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PubMed1993

Effect of recombinant-tissue plasminogen activator, low molecular weight urokinase and unfractionated heparin on platelet aggregation.

We studied the interaction of two thrombolytic agents, recombinant-tissue plasminogen activator (r-TPA) and low molecular weight urokinase (UK), with platelet aggregation in the absence or presence of unfractionated heparin (UH). With platelet rich plasma (PRP), a dose dependent inhibition was seen for both r-TPA and UK. However, this effect was more evident in the presence of r-TPA. UH did not modify this effect. However, it enhanced platelet aggregation induced by ADP and decreased the aggregation induced by collagen (COL) as already shown by us. With washed platelets, only r-TPA decreased platelet aggregation in a dose dependent manner in the presence of COL and only at the highest dose (100 micrograms) in the presence of TH. The presence of ten units of plasminogen (PLG) together with 10 micrograms of r-TPA or 1250 units of UK totally inhibited TH-induced platelet aggregation. UH reversed this effect. In contrast, when COL was the aggregating agent, the inhibition of platelet aggregation in presence of PLG, seems to be further increased by UH. Since UH is an adjunct of thrombolytic therapy to prevent rethrombosis, this double edged sword could partially explain the lack of therapeutic effect in some patients.

Adenosine Diphosphate↗
PubMed1991

14,15-Epoxyeicosatrienoic acid inhibits platelet aggregation in mouse cerebral arterioles.

BACKGROUND AND PURPOSE: Epoxygenase metabolites of arachidonic acid are produced by several tissues and have been shown to inhibit in vitro platelet aggregation. The purpose of the present investigation was to determine whether 14,15- or 8,9-epoxyeicosatrienoic acid, epoxygenase derivatives of arachidonic acid, affect the speed of platelet aggregation in in vivo mouse cerebral arterioles. METHODS: We performed a craniectomy in 116 anesthetized male mice and observed the pial arterioles by microscopy. We induced in situ platelet aggregation using a mercury light and intravascularly injected fluorescein dye. RESULTS: Indomethacin (0.5 mg/kg i.p.), a known cyclooxygenase inhibitor, and 14,15-epoxyeicosatrienoic acid (0.3 mg/kg i.v.) increased the time necessary for the light plus dye to induce the first arterial platelet aggregate by 35% and 26%, respectively, whereas 8,9-epoxyeicosatrienoic acid (0.3 mg/kg i.v.) had no effect. Analysis of mouse serum by radioimmunoassay showed that the degree of inhibition of platelet aggregation by indomethacin and epoxyeicosatrienoic acids correlated with the degree of inhibition of thromboxane production. CONCLUSIONS: We conclude that 14,15-epoxyeicosatrienoic acid is a potent inhibitor of in vivo platelet aggregation but cannot conclusively confirm that its effect on aggregation occurs via its reduction of platelet thromboxane A2. Because epoxyeicosatrienoic acids are produced by several tissues, including brain and vascular tissue, they may be important in vivo modulators of platelet aggregation and hemostasis.

8,11,14-Eicosatrienoic Acid↗
PubMed1999

Effect of ticlopidine on exercise-induced platelet aggregation and exercise tolerance time in patients with ischemic heart disease.

Platelet aggregation is one of the most important mechanisms for acute myocardial infarction during exercise. We sought to evaluate the effect of ticlopidine (TP) on platelet aggregation (PA) during exercise in patients with ischemic heart disease (IHD). We studied 38 patients with IHD, 26 patients with effort angina pectoris, and 12 patients with a previous myocardial infarction. In protocol I, subjects were divided into two groups. Drugs altering platelet aggregation were withheld 2-4 weeks before the study in 25 patients (control group). TP (200 mg/day) was administered for 7 days in 13 patients (ticlopidine group). A symptom-limited modified Bruce protocol treadmill exercise test was performed. PA was measured at rest and after exercise by using optical densitometry induced by adenosine diphosphate (ADP). PA ratio (percentage of maximum) was compared. In protocol II, in 12 patients, treadmill exercise test and PA measurement were performed with and without TP. PA significantly increased after exercise in control (from 51.7+/-23.3% to 64.4+/-27.7%, p < 0.01) and ticlopidine (from 31.9+/-10.5% to 42.0+/-20.4%, p < .01) groups; however, its grade was lower in the ticlopidine group than in the control group. After exercise, PA was lower in the ticlopidine group than in control group (42.0+/-20.4% vs. 64.4+/-27.7%; p < 0.01). In the same patients, PA was lower with TP than without TP after exercise. Treadmill exercise-tolerance time was greater in the ticlopidine group than in the control group, but not statistically significant (762.3+/-139.2 vs. 711.6+/-169.6 s; NS). Exercise-tolerance time was significantly greater with TP than without TP in same patient (791.7+/-98.9 vs. 733.3+/-152.8 s; p < .05). TP suppressed the increase of PA during exercise and increased the exercise-tolerance time in patients with IHD.

