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PubMed1986

Heparin-induced platelet aggregation: dose/response relationships for a low molecular weight heparin derivative (PK 10169) and its subfractions.

Addition of heparin or heparin derivatives to citrate anticoagulated platelet-rich plasma caused platelet aggregation in a dose-dependent manner. Utilizing heparin, a low molecular weight heparin derivative (PK 10169) and its various subfractions, we determined dose/response relationships for platelet aggregation and found that the ability of these agents to cause platelet aggregation was dependent upon the molecular weight of the individual subfraction used. In comparison to unmodified porcine mucosal heparin, the lower molecular weight derivative (PK 10169) yielded a dose/response curve that was shifted down and to the right, and indicated that this agent was less potent in causing platelet aggregation. In addition, as the molecular weight of PK 10169 subfractions decreased, their dose/response curves were progressively shifted down and to the right. The lowest molecular weight subfraction was essentially without platelet aggregating activity. We also measured the anti IIa and anti Xa activities of these agents and concluded that these activities did not appear to correlate with platelet aggregating activity. Platelet aggregation studies with PK 10169 subfractions of high and low affinity for antithrombin III (AT III) indicated that the platelet aggregating activity of these compounds may not be related to their affinity for AT III, but results were not definitive.

Antithrombin III↗
PubMed2002

Effects of alcohol ingestion post-exercise on platelet aggregation.

The present study examined the influence of ingesting a moderate dose of alcohol on platelet count and platelet aggregation during recovery following exercise. Nineteen subjects (11 male and 8 female) were studied immediately after a standardised cycle ergometer test and during the 24-h period of recovery. In random order, alcohol (0.7 g/kg body mass) was given 1 h after exercise on one test occasion, while an equal volume of alcohol-free solution was administered on the other. Venous blood samples were obtained at baseline, post-exercise, and at 1, 5, and 22 h post-alcohol ingestion. Blood alcohol level increased significantly 1 h after the ingestion of alcohol, but decreased and returned to the resting baseline level at 5 h during recovery. Males and females subjects exhibited similar mean values of platelet count, platelet aggregation, and beta-thromboglobulin concentration at rest and following exercise and recovery. A significant increase in platelet count and a decrease in platelet aggregation using adenosine diphosphate (ADP) was found following exercise. Although plasma beta-thromboglobulin level (pooled data for males and females) showed an increase by 26.0% (from a mean pre-exercise value of 22.3-28.1 IU/ml), this rise was not significant (P>.05). The post-exercise increase in platelet count was mainly due to exercise-induced plasma volume loss. During recovery, while the increase in platelet count post-exercise returned to the baseline level in control and alcohol trials, the optical density of platelet aggregation remained significantly depressed at 5-h during recovery in the alcohol trial but not in the normal control condition. It is concluded that exercise induces significant reduction in platelet aggregation and the consumption of alcohol after physical exercise delays the normal return of platelet aggregation to the resting baseline levels during recovery.

Adenosine Diphosphate↗
PubMed1985

Prejunctional adrenergic inhibition by aggregating platelets in canine blood vessels.

Experiments were performed to determine the effect of aggregating platelets on adrenergic neurotransmission. Rings of canine saphenous veins and left circumflex coronary arteries were incubated with [3H]norepinephrine and suspended for superfusion. Aggregating platelets and exogenous 5-hydroxytryptamine decreased the overflow of [3H]norepinephrine evoked by electrical stimulation of the adrenergic nerve endings. The reduction of transmitter overflow caused by 5-hydroxytryptamine was prevented by the serotonergic antagonist methiothepin in a concentration that did not significantly affect the release of 5-hydroxytryptamine or thromboxane B2 from the aggregating platelets. Methiothepin decreased but did not abolish the inhibitory effect of aggregating platelets on neurotransmitter overflow. These experiments demonstrate that 5-hydroxytryptamine and other substances released from aggregating platelets can exert prejunctional inhibition of adrenergic neurotransmission in isolated blood vessels.

Animals↗
PubMed1985

A method of testing platelet aggregation in native whole blood.

A method of testing collagen induced platelet aggregation and ATP release in native (= non anticoagulated) whole blood by monitoring the electrical impedance in the Chrono Log Whole Blood Aggregometer is reported. It is the first simple method by which aggregation of human platelets can be measured in their natural environment. In normal individuals lower threshold collagen concentrations could induce platelet aggregation as determined with this method than in the other tested methods (impedance method with citrated blood, optical method in platelet rich plasma). The aggregation response was not inhibited by hirudin or heparin in therapeutic dose. The luminescence channel of the Whole Blood Aggregometer permits measurements of ATP release in native whole blood.

Adult↗
PubMed1992

Effects of aspirin, dipyridamole, nifedipine and cavinton which act on platelet aggregation induced by different aggregating agents alone and in combination.

The effects of aspirin, nifedipine, dipyridamole and cavinton on platelet aggregability in patients with atherosclerosis has been studied using various agents to induce aggregation. The drugs reduced platelet aggregability when aggregation was induced by ADP, adrenaline, or collagen alone. However, if platelet aggregation were induced by combinations of the agonists (including combinations of ADP with either adrenaline or platelet-activating factor (PAF), adrenaline with PAF, and collagen with ADP), the anti-aggregant effects of aspirin, dipyridamole, and cavinton were significantly reduced. The effect of nifedipine was less markedly reduced, especially by combinations which included adrenaline. The data suggest that positive agonist interactions may lead to a reduction in the therapeutic activity of antiplatelet drugs.

Adenosine Diphosphate↗
PubMed2003

Platelet aggregation, thromboxane production and thrombogenic ratio in postmenopausal women consuming high oleic acid-sunflower oil or palmolein.

BACKGROUND: Saturated fatty acids exert controversial effects on platelet aggregation and eicosanoid production. AIM: To investigate the effect of a dietary exchange between palmitic acid and oleic acid on both platelet aggregation and thromboxane B2 (TXB(2)) production, and on urine TXB(2), prostacyclin I2 (PGI(2) as 6-keto-protaglandin F(1)alpha), and the thrombogenic ratio (TXB(2)/6-keto-protaglandin F(1)alpha) in fourteen postmenopausal women. EXPERIMENTAL DESIGN: Women were assigned to two consecutive 28-d dietary periods that were high in cholesterol (~400 mg/d) and fat (~46%en). In the first period all subjects followed an oleic acid-rich diet prepared with high oleic acidsunflower oil. This was followed by a second period rich in palmitic acid in the form of palmolein. DETERMINATIONS: Nutrient intakes, ADP-platelet aggregation, platelet TXB(2) production, urine TXB(2) and 6-keto-protaglandin F(1)alpha were measured during two dietary periods and the results obtained correlated to serum cholesterol, lipoproteincholesterol and peroxides, apolipoproteins and plasma tocopherol. RESULTS: The palmolein diet led to an increase in the platelet aggregation rate (p < 0.05) and in the time for the maximal aggregation rate (p < 0.02). No significant differences were observed in platelet TXB(2) production. Palmolein increased urine TXB(2) in pg/mL (p < 0.05) and pg/min (p < 0.01), whereas the thrombogenic ratio (TXB(2)/6-keto-protaglandin F(1)alpha) did not change. Most changes were related to oil change, few to serum cholesterol level (< or > or = 6.2 mmol/L) or age (< or > or = 65 yr). CONCLUSIONS: Palmolein diet activates platelet aggregation more in normocholesterolemics. Though palmolein increased thromboxane and tended to increase prostacyclin in urine in normo- and hypercholesterolemic women, the thrombogenic ratio did not change. These effects were related to the LDL and HDL concentration increases and to the absence of change in the total cholesterol/HDL-cholesterol ratio found following the dietary intervention.

Aged↗
PubMed1992

Platelet alpha 2 adrenoceptor characteristics during the morning increase in platelet aggregability.

The incidence of myocardial infarction and sudden cardiac death increases in the morning, as do platelet aggregability and sympathetic activity. We considered the possibility that increased platelet aggregability in the morning was due to an increase in platelet alpha 2 adrenergic receptor number or agonist binding affinity, or to a temporal disparity between the increase in sympathetic activity that accompanies arising and the anticipated decrease in platelet high affinity alpha 2 adrenoceptors. To evaluate these possibilities, we studied eight healthy male volunteers (20-35 years) before and 1-1.5 and 3-4 h after they arose at 08.00 h and performed routine morning activities. Platelet aggregability was determined in platelet-rich plasma; alpha 2 adrenoceptor density and agonist binding affinity were determined in intact platelets and in membrane preparations using the alpha 2 selective ligand [3H]-yohimbine. The threshold concentration of epinephrine required to produce biphasic aggregation decreased (i.e. platelet aggregability increased) from 3.6 +/- 1.2 to 0.9 +/- 0.3 microM (P less than 0.05) after arising. However, alpha 2 adrenoceptor density (380 +/- 71 to 365 +/- 51 sites per platelet) and agonist binding affinity assessed simultaneously did not change after arising, suggesting that the increase in platelet aggregability is due to factors extrinsic to the platelets or to an intra-platelet mechanism distal to the receptor level.

Adenosine Diphosphate↗
PubMed1989

Circadian variation in circulating platelet aggregates.

Acute coronary events are more likely to occur in the morning and it has recently been shown that platelet aggregability increases significantly then. To determine whether circulating platelet aggregates show such a circadian variation, we measured in vivo platelet aggregation in atherosclerotic patients and healthy subjects at three-hour intervals throughout a 24-hour period. We found a significant variation in circulating platelet aggregates, the highest being at 6 a.m. and the lowest at 9 a.m. We suggest that it may be important to consider the duration of action of anti-aggregating drugs and timing their administration with respect to circadian variation in circulating platelet aggregates.

Adult↗
PubMed1991

A monoclonal antibody to a 67 kD cell membrane glycoprotein directly induces persistent platelet aggregation independently of granule secretion.

The transition from reversible to persistent platelet aggregation has been difficult to study because of interference both from preceding primary aggregation and from the events associated with granule secretion during secondary aggregation. As a result it remains unclear whether the persistence of aggregation involves some secretion-independent specific platelet surface reactions. Here we show that a monoclonal antibody (MAb), LeoAl, against a newly described 67 kD platelet membrane glycoprotein induced active platelet aggregation consisting of two distinct phases. The first secretion-independent phase was in several respects (extracellular protein, divalent cation, and pH dependence) different from primary aggregation, but closely resembled the transition from primary to secondary aggregation observed at certain concentrations of physiological agonists. The second, faster phase was indistinguishable from secretion-dependent aggregation to various stimulants. It was shown that p67, GPIIb-IIIa and FC gamma RII are all involved in the observed aggregation, probably through their close topographical association. It is suggested that LeoAl-induced aggregation can be used as a model to study the receptors, ligands and metabolic pathways specifically involved in the transition from reversible to persistent platelet aggregation.

Antibodies, Monoclonal↗
PubMed1991

[Effect of rhyncophylline on platelet aggregation and experimental thrombosis].

Rhyncophylline (Rhy) produced a potent inhibition of rat platelet aggregation in ex vivo. TXA2 generation in platelet rich plasma from rats treated with Rhy obviously decreased in the collagen-induced group, but was not altered in the AA-induced group. These results suggest that Rhy suppressed the release of AA from platelet phospholipids stimulated by collagen, and this may be one of the mechanisms related to its action on platelet aggregation. Pretreatment with ASA, but not Rhy, reduced plasma PGI2 in rats. In the in vitro system, the PGI2 synthesis in rat aorta was shown to be inhibited by ASA but was not by Rhy. Rhy significantly reduced the number of mice died due to thrombosis by platelet aggregates. ASA prevented collagen plus adrenaline induced thrombotic death while Rhy prevented both ADP and collagen plus adrenaline induced thrombotic death.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Whole blood platelet aggregation in dogs with liver disease.

Whole blood platelet aggregation was determined in response to collagen, arachidonic acid, and adenosine diphosphate in 20 dogs with liver disease and in 20 control dogs. Platelet aggregation in response to collagen and arachidonic acid was reduced in dogs with liver disease, compared with control dogs (P less than 0.05), whereas there was no significant difference in platelet response to adenosine diphosphate between the 2 groups of dogs. Adenosine diphosphate was found not to be a reliable aggregation agent for determination of whole blood platelet aggregation in dogs. Dogs whose platelets did not aggregate in response to collagen and/or arachidonic acid manifested bleeding tendencies that could be attributed to platelet dysfunction.

Adenosine Diphosphate↗
PubMed1981

The effects of neuroleptic drugs on 5-hydroxytryptamine induced platelet aggregation in schizophrenic patients.

1 The effects of treatment with a range of neuroleptic drugs on 5-hydroxytryptamine (5-HT) induced platelet aggregation in vivo were examined in a group of recently admitted psychiatric patients and in a larger group of chronic schizophrenic patients. 2 Five of seven recently admitted patients treated with chlorpromazine showed enhanced aggregation. Four of seven patients treated with fluphenazine, flupenthixol, trifluoperazine and haloperidol showed enhancement. 3 Enhanced aggregation responses were observed in only 20% of chronic schizophrenic patients being treated with a neuroleptic drug. 4 The relationship between changes in platelet aggregation and clinical changes in recently admitted patients was variable and platelet aggregation responses were not predictive of response to treatment. 5 Chronic schizophrenic patients with enhanced aggregation showed significant week to week variation in platelet aggregation response. Variability of responses was not related to the drug used or to the dose administered. There was some evidence that higher plasma concentrations of neuroleptic drugs were associated with enhanced platelet aggregation responses. 6 Treatment with neuroleptic drugs leads to enhancement of platelet aggregation responses induced by 5-HT. The frequency and reliability with which such responses can be elicited is unpredictable and the value of platelet aggregation responses as an empirical guide to treatment with neuroleptic drugs is therefore open to question.

Antipsychotic Agents↗
PubMed2000

Endothelin-B-receptors-dependent-inhibition of platelet aggregation in the CD-1 mouse.

An experimental protocol of adenosine diphosphate-(ADP) induced platelet aggregation in the mouse was designed in order to study the roles played by endothelin-A (ET(A)) and endothelin-B (ET(B)) receptors in the ET-1-induced inhibition of ex vivo platelet aggregation. The pressor effects of ET-1 or IRL-1620 were firstly determined in vivo in anesthetized (ketamine/xylazine) CD-1 mice (males and females; 25-30 g). All agents were administered intravenously (via the jugular vein) and blood samples were collected from the carotid artery into heparinized Eppendorfs (15 U/ml). To obtain platelet-rich plasma (PRP) the blood was immediately centrifuged for 12 min at low speed (1100 g). Platelet-poor plasma (PPP) was then prepared by centrifugation of the whole blood sample at high speed (3700 g) for 30 min. PPP was used to calibrate the aggregometer at 100% transmission. Platelet aggregation was monitored ex vivo as a change in light transmission through PRP following the injection of ADP (5 microM). ET-1 (0.01-2.0 nmol/kg) induced a significant and dose-dependent inhibition of platelet aggregation ex vivo (12-84%). The selective ET(B) agonist, IRL-1620 (0.05-2.0 nmol/kg), also triggered a marked inhibition of platelet aggregation. Indomethacin (10 mg/kg), a nonselective cyclooxygenase inhibitor, abolished the inhibitory effect of ET-1. The selective ET(A) antagonist, BQ-123 (1 nmol/kg), abolished the in vivo pressor effect of exogenous ET-1, without affecting its anti-aggregatory activity. The selective ET(B) antagonist, BQ-788 (0.5 nmol/kg), did not modify the elevation of blood pressure produced by the ET-1; however, it did abrogate dose-dependently the inhibitory effect of ET-1 on platelet aggregation. These results suggest that the anti-aggregatory effect of ET-1, in anesthetized CD-1 mice, relies mainly upon the activation of ET(B) receptors. The mechanism whereby ET-1 exerts this effect, is partially indirect and requires at least the production and the release of prostanoids (possibly PGI2) into the blood stream.

Animals↗
PubMed1995

Effects of stonustoxin (lethal factor from Synanceja horrida venom) on platelet aggregation.

Stonustoxin (SNTX) is a 148,000 mol. wt lethal factor isolated from Synanceja horrida venom. It induces species-restricted red cell haemolysis which correlates with its effects on platelet aggregation in whole blood. SNTX induced a concentration-dependent and irreversible platelet aggregation in rabbit or rat but not in human or mouse whole blood. The degree of haemolysis and platelet aggregation induced by SNTX in rabbit or rat whole blood were concentration dependent. At concentrations of SNTX where only slight or no haemolysis was observed, no platelet aggregation occurred. Although SNTX itself could not induce platelet aggregation in rabbit or rat platelet-rich plasma (PRP), it had biphasic effects on collagen- or ADP-induced platelet aggregation in PRP. It inhibited collagen- or ADP-induced platelet aggregation at high concentrations (0.08-0.8 micrograms/ml) but the response was potentiated by lower stonustoxin concentrations (0.008-0.016 micrograms/ml). The inhibition of collagen- or ADP-induced platelet aggregation might be due to the lytic activity of SNTX on the platelets.

Animals↗
PubMed1989

Hypercholesterolemia causes generalized impairment of endothelium-dependent relaxation to aggregating platelets in porcine arteries.

The role of the endothelium in response to aggregating platelets was examined in porcine coronary and peripheral (carotid, femoral and renal) arteries from normal and hypercholesterolemic pigs. Male Yorkshire pigs were fed either a normal diet or a 2% high cholesterol diet for 10 weeks. Endothelium-dependent responses were examined in vitro. In all arteries from control animals, aggregating platelets caused endothelium-dependent relaxations, which were augmented by ketanserin (a 5-HT2-serotonergic blocker), attenuated by apyrase (an adenosine diphosphatase and triphosphatase) or methiothepin (a combined 5-HT1 and 5-HT2-serotonergic blocker) and were almost abolished by a combination of apyrase and methiothepin. The platelet-induced relaxations were most pronounced in the coronary arteries. Adenosine diphosphate caused endothelium-dependent relaxations, which were significantly attenuated by apyrase. Serotonin also caused endothelium-dependent relaxations, which were significantly attenuated by methiothepin but augmented by ketanserin. The endothelium-dependent relaxations to adenosine diphosphate were most pronounced in coronary arteries and those to serotonin in coronary and renal arteries. In cholesterol-fed animals, the endothelium-dependent relaxations to aggregating platelets, adenosine diphosphate and serotonin were impaired in all four arteries. These experiments indicate that 1) the endothelium exerts inhibitory effects against aggregating platelets in porcine coronary and peripheral arteries; 2) platelet-induced endothelium-dependent relaxations are achieved by purinergic and 5-HT1-serotonergic receptors on the endothelium; and 3) hypercholesterolemia reduces the endothelium-dependent relaxations to aggregating platelets in a generalized manner because it impairs the relaxations to adenosine diphosphate and serotonin released from the platelets.

Animals↗
PubMed1986

Interaction of local anaesthetics with blood platelet aggregation.

The effect of three newly synthesized local anaesthetics on platelet aggregation, serotonin release and integrity of platelets was investigated. Pentacaine, heptacaine and carbisocaine were found to be about 10 times more active than "classic" local anaesthetics. They inhibited platelet aggregation stimulated by collagen, thrombin and ADP at the concentrations of 0.01, 0.1 and 1 mmol/l respectively. At millimolar concentrations the test local anaesthetics liberated serotonin from platelets and disintegrated platelet membranes. Pentacaine was the most effective, followed by heptacaine and carbisocaine. The authors suppose that the perturbation induced in platelet membranes by local anaesthetics could be responsible for inhibition of platelet aggregation and release of serotonin.

Anesthetics, Local↗
PubMed1998

Inhibition of rat platelet aggregation by mycalolide-B, a novel inhibitor of actin polymerization with a different mechanism of action from cytochalasin-D.

In vitro effects of mycalolide-B (MB), isolated from marine sponge, were investigated with regard to the activation of rat platelets. Collagen-induced platelet aggregation in platelet-rich plasma (PRP) was slightly but significantly potentiated by lower concentrations of MB (0.3 and 1 microM) but was inhibited by higher concentrations (3 and 10 microM). ADP-induced platelet aggregation in PRP was also significantly prevented by MB (1-10 microM). Potentiation of ADP-induced aggregation by MB (0.3 microM) was hardly observed. G-actin contents, determined by DNase I inhibition assay, were increased in resting washed platelets incubated with MB (3 microM). In contrast, cytochalasin-D (CD) at 3 microM slightly reduced G-actin contents in resting platelets. After platelet aggregation with collagen (3 microg/ml) or ADP (10 microM), G-actin contents in platelets were reduced, indicating de novo actin polymerization. MB (3 microM) and CD (3 microM) abolished both ADP (10 microM)- and collagen (3 microg/ml)-induced platelet aggregation and actin polymerization in washed platelets. MB (1-10 microM) had no effects on intracellular Ca2+ concentrations in ADP (10 microM)-stimulated platelets. [125I]-fibrinogen binding to activated platelets with ADP (10 microM)(was inhibited by MB (0.3-3 microM) in a concentration-dependent manner. Thrombin-induced platelet-fibrin clot retraction was inhibited by MB (1 and 10 microM). These results suggest that MB inhibits platelet activation by interfering with actin polymerization through a different mechanism of action from CD. MB may be a useful tool for studying the role of actin polymerization in various cells.

Actins↗