of xanthines inhibited platelet aggregation and ATP release induced by PAF, therapeutic concentrations are unlikely to inhibit PAF-induced effects.

Adenosine Diphosphate↗
PubMed1996

Intracellular levels of cyclic AMP and cyclic GMP differentially modify platelet aggregate size in human platelets activated with epinephrine or ADP.

We investigated the effects on human platelet aggregation of several agents that increase either intracellular cyclic AMP or cyclic GMP, using a platelet aggregometer that allows quantification of the size and number of platelet aggregates. During the initial phase of aggregation induced by epinephrine and ADP, small aggregates consisting of < 100 cells predominated; large aggregates formed later. Prostaglandin I2 (PGI2), which increases intracellular cyclic AMP, suppressed the formation of small as well as large aggregates induced by epinephrine, with ID50 values of 10.7 +/- 2.8 and 3.8 +/- 0.5 nM, respectively. ADP-induced formation of small and large aggregates was also inhibited by PGI2, with similar ID50 values. Dibutyryl cyclic AMP (db cyclic AMP), a cell-permeant form of cyclic AMP, also inhibited small and large aggregate formation induced by epinephrine or ADP, with ID50 values of 420-560 microM for small aggregates and 139-166 microM for large aggregates, respectively. On the other hand, nitroprusside, which increases intracellular cyclic GMP, inhibited only the formation of large aggregates, with an ID50 value of 454 +/- 191 nM for epinephrine-induced activation and of 2.1 +/- 0.6 microM for ADP-induced activation. Nitroprusside at 1 mM did not affect the formation of small aggregates induced by epinephrine, whereas that of large aggregates was completely blocked at 10 microM. 8-Bromo cyclic GMP (8-br cyclic GMP) also inhibited only the formation of large aggregates, with ID50 values of 140-170 microM, but not that of small aggregates induced by epinephrine and ADP. Milrinone, which increases the intracellular level of both cyclic AMP and cyclic GMP, suppressed the formation of small and large aggregates induced by epinephrine and ADP. These findings suggest that cyclic AMP and cyclic GMP differentially modify the size of aggregates formed during epinephrine or ADP activation.

Adenosine Diphosphate↗
PubMed2001

Monitoring the effects of platelet glycoprotein IIb/IIIa antagonists with a microtiter plate method for detection of platelet aggregation.

Measurement of platelet aggregation in platelet-rich plasma (PRP) is a fundamental tool in platelet studies, despite the fact that the technique required for this is time-consuming, may need large volumes of blood, and require particular skill and special equipment. The use of a microplate reader seems useful to perform platelet aggregation more rapidly and with less material. So, the aim of the present study was to validate a simple and rapid method which enables performance of kinetic measurements of platelet aggregation directly in a microtiter plate reader. Platelet aggregation was carried out in 96-well, flat-bottomed microtiter plates. Samples of PRP (140 microl/well) were placed in a microtiter plate. Agonists (10 microl/well) were added using an electronic multichannel dispenser directly before the reading was started. Measurements of the optical density were performed at 650 nm using a THERMOmax microplate reader (Molecular Devices, Sunnyvale, USA). During the run time the plate was incubated at 37 degrees C and was mixed with the automix function of the reader. The technique was verified by comparing dose-response curves of platelet agonists and glycoprotein IIb/IIIa antagonists, obtained with the standard aggregometer and with the microtiter plate reader. Platelet aggregation in microtiter plates is simple and rapid. It offers the advantages of lowering the test volumes and the possibility to perform about 90 tests simultaneously. The method was successfully applied to measure platelet inhibition by glycoprotein IIb/IIIa antagonists.

Adenosine Diphosphate↗
PubMed2005

Platelet aggregation testing in platelet-rich plasma: description of procedures with the aim to develop standards in the field.

Platelet function testing consisting of platelet aggregation and secretion often is requested in the clinical evaluation of patients with bleeding problems. At present, there are no uniform clinical laboratory standards for the performance or interpretation of these studies. The present report describes one laboratory's methods and interpretations of platelet aggregation and secretion studies of platelet-rich plasma using each of the common platelet agonists. Diagnostic categories for the evaluation of the platelet function testing are presented. The diagnostic categories then are applied to the evaluation of 61 patients referred to our medical center for these studies. The aims of this report are to present clinical platelet aggregation and secretion studies and to provide a working schema to evaluate these results. Our intent is to stimulate interest in the development of professional guidelines for platelet function testing in the clinical laboratory.

Adenosine Diphosphate↗
PubMed1992

Species differences in platelet aggregation induced by platelet-activating factor (PAF).

Species differences in platelet aggregation induced by platelet-activating factor (PAF) were investigated by using the same procedure of platelet preparation and biological assay. Washed platelets of six different species (horses, dogs, rats, rabbits, sheep and guinea pigs) were prepared employing the same method and platelet aggregation was induced by C16-PAF. Horse platelets were most sensitive to PAF (8.0 x 10(-12) M) and rabbit platelets activated by 5.0 x 10(-11) M PAF were also sensitive enough to detect PAF in clinical samples.

Animals↗
PubMed2000

Differential in vitro effects of the platelet glycoprotein IIb/IIIa inhibitors abixicimab or SR121566A on platelet aggregation, fibrinogen binding and platelet secretory parameters.