Adenosine Diphosphate↗
PubMed1996

Effects of dietary n-3/n-6 and polyunsaturated fatty acid/saturated fatty acid ratios on platelet aggregation and lipid metabolism in rats.

We studied the effects of dietary lipids on platelet aggregation and lipid metabolism in rats by varying the n-3/n-6 ration while maintaining the polyunsaturated fatty acid/saturated fatty acid (P/S) ratio fixed, and vice versa. After two weeks, the platelet counts decreased as the dietary n-3/n-6 ratio rose, and platelet aggregation was sufficiently suppressed at the ratio of 0.2. Differences in the dietary P/S ratio, however, did not affect either the platelet counts nor platelet aggregation. As the dietary n-3/n-6 ratio rose, the proportion of arachidonic acid (AA) in the plasma and the phospholipids (PL) of the platelets and aorta decreased gradually, whereas the proportion of eicosapentaenoic acid (EPA) in each tissue increased gradually. The proportion of EPA was higher in the platelets than in the aorta, while that of docosahexaenoic acid (DHA) was higher in the latter. The production of platelet thromboxane A2 (TXA2) and aortic prostacyclin (PGI2) showed sharp declines, from the values for the n-3/n-6 ratio of 0.02 (control) to those for 0.5. These results suggest that the n-3/n-6 ratio of dietary fats necessary to ensure the suppression of platelet aggregation in normal rats would be at least 0.2 and no more than 0.5.

Animals↗
PubMed1975

Influence of vitamin E on platelet aggregation and thrombocythemia in the rat.

Collagen-induced platelet aggregation was increased in 9-10 wk old vitamin E deficient rats although there was no difference in platelet count between deficient and control animals. With a more prolonged deficiency (at 15 wk) both platelet aggregation and platelet counts were elevated in the vitamin E deficient animals.

Age Factors↗
PubMed1984

In vivo study of platelet aggregation in rats.

A simple in vivo method for the study of platelet aggregation in rats is described. The presence of circulating platelet aggregates in the blood of rats is shown after induction of intravascular platelet aggregation. This aggregation can be triggered either acutely, for example with ADP and collagen, or chronically, for example with a thrombogenic diet. The antagonist activity of acetylsalicylic acid indicates that this method can be used to evaluate anti-thrombotic drugs.

Adenosine Diphosphate↗
PubMed2004

Intense exercise increases shear-induced platelet aggregation in men through enhancement of von Willbrand factor binding, glycoprotein IIb/IIIa activation, and P-selectin expression on platelets.

Vigorous exercise transiently enhances the risk of primary cardiac arrest. Shear-induced platelet aggregation (SIPA) is an important mechanism in arterial thrombogenesis. This study investigates whether intense exercise affects SIPA, and elucidates mechanisms that underlie SIPA. Eighteen sedentary healthy men engaged in intense exercise (about 80% of maximal oxygen consumption) for 40 min on a bicycle ergometer. Platelet aggregation, binding of von Willebrand factor (vWF) to platelets, and activation of glycoprotein (GP) IIb/IIIa and expression of P-selectin on platelets induced by shear stress were analyzed both before and immediately after exercise. Analytical results demonstrated that: (1). the levels of plasma vWF antigen and activity were enhanced after intense exercise, (2). intense exercise increased either shear- or ristocetin-induced platelet aggregation and was accompanied by an increase in vWF binding to platelets and vWF-mediated GP IIb/IIIa activation at high shear flow, and (3). shear-induced P-selectin expression in the absence or the presence of exogenous vWF was enhanced by intense exercise. Therefore, we conclude that intense exercise promotes the extent of SIPA, possibly by enhancing the ability of vWF to bind to platelets and the subsequent activation of GP IIb/IIIa complexes, as well as the expression of P-selectin in response to shear stress, which in turn may augment the risk of vascular thrombosis.

