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PubMed1990

[Effects of ketotifen on rabbit platelet aggregation and platelet activating factor formation from rat neutrophils].

The effects of ketotifen (Ket) on rabbit platelet aggregation induced by platelet activating factor (PAF), ADP and arachidonic acid (AA) and PAF formation from A-23187-stimulated rat neutrophils in vitro were studied. PAF (15-100 pmol/L) induced rabbit platelet aggregations, with an EC50 of 33 pmol/L. Ket shifted the PAF dose-dependent platelet aggregation curve to the right in a parallel fashion with no depression of the maximal response and reversed the secondary aggregation phase, suggesting that Ket had competitive antagonistic activity against PAF-induced platelet aggregation. It also showed inhibitory effects on platelet aggregations induced by ADP 10 mumol/L and AA 50 mumol/L, the IC50 were 94.5 and 143.5 mumol/L respectively. However, it failed to influence PAF formation from rat neutrophils stimulated by A-23187 2.5 mumol/L in vitro. The inhibitory effects of Ket on platelet activation, particularly PAF-induced platelet aggregation, may contribute to its anti-asthmatic properties.

Animals↗
PubMed1992

Circulating aggregated platelets, number of platelets per aggregate, and platelet size during acute myocardial infarction.

Circulating aggregated platelets (total, reversibly and irreversibly aggregated), the number of platelets per aggregate and "big" platelets were measured by a modification of the Wu and Hoak method in 42 patients on the first, second and fifth day of acute myocardial infarction (AMI). Among them, 30 had an uncomplicated course and 12 patients had complications that occurred between the 5th and 10th day of hospitalization (7 patients had reinfarction and 5 died). In all patients the measured parameters were elevated compared with those of control subjects. There was a significant increase, especially after the first observation day, in the values of total aggregated platelets (37 +/- 11% vs 26 +/- 12%, p < 0.001), reversibly aggregated platelets (27 +/- 9% vs 17 +/- 8%, p < 0.001) and the average platelets per aggregate (8.6 +/- 0.3 vs. 2.3 +/- 0.4) in patients with versus without complications. In considering the role of platelets in the development of AMI, these findings may add information to the role of platelets in determining the course of AMI.

Blood Platelets↗
PubMed2002

Interaction between ATP and catecholamines in stimulation of platelet aggregation.

Platelets, on activation by endothelial damage, release ADP, ATP, serotonin, epinephrine, and norepinephrine. Although ATP is known to augment the action of norepinephrine in cardiovascular and endocrine systems, the possible interaction between ATP and catecholamines in regulation of platelet reactivity has not been reported. The addition of ATP (1-5 microM) to human platelet-rich plasma did not induce platelet aggregation; however, it selectively augmented the aggregatory response to norepinephrine and epinephrine, but not to serotonin. This potentiating action of ATP was dose dependent and was not due to contamination by, or hydrolysis to, ADP. The action of ATP was blocked by 10 microM of adenosine 3'-phosphate 5'-phosphosulfate, a selective P(2)Y(1) receptor antagonist. ATP alone did not cause release of intracellular Ca(2+), but produced a significant Ca(2+) response in the presence of norepinephrine. In contrast, the P(2)X(1) receptor agonists P(1),P(6)-diadenosine-5' hexophosphate and alpha,beta-methylene-ATP had no effect on norepinephrine-induced platelet aggregation even when added at 100 microM. This synergistic interaction between ATP and norepinephrine in stimulating platelet aggregation may have significant clinical implications and suggests a prothrombotic role for ATP in stress.

Adenosine Triphosphate↗
PubMed1976

The effect of vitamin E on platelet aggregation.

Platelet aggregation studies were performed in five men with coronary artery disease and angina pectoris and five men with nonspecific chest pain before and after receiving 1,000 I.U. of alpha-tocopherol acetate orally per day for 8 days. There was no significant difference in the platelet aggregation response to three concentrations of ADP and two concentrations of epinephrine between the pre- and post-vitamin E periods among the 10 patients. If tocopherol acetate (vitamin E) has any beneficial effect on the prevention of thromboemolism or in the treatment of angina pectoris and peripheral vascular disease, it is not via inhibition of platelet aggregation.

Adenosine Diphosphate↗
PubMed1981

In vitro effect of ethanol on ADP and collagen-induced platelet aggregation.

Platelet aggregation was measured by Born's method. Plasma from Sprague-Dawley rats and inbred albino rabbits was used. 20% ethanol in 0.9% (w/v) NaCl was added to plasma at final concentrations of 56.5 mM, 85.9 mM 171.5 mM and 343.1 mM or to whole blood at final concentrations of 8.7 mM, 17.4 mM, 52.5 mM, 171.5 mM and 343.1 mM. Experiments using 0.9% NaCl volumes equivalent to the added ethanol volume were also conducted. Dose-response aggregation tests showed that a decrease in ADP- and collagen-induced aggregation existed when ethanol was mixed with rat or rabbit blood prior to the preparation of platelet-rich plasma. There was no effect on ADP-induced platelet aggregation when ethanol was mixed with rat or rabbit plasma. Collagen-induced aggregation was impaired only in rat plasma when ethanol concentration reached 343.1 mM. These results suggested that ethanol modified platelet function possibly via red cells.

Adenosine Diphosphate↗
PubMed2001

Mechanisms of platelet aggregation.

Platelet aggregation is initiated by receptor activation coupled to intracellular signaling leading to activation of integrin alphaIIbbeta3. Recent advances in the study of platelet receptors for collagen, von Willebrand factor, thrombin, and adenosine diphosphate are providing new insights into the mechanisms of platelet aggregation.

Animals↗
PubMed1983

Microscopic measurements of platelet aggregation reveal a low ADP-dependent process distinct from turbidometrically measured aggregation.

Platelet aggregation measured from the decrease in the number of nonaggregated platelets (PA) is compared with that measured from the increase in %T (TA) after ADP addition to a stirred platelet suspension. A number of properties distinguish PA from TA. Half-maximal extent of PA, measured at 3 or 10 sec after ADP addition is attained at significantly lower ADP concentrations ([ADP]) than for TA (velocity and extent), and in particular at [ADP] equal to or less than that required for shape change. PA appears minimally refractory to ADP under conditions causing maximal refractoriness of TA. Examination of the effect of three inhibitors of platelet aggregation acting on extracellular ionized calcium (EDTA) and on platelet adenylate cyclase (PGE1) and phosphodiesterase (anagrelide; BL-4162A) indicates that PA is generally less sensitive to these inhibitors than TA but, of greater significance, that PA and TA reveal aggregation processes with differing ADP sensitivities. It is suggested that these differences reflect different processes determining the strength of interplatelet interactions. Conventional aggregometry is insensitive for measuring the low ADP-dependent aggregation process.

Adenosine Diphosphate↗
PubMed1998

Analysis of low-speed rotational atherectomy for the reduction of platelet aggregation.

Platelet activation is an important determinant of acute outcomes of percutaneous intervention. The objective of this study was to assess the effect of rotational atherectomy on platelet activation in an in vitro model. Freshly collected heparinized porcine blood was exposed to a 2.0-mm Rotablator burr rotating at one of three speeds: 180,000, 140,000, or 0 rpm. The specimens were analyzed immediately for concentration and size of platelet aggregates and plasma-free hemoglobin. There were significantly more platelet aggregates of >20-microm diameter at higher speeds (7,434+/-2,193 at 180,000, vs. 2,269+/-627 at 140,000, vs. 633+/-258 aggregates/ml at 0 rpm; P < 0.001). Plasma-free hemoglobin, a simple measure of cell damage, decreased with decreasing rotational speed (429+/-168 mg/dl at 180,000, vs. 88+/-44 mg/dl at 140,000, vs. 9+/-9 mg/dl at 0 rpm; P < 0.0001). In vitro, platelet activation decreases with decreasing burr speed, suggesting that the use of the Rotablator system at its minimum approved speed (140,000 rpm) could prove clinically beneficial.

Animals↗
PubMed1995

Effects of tetrandrine on rabbit platelet aggregation and platelet activating factor generation.

AIM: To study the effects of tetrandrine (Tet) on platelet aggregation and platelet activating factor (PAF) generation in rabbit platelet-rich plasma (PRP). METHODS: The aggregation rate of platelets induced by calcimycin (Cal) and PAF and the inhibition rate of Tet on platelet aggregation were measured. The amount of PAF in PRP stimulated with Cal and treated with Tet was also measured. RESULTS: Cal 1-8 mumol.L(-1) and PAF 9.5-190.5 pmol.L(-1) induced platelet aggregation. At the final concentrations of 4-64 mumol.L(-1), Tet inhibited the aggregation induced by Cal 4 mumol.L(-1) and PAF 142.9 pmol.L-1. The IC50 (95% confidence limits) were 8.6 (6.0-12.2) mumol.L-1 for Cal and 14.0 (6.4-30.4) mumol.L(-1) for PAF. In the PRP aggregation by Cal, there was a marked increase in PAF content. Tet dependented the release of PAF from platelets by Cal in a concentration-dependent manner, with IC50 of 21 (8-54) mumol.L(-1). CONCLUSION: The inhibition effect of Tet on platelet aggregation might be concerned with the reduction of endogenous PAF generation.

Alkaloids↗
PubMed1977

Autoprothrombin ii-a, thrombin, and epinephrine: interrelated effects on platelet aggregation.

Platelets aggregate with thrombin-free autoprothrombin II-A. Aggregation was dependent on an intact release mechanism since inhibition of aggregation occurred with adenosine, colchicine, or EDTA. Autoprothrombin II-A reduced the sensitivity of platelets to aggregate with thrombin, but enhanced epinephrine-mediated aggregation. Autoprothrombin II-A directly competes for membrane sites sensitive to thrombin. It allows complexes to from with epinephrine. There was no absolute requirement for autoprothrombin II-A since epinephrine aggregated dog platelets at the identical optimum concentration following Coumadin treatment.

Animals↗
PubMed1976

The effect of cytosine arabinoside on platelet aggregation.

Platelet aggregation induced by ADP, collagen, epinephrine, and thrombin was studied in patients with acute leukemia in complete remission, before and after a continuous 5-day intravenous infusion of cytosine arabinoside at a dose of 100 mg/m2 per day. Aggregation was also measured in normal subjects with cytosine arabinoside added in vitro. Cytosine arabinoside had no significant effect on platelet aggregation after either in vitro or in vivo administration.

Acute Disease↗
PubMed1996

Inhibitory effects of Acanthopanax gracilistylus saponins on human platelet aggregation and platelet factor 4 liberation in vitro.

AIM: To study the effects of Acanthopanax gracilistylus var pubescens Li saponins (AGVPS) on human platelet aggregation and platelet factor 4 (PF4) liberation in vitro. METHODS: Human platelet aggregations induced by ADP, adrenaline, and collagen were measured turbidimetrically. The aggregation curve was recorded on a platelet aggregometer and the maximal aggregation rate (ARmax), effective deaggregation rate in 5 min (DR5 min) and lag time (LT) were autocalculated by the built-in microcomputer; PF4 liberation from human platelets stimulated by ADP and collagen was determined by recording the heparin thrombin clotting time (HTCT). Thrombosis was tested by weighing the wet and dry thrombi formed in a siliconized revolving ring. RESULTS: AGVPS inhibited in vitro the ARmax with IC50 of 1.33 (95% confidence limits: 1.09-1.63, ADP-induced), 1.66 (1.54-1.79, adrenaline-induced), and 4.2 g.L-1 (0.6-29, collagen-induced). The DR5 min (on ADP-induced aggregation) and LT (collagen-induced) were also increased as well. Meanwhile, AGVPS 0.63-2.50 g.L-1 prolonged HTCT on ADP- and collagen-stimulated PF4 liberation. At 0.34-1.39 g.L-1, AGVPS reduced the wet and dry weight of thrombi formed in vitro. CONCLUSION: AGVPS inhibits human platelet aggregation, liberation, and thrombosis in vitro, suggesting its possible antithrombotic action in man.

Adult↗
PubMed1991

Effect of calcium channel blocker (diltiazem) on platelet aggregation.

Platelet aggregation with collagen, ADP and sodium arachidonate was significantly inhibited by 0.48 and 0.24 mg/ml of diltiazem but no significant effect occurred with 0.024 mg/ml of diltiazem. It is suggested that the antiplatelet property of diltiazem may be utilized in clinical setting and diltiazem may be tried synergistically with other antiplatelet drugs.

Diltiazem↗
PubMed2005

Effects of SolCD39, a novel inhibitor of Platelet Aggregation, on Platelet Deposition and Aggregation after PTCA in a Porcine Model.

INTRODUCTION: This study evaluated CD39 in a porcine model of balloon angioplasty and in plasma of patients undergoing percutaneous intervention. CD39 (E-NTPDase1), is the endothelial ecto-ADPase inhibiting platelet function via hydrolysis of released platelet ADP. METHODS AND RESULTS: A recombinant soluble form of CD39 (solCD39) given intravenously to pigs had an elimination half life of 5--7 days, increased the bleeding time to an extent similar to aspirin, and inhibits platelet aggregation by>90%. Platelet counts and clot retraction remained normal following solCD39 administration. In a pig model of acute coronary balloon injury, solCD39 resulted in non-statistically significant decreases in platelet (7.7+/-1.4 versus 11.7+/- 3.4) and fibrin (3.5+/- 0.4 versus 4.2+/- 0.7) deposition ratios. Adding ex vivo to human platelet rich plasma (PRP) solCD39 produced nearly 100% inhibition of ADP-induced platelet aggregation. A dose-response effect of solCD39 on platelet aggregation induced by collagen or a thrombin receptor activating peptide (TRAP(SFLLRN)) was noted in PRP obtained from volunteers and patients receiving aspirin, clopidogrel or ticlopidine. SolCD39 also provided additional and complete inhibition of TRAP-induced platelet aggregation in PRP from patients who had received abciximab, aspirin and clopidogrel. CONCLUSIONS: SolCD39, a novel inhibitor of platelet activation and recruitment with a relatively long half-life appears to be well tolerated and is a potent inhibitor of ADP-, collagen-, or TRAP-induced platelet activation. Its potential use in percutaneous coronary intervention requires further study. ABBREVIATED ABSTRACT: E-NTPDase1/CD39 is the endothelial ecto-ADPase responsible for inhibition of platelet function. A recombinant soluble form (solCD39) had an elimination half life of 5-7 days in pigs, elevated bleeding times similar to aspirin, did not affect clot retraction, and inhibited platelet aggregation by > 90%. When combined with standard heparin therapy in a pig model of acute coronary balloon injury, solCD39 resulted in a trend toward a decrease in platelet and fibrin deposition. SolCD39 added ex vivo to human platelet rich plasma yielded nearly 100% inhibition of ADP-induced platelet aggregation and provided further inhibition when combined with standard therapy.

Adenosine Diphosphate↗
PubMed1981

Improvement of bleeding time, platelet aggregation and platelet count during CAPD treatment.

Mean bleeding time in 11 uraemic patients improved from 11.2 (range 3.5--20) before the 5.8 (range 2.5--20) minutes during CAPD treatment (p less than 0.025). Bleeding time became normal in six out of seven patients with a prolonged bleeding time prior to CAPD. There was a concomitant improvement in platelet aggregation. Mean platelet count rose from 195 (range 117--414) to 311 (148--522) x 10(9)/L (p less than 0.01). A significant correlation was found between the change in bleeding time and in platelet aggregation induced by ristocetin, but not between the change in bleeding time and the platelet count. Our results suggest that CAPD treatment improves the uraemic bleeding tendency, even in patients on previous haemodialysis treatment.

Adenosine Diphosphate↗
PubMed1976

The effect of thrombocytopenia on the determination of platelet aggregation.

Platelet aggregation has been widely assumed to be unmeasurable in thrombocytopenic samples. Using a sensitive differential self differential self-calibrating aggregometer, and standard aggregating agents, aggregation was measured in serially diluted platelet-rich plasma. Aggregation induced by ADP or collagen was reproducible at platelet counts as low as 50,000 per cu. mm., and with epinephrine aggregation was reproducible at platelet counts as low as 75,000 per cu. mm.

Adenosine Diphosphate↗
PubMed1996

Platelet lipoxygenase inhibitors attenuate thrombin- and thromboxane mimetic-induced intracellular calcium mobilization and platelet aggregation.

Platelets metabolize arachidonic acid via cyclooxygenase and lipoxygenase (LO) enzymatic pathways. Although platelets produce large amounts of arachidonic acid metabolites via the LO pathway, little is known regarding the physiological significance of these products. We used three structurally dissimilar LO inhibitors, 5,8,11-eicosatriynoic acid (ETI), baicalein and phenidone, and found that LO inhibition attenuated thrombin- and U46619 (a thromboxane mimetic)-induced increases of platelet intracellular calcium ([Ca++]i) in washed human platelets. LO inhibitors also reduced platelet aggregation induced by thrombin and U46619. The effect of ETI on reducing the thrombin-induced [Ca++]i elevation persisted even when cation channels were blocked, suggesting that LO inhibitors modify release of Ca from intracellular stores. Stimulating endogenous LO product formation potentiated thrombin-induced [Ca++]i responses and aggregation, and these effects were eliminated by ETI. ETI did not alter inositol 1,4,5-trisphosphate production in stimulated platelets, but increased platelet cyclic AMP production in thrombin- or forskolin-stimulated platelets. These results suggest that LO products are regulators of platelet [Ca++]i mobilization and aggregation in response to some agonists, and that LO inhibitors may work in part by modifying platelet cyclic AMP metabolism.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1996

Plasma platelet aggregating factor and platelet aggregation studies in pre-eclampsia.

OBJECTIVE: A plasma platelet aggregation factor (PAF) has been implicated in the pathogenesis of platelet activation in thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS). Similar mechanism may be operative in pre-eclampsia. METHODS: Coagulation profile and detailed in vitro platelet aggregation with various agonists were studied. PAF was demonstrated by spontaneous aggregation of normal platelets with test plasma. Non-parametric Wilcoxon's rank sum test and Krauskal Wally's one way analysis of variance were applied. RESULT: Twenty-two pre-eclamptic patients and 20 normal pregnant controls were studied. Anti-thrombin III levels were within normal range and fibrin degradation products were only border line raised ( > 10 < 40 micrograms/ml) in 14 (65.4%) patients. In vitro platelet aggregation was abnormal in 17 (77.2%) patients. PAF was demonstrable in 10 of 22 (45.5%) patients. CONCLUSION: Platelet aggregation studies indicated the presence of both activated (hyperaggregable) as well as exhausted (hypoaggregable) platelets in circulation. PAF demonstrable in 45.4% pre-eclampsia patients would suggest its role in the pathogenetic mechanism of platelet activation in this disease.

Adult↗