The aim of this study was to compare fibrinogen binding, inhibition of platelet aggregation and secretory potential of the MAb abciximab (0.5-5 microg/mL) and the peptidomimetic compound SR121566A (15-250 ng/mL) in vitro in whole blood. Fibrinogen binding was followed by flow cytometry; platelet function was evaluated by light transmittance and by impedance aggregometry. Secretory functions of platelets were evaluated using ATP as marker for early secretion by dense granulae and P-selectin (CD62) for alpha-granular secretion as well as CD63 for lysosomal degranulation. Results showed that fibrinogen binding induced by 5 microM TRAP was maximally inhibited greater than 80% at 3 microg/mL abciximab or at 250 ng/mL SR121566A. At these concentrations of antagonists, platelet aggregation induced by 5 microM ADP or 2 microg/mL collagen was inhibited completely. Expression of CD62 was reduced 34% with abciximab or 15% with SR121566A; CD63 expression was reduced 22% with both agents. With both agents, the EC50 for inhibition of CD62 and CD63 expressions was in similar magnitudes than the EC50 for fibrinogen binding inhibition. With 3 microg/mL abciximab, ATP secretion was maximally reduced to 50% of the control, whereas SR121566A at 250 ng/mL had no inhibitory effect on this parameter. A slight increase in ATP secretion was seen with 0.5 microg/mL abciximab and with SR121566A in concentrations of less than 45 ng/mL. The data suggest a discoupling between the anti-aggregatory and the antisecretory effects of IIb/IIIa antagonists. Because it is not established to what extend CD62 or CD63 expression can be reduced by any means, the reduction by 20-30% obtained by 3 microg/mL abciximab or 250 ng/mL SR121566A might already be the maximum possible inhibition by these agents.

Adenosine Triphosphate↗
PubMed2000

Effects of acute, moderate ethanol consumption on human platelet aggregation in platelet-rich plasma and whole blood.

BACKGROUND: Platelet-inhibitory effects of alcohol potentially contribute to the reduced risk of coronary heart disease associated with moderate drinking. However, few studies have directly examined the effects of acute consumption of a moderate dose of alcohol on aggregation of platelets from healthy human subjects. In the present study, we examined those effects, with the use of multiple platelet agonists and two aggregation measurement techniques, as part of an ongoing series of studies that evaluate the actions of ethanol on platelet function. METHODS: Human subjects consumed alcohol at a dose equivalent to one drink (0.25 ml/kg) or two drinks (0.5 ml/kg). One hour after ingestion, anticoagulated blood was collected and agonist-induced aggregation of platelets was measured in both whole blood and in platelet-rich plasma. RESULTS: Inhibition of aggregation by ethanol consumption was observed in whole blood (measured as maximum change in impedance) and reached statistical significance (p < 0.05) in the 0.5 ml/kg alcohol group for two collagen concentrations (0.625 and 1.25 microg/ml) as well as for the highest concentration of adenosine diphosphate tested (p < 0.05). Inhibition was 15.4%, 22.6%, and 10.5%, respectively, for these three situations. In platelet-rich plasma, after consumption of 0.5 ml/kg ethanol, aggregation (measured as maximum change in optical density) in response to 1.25 microg/ml collagen was significantly inhibited (p < 0.05); no other significant inhibition was observed at either dose of alcohol in any other cases with platelet-rich plasma. In comparison of male and female subjects, there was a statistically significant difference (p < 0.05) in the degree of inhibition by ethanol consumption (0.5 ml/kg) of whole-blood platelet aggregation induced by collagen, whereby female aggregation was inhibited to a greater extent than male. CONCLUSIONS: This study shows that alcohol, at physiologically relevant doses, below those investigated in most previous human studies, has a dose-dependent inhibitory effect on platelet aggregation. Such an effect could potentially contribute to the beneficial effects of alcohol consumption against coronary artery disease. The inhibitory action is most readily measured with whole-blood platelet aggregometry, with the use of collagen as the agonist. This observation is consistent with the view that alcohol reduces platelet sensitivity to thrombotic stimuli by inhibition of arachidonic acid release and, therefore, subsequent thromboxane synthesis.

Adenosine Diphosphate↗
PubMed2006

Porphyromonas gingivalis-induced platelet aggregation in plasma depends on Hgp44 adhesin but not Rgp proteinase.

Evidence from recent epidemiological studies suggests a link between periodontal infections and increased risk of atherosclerosis and related cardiovascular and cerebrovascular events in human subjects. One of the major pathogens of periodontitis, Porphyromonas gingivalis, has the ability to aggregate human platelets in platelet-rich plasma (PRP). Mechanism of P. gingivalis-induced platelet aggregation in PRP was investigated. Proteinase inhibitors toward Arg-gingipain (Rgp) and Lys-gingipain (Kgp) did not suppress P. gingivalis-induced platelet aggregation in PRP, whereas the Rgp inhibitor markedly inhibited P. gingivalis-induced platelet aggregation using washed platelets. Mutant analysis revealed that P. gingivalis-induced platelet aggregation in PRP depended on Rgp-, Kgp- and haemagglutinin A (HagA)-encoding genes that intragenically coded for adhesins such as Hgp44. Hgp44 adhesin on the bacterial cell surface, which was processed by Rgp and Kgp proteinases, was essential for P. gingivalis-induced platelet aggregation in PRP. P. gingivalis cell-reactive IgG in plasma, and FcgammaRIIa receptor and to a lesser extent GPIbalpha receptor on platelets were found to be a prerequisite for P. gingivalis-induced platelet aggregation in PRP. These results reveal a novel mechanism of platelet aggregation by P. gingivalis.

Adhesins, Bacterial↗