Adult↗
PubMed1991

[Platelet aggregation during adjuvant chemotherapy with CMF].

We have studied platelet aggregation in fourteen pre- and post-menopausal women treated with cyclic adjuvant CMF chemotherapy for mammary cancer with positive axillary nodes, previously operated. Aim of the investigation is to evaluate the effect of chemotherapy on platelet aggregation. The obtained results demonstrate that CMF therapy does not modify platelet aggregation in both pre- and post-menopausal patients.

Adenocarcinoma↗
PubMed1993

[Effects of platelet aggregating inhibitor on pulmonary metastases of tumor cells after surgical resection].

DN-9693, c-AMP: phosphodiesterase inhibits platelet aggregation induced by metastasizing tumor cells and blood-borne metastases of these tumors. Effects of this drug on pulmonary metastases was studied in wKA rats, which were sc implanted with 4-dimethylaminoazobenzene (DAB) induced KDH-8 tumor cells. KDH-8 cells (10(5)) were sc inoculated on day 0 and excised on day 20. DN-9693 was ip injected at a dose of 150 micrograms twice a day for 7 days pre operatively (-7 - 0) or perioperatively (-3 - +3) or postoperatively (0 - +7). The rats were sacrificed on day 20 after surgery, and lung weight and the number of surface pulmonary nodules were measured. Both were significantly decreased in the group of perioperative and postoperative administration of DN-9693. The survival of these rats were furthermore prolonged when Cyclophosphamide (40 mg/kg) was sc injected 3 days after surgical resection. KDH-8 tumor cells (10(4)) were iv inoculated on day 0, and DN-9693 was ip injected at a dose of 150 micrograms twice a day for 7 days on day 0 approximately 7. Rats were sacrificed on day 20, and same studies as above were done. In this artificial pulmonary metastases, the decrease of the number of lung nodules was observed in WKA rat treated with DN-9693. Platelet aggregation induced by KDH-8 tumor cells was inhibited by ADP inhibitor (apyrase, CP/CPK) and thrombin inhibitor (heparin, MD-805); KDH-8 tumor cells induced platelet aggregation by two different mechanisms: ADP-mediated aggregation and thrombin-mediated aggregation. This platelet aggregation by KDH-8 tumor cells was inhibited by DN-9693 with dose-dependency. DN-9693 had no direct anti-tumor effects either in vivo or in vitro. The results indicates that this drug prevents pulmonary metastases by inhibiting platelet aggregation.

Animals↗
PubMed1993

SIN-1 partially and RGDS totally counteracts platelet aggregation as assessed in vitro by two independent whole blood methods.

The cyclic GMP stimulant SIN-1 and the GP IIB/IIIA receptor antagonist RGDS were compared with regard to platelet antiaggregatory effects as measured in vitro by filtragometry and by whole blood aggregometry. In filtragometry platelet aggregation is measured as the time to partial occlusion of a filter in the test unit. Beta-thromboglobulin concentrations increased over the filter (p < 0.002) indicating that in filtragometry part of the mechanism of aggregation could be platelet activation across the filter. In whole blood aggregometry platelet aggregation is induced by a chemical stimulant. As tested in blood from healthy volunteers, linear dose-effect relations were found with both methods, for SIN-1 in the 10(-7)-10(-6) M range (p < 0.02, filtragometry and p < 0.05, whole blood aggregometry) and for RGDS in the 10(-5)-10(-4) M range (p < 0.0001, filtragometry and p < 0.02, whole blood aggregometry). At the highest dose RGDS totally counteracted platelet aggregation in both test systems. Maximal SIN-1 platelet antiaggregatory effects were less (p < 0.04, filtragometry and p < 0.01, whole blood aggregometry) than for RGDS. SIN-1 concentrations in the 10(-4) M range had no further antiaggregatory effects. In conclusion, with two principally different methods for the assessment of whole blood platelet aggregation, SIN-1 was found to be a partial antagonist while RGDS a total antagonist.

Amino Acid Sequence↗
PubMed2000

[Effects of nitrates and beta-blockers on platelet aggregation in patients with coronary heart disease].

Our study aimed at evaluating an effect of the selected nitrates and beta adrenoceptor blockers on platelet aggregation in patients (pts) with coronary artery disease (CAD). The study included 168 male patients (M), aged between 33 and 72 years (mean age 51 +/- 7). 61 M given isosorbide dinitrate were divided into three groups: in the group I and II an effect of the drug on the platelet aggregation following a single 10 mg (I) and 20 mg (II) dose has been evaluated; in group III an effect of the drug after a two-week treatment has been evaluated. 14 male patients (group IV) were given 5-mononitrate 40 mg daily for two weeks. 85 male patients, treated with propranolol have also been divided into three groups. In group V and group VII an effect of propranolol on platelet aggregation following a single dose of 40 mg and 80 mg has been evaluated respectively. In the group VII an outcome of a two-week propranolol therapy has been assessed. Eleven patients (group VIII) received nadolol in a dose of 40-80 mg daily for two weeks. Platelet aggregation induced by adenosine diphosphate (ADP) in concentration of 1 mM/ml and 5 mM/ml (groups I, II, III, V, VI, VII) and only of 1 microM/ml (groups IV, VIII) was evaluated with Born's method. In patients with CAD only isosorbide dinitrate inhibits platelet aggregation. This effect has been noted following a single dose as well as a two-week treatment. Other drugs (5-mononitrate, propranolol, nadolol) transiently increase platelet aggregation, but became either ineffective after two-week therapy (5-mononitrate, nadolol) or increase (propranolol) platelet aggregation. Tendency to inhibit (sorbonit) or to increase (propranolol) platelet aggregation has been more pronounced with higher concentration of aggregating factor.

Adrenergic beta-Antagonists↗
PubMed2001

The role of platelet factor 4 in platelet aggregation induced by the antibodies implicated in heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is a severe side effect of heparin treatment. Recent studies using immunological methods demonstrated that antibodies contained in plasma, or in purified total immunoglobulin (Ig)G from patients suffering HIT, recognize as target antigen the complex heparin/platelet factor (PF4). In the present study, the role of PF4 in in-vitro platelet aggregation induced by purified total IgG or platelet-poor plasma from patients suffering HIT was investigated. In order to demonstrate the functional role of PF4, an anti-PF4 antibody that specifically blocked PF4 was used. In an experimental system composed of washed platelet suspension, incubation of F(ab')2 fragments (0.125 microg/ml) of the polyclonal anti-PF4 antibody resulted in complete inhibition of platelet aggregation triggered by purified total IgG from patients suffering HIT and heparin. In platelet-rich plasma, a significantly higher concentration (4.25 microg/ml) of the anti-PF4 F(ab')2 was required to inhibit platelet aggregation induced by HIT-PPP and heparin. Intermediate concentrations of the anti-PF4 antibody partially inhibited platelet aggregation. In plasma milieu, the concentration of PF4 was about five-fold higher in comparison with that measured in the purified system. The intensity of platelet aggregation depended on the concentration of HIT-IgG. Platelet aggregation was abolished in the presence of high concentrations of heparin (superior or equal to 10 IU/ml). The present study shows that PF4 is essential for platelet aggregation triggered by the antibodies related to HIT in the presence of heparin. The concentration of PF4 that is available to bind with heparin or with the HIT-related antibodies is critical for platelet aggregation induced by HIT antibodies.

Antibodies↗
PubMed1987

Effect of human tumor cells on platelet aggregation: potential relevance to pattern of metastasis.

Tumor metastasis may be facilitated by interaction of tumor cells with platelets. It is not known, however, whether solid tumors which have predisposition to pulmonary metastasis affect platelets differently than lymphoid tumors, which rarely spread to lungs. We therefore examined the effects of cultured osteogenic sarcoma (MG-63, U2-OS), as well as leukemia (NALM-16, LAZ-221, K-562) and lymphoma (RAJI, MOlt 4) cells, on human platelet aggregation. Human osteogenic sarcoma (MG-63) cells alone induced platelet aggregation, whereas U2-OS cells induced platelet aggregation only after preincubation of platelets with subthreshold concentrations of epinephrine. In contrast, neither leukemia nor lymphoma cells affected platelet aggregation. These observations suggest that the platelet proaggregatory potential of tumor cells is variable and that the platelet stimulatory effects of osteogenic sarcoma cells may relate to their high risk of pulmonary metastasis.

Adenosine Diphosphate↗
PubMed1990

Adenosine inhibits the rise in intracellular calcium and platelet aggregation produced by thrombin: evidence that both effects are coupled to adenylate cyclase.

Platelet aggregation and secretion are associated with a rise in intracellular calcium concentration ([Ca2+]i). Adenosine has been postulated as an endogenous inhibitor of platelet aggregation. The antiaggregatory effects of adenosine are related to activation of adenylate cyclase. We studied the effect of adenosine on the rise in [Ca2+]i and platelet aggregation produced by thrombin. Human platelets were obtained from dextrose/citrate-treated plasma. [Ca2+]i was determined by fluorescence-dye techniques (fura-2). Adenosine inhibited the slope of the first phase of aggregation and the rise in [Ca2+]i produced by thrombin, in a dose-dependent manner. The dose that produced 50% inhibition of both aggregation and the rise in [Ca2+]i was approximately 500 nM. The effects of adenosine on [Ca2+]i were shared by its stable analogs, 5'-N-ethylcarboxamidoadenosine being approximately 10-fold more potent than (-)N6-phenylisopropyladenosine, suggesting that these effects were mediated through adenosine A2 receptors. Furthermore, caffeine antagonized the inhibitory effects of adenosine on platelet aggregation and [Ca2+]i. The effects of adenosine on [Ca2+]i appear to be mediated through a rise in intracellular cAMP, because they were prevented by the adenylate cyclase inhibitor 2',5'-dideoxyadenosine (1 mM) and were potentiated by phosphodiesterase inhibition with papaverine (1 microM). Adenosine also inhibits the rise in [Ca2+]i produced by thrombin in a calcium-free medium, suggesting that adenosine inhibits both calcium influx and the release of calcium from intracellular stores.

Adenosine↗
PubMed1993

Role of platelet membrane glycoproteins Ib/IX and IIb/IIIa, and of platelet alpha-granule proteins in platelet aggregation induced by human osteosarcoma cells.

We have previously shown that the platelet-aggregating activity of human MG-63 and HOS osteosarcoma cells depends at least in part upon tumor cell surface-associated thrombospondin, and suggested that platelet-osteosarcoma cell interactions could occur through interactions with specific platelet membrane receptors. In this study, the platelet-aggregating activity of MG-63 and HOS cells was studied by using a variety of platelet disorders. Both osteosarcoma cell lines induced a biphasic platelet aggregation response when added to normal platelet-rich plasma, while the second phase of aggregation was absent when added to gray platelets (deficiency in alpha-granule proteins) and to aspirin-treated platelets. Platelets from two unrelated patients with type I Glanzmann's thrombasthenia (deficiency in glycoprotein (GP) GPIIb/IIIa) did not aggregate at all with osteosarcoma cells. Using giant platelets from three patients with Bernard-Soulier syndrome (deficiency in GPIb/IX), the aggregation response induced by MG-63 and HOS cells was monophasic and reversible when compared to normal-sized platelets and to giant platelets from a patient with May-Hegglin anomaly (no membrane GP defect). Because GPIb serves as a receptor for von Willebrand factor during hemostasis, aggregation experiments were also conducted with the platelet-rich plasma of two patients with a low plasma von Willebrand factor concentration (type I von Willebrand's disease) before and after the infusion of deamino-D-arginine vasopressin. MG-63 and HOS cells induced biphasic platelet aggregation both before and after deamino-D-arginine vasopressin treatment, while the ristocetin-dependent binding of von Willebrand factor to platelets only occurred after deamino-D-arginine vasopressin treatment. Preincubation of normal platelet-rich plasma with monoclonal antibody SZ-2 directed against the von Willebrand binding domain of GPIb did not inhibit the platelet-aggregation activity of osteosarcoma cells, whereas anti-GPIb antibody SZ-2 did inhibit ristocetin-induced platelet agglutination. In addition, anti-GPIX antibodies did not affect platelet-osteosarcoma cell interactions. In conclusion, our data demonstrate that the first phase of the platelet-aggregating activity of human osteosarcoma cells is initiated by the interaction of these tumor cells with platelet membrane GPIIb/IIIa, whereas the second phase, even if plasma von Willebrand factor is deficient, involves platelet membrane GPIb and the participation of platelet alpha-granule proteins in membrane-mediated events, making aggregation irreversible.

Antibodies, Monoclonal↗
PubMed1982

Functional fractionation of platelets: aggregation kinetics and glycoprotein labeling of differing platelet population.

Platelet heterogeneity has been studied with a technique called functional fractionation which employs gentle centrifugation to yield subpopulations ("reactive" and "less-reactive" platelets) after exposure to small doses of aggregating agent. Aggregation kinetics of the different platelet populations were investigated by quenched-flow aggregometry. The larger, "reactive" platelets were more sensitive to ADP (Ka = 1.74 microM) than the smaller "less-reactive" platelets (Ka = 4.08 microM). However, their maximal rate of aggregation (Vmax, % of the platelets aggregating per sec) of 23.3 was significantly lower than the "less-reactive" platelets (Vmax = 34.7). The "reactive" platelets had a 2.2 fold higher level of cyclic AMP. Platelet glycoproteins were labeled using the neuraminidase-galactose oxidase--[H3]-NaBH4 technique. When platelets were labeled after reversible aggregation, the "reactive" platelets showed a two-fold decrease in labeling efficiency (versus control platelets). However, examination of whole cells or membrane preparations from reversibly aggregated platelets revealed no significant difference in Coomassie or PAS (Schiff) staining. These results suggest that the large, "reactive" platelets are more sensitive to ADP but are not hyperaggregable in a kinetic sense. Reversible aggregation may cause a re-orientation of membrane glycoproteins that is apparently not characterized by a major loss of glycoprotein material.

Adenosine Diphosphate↗
PubMed2004

Platelet aggregation induced by the C-terminal peptide of thrombospondin-1 (4N1-1) is inhibited by epigallocatechin gallate but not by prostaglandin E1.

The C-terminal peptide of thrombospondin (4N1-1) stimulates distinct signalling pathways but induces an activation-independent platelet aggregation. This study demonstrates inhibitory effects of epigallocatechin gallate (EGCG), a major flavonoid component of green tea, on 4N1-1-induced aggregation of washed human platelets. Thrombin (0.1 U/ml)-induced platelet aggregation was completely inhibited by prostaglandin E1 (PGE1, 300 nM). In contrast, platelet aggregation induced by 4N1-1 (100 microM) was not affected by PGE1. However, epigallocatechin gallate (EGCG), but not other catechins from green tea, concentration-dependently inhibited 4N1-1-induced platelet aggregation. Thus, dietary components, such as EGCG, may inhibit platelet function even under conditions, when 'classical' platelet inhibitors, such as cAMP-elevating agents, are not effective.

Alprostadil↗
PubMed1980

1-arachidonyl-monoglyceride causes platelet aggregation: indirect evidence for an acylglycerol acylhydrolase involvement in the release of arachidonic acid for prostaglandin synthesis.

Phosphatidylcholine liposomes containing 1-arachidonyl-monoglyceride were found to cause aggregation of human platelets. In contrast, addition of phosphatidylcholine liposomes, 1-arachidonyl-monoglyceride, or phosphatidylcholine liposomes containing I-oleoyl-monoglyceride to a similar platelet preparation had no effect. Aggregation stimulated by 1-arachidonyl-monoglyceride was inhibited by 100 microM aspirin or 1 microM indomethacin, suggesting that the arachidonic acid is first released by; a platelet acylglycerol acylhydrolase and then converted to PGG2 and thromboxane A2 which initiate the platelet aggregation. Changes in platelet morphology in response to 1-arachidonyl-monoglyceride were similar to those reported previously to occur following stimulation of platelets by arachidonic acid or PGG2 providing further support for this concept. EDTA inhibited aggregation of platelets but no shape change or granule centralization in response to 1-arach-idonyl-monoglyceride. PGE1 and theophylline inhibited both aggregation and morphological changes. These results with inhibitors are similar to the effects of these inhibitors on PGG2 and provide further evidence for similarity between the action of 1-arachidonyl-monoglyceride and PGG2. The results provide important evidence to support the concept that an acylglycerol acylhydrolase may be involved in arachidonic acid release and platelet aggregation.

Arachidonic Acids↗