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PubMed1998

Activation of leukocytes in whole blood samples by N-formyl-methionyl-leucyl-phenylalanine (FMLP) enhances platelet aggregability but not platelet P-selectin exposure and adhesion to leukocytes.

Adhesion of platelets to neutrophils and monocytes is believed to play an important role in intercellular communication. Evidence has been provided that such heterotypic cell-cell contacts via adhesion molecules may be directly involved in intercellular signal transduction as well as facilitate the action of soluble signal transmitters, e.g. cathepsin G, PAF or nitric oxide. With respect to platelet activation, stimulatory and inhibitory effects of leukocytes have been reported, and the results obtained seem to be influenced by the experimental conditions. We investigated the effect of leukocyte stimulation on platelet behaviour in samples of human citrated whole blood. Adding the chemotactic peptide FM LP, which stimulates neutrophils and monocytes but not lymphocytes and platelets, to stirred whole blood samples resulted in a significant enhancement ( P < 0.01) of spontaneous as well as ADP-induced platelet aggregation (25 vs 33% and 66 vs 69% , respectively). In contrast stirring-induced as well as ADP-induced increase of P-selectin exposure (33 and 107% , respectively) was not affected by FMLP. In unstirred whole blood samples, about 10 to 20% of neutrophils and monocytes had bound platelets to their surfaces, and the number of these heterotypic conjugates was enhanced about twofold during spontaneous platelet aggregation. Addition of FMLP significantly reduced the stirring-induced formation of platelet-neutrophil conjugates but not of platelet-monocyte conjugates. These results indicate that neutrophil and/or monocyte activation in whole blood may enhance platelet aggregation, but not secretion (CD62P exposure) and formation of heterotypic platelet-leukocyte conjugates.

Journal Article↗
PubMed1993

Short-term and long-term role of platelet activating factor as a mediator of in vivo platelet aggregation.

BACKGROUND: Platelet activating factor (PAF) is a phospholipid released upon stimulation by a variety of cells and has been implicated in several pathophysiological events such as asthma and inflammatory diseases. However, although the ability to aggregate platelets in vitro was the first biological activity ascribed to PAF, its role in contributing to the in vivo formation of arterial thrombi has not been thoroughly clarified. METHODS AND RESULTS: Intravascular platelet aggregation was initiated in two different animal models of arterial stenosis and endothelial injury. An external constrictor was positioned around rabbit carotid arteries and canine coronary arteries. After placement of the constrictor, a typical pattern of flow developed in the stenotic vessels. This pattern of flow, characterized by progressive reductions of carotid or coronary blood flow followed by spontaneous or induced restorations of flow (cyclic flow variations, CFVs), is related to recurrent platelet aggregation at the site of the stenosis followed by dislodgment of the thrombus. After observing CFVs for 30 minutes, BN52021 (up to 1.2 mg/kg), a potent and selective PAF antagonist, was given intravenously to rabbits (n = 12) and dogs (n = 10). BN52021 completely inhibited CFVs in 10 of 12 rabbits, whereas it was relatively ineffective in abolishing CFVs in dogs (only 2 of 10 animals inhibited). This different effect of BN52021 was not explained by too small a dose of the drug to achieve a complete blockade of PAF receptors in dogs, since ex vivo platelet aggregation was completely inhibited in both rabbits and dogs in response to exogenous PAF at concentrations up to 10(-5) mol/L. In a second group of 10 dogs, the hypothesis that PAF may become an important mediator of CFVs in dogs only several hours after endothelial injury was tested. After 30 minutes of baseline CFVs, these animals received a bolus of BN52021 up to 1.2 mg/kg. After this treatment, CFVs were completely abolished in 2 of 10 animals. The remaining 8 dogs were followed for an additional 8-hour period, at the end of which a second bolus of BN52021 was given. At this time, BN52021 was effective, as CFVs were abolished in 6 of 8 animals. These effects of BN52021 at 8 hours were not the consequence of a cumulative dose of the compound, since ex vivo platelet aggregation in response to PAF returned to baseline values immediately before administering the second dose. To identify possible sources of PAF other than aggregating platelets at the site of arterial stenosis, dogs in a third group were killed after 30 minutes (n = 7) and after 8 hours (n = 8) of CFVs. Histological sections of the stenotic coronary artery showed a marked leukocyte infiltration in these arterial segments after 8 hours of CFVs, whereas sections from dogs killed after 30 minutes showed only moderate or no infiltration. CONCLUSIONS: These data demonstrate that PAF plays an important role as a mediator of platelet aggregation in vivo in rabbits and dogs. In the canine model, PAF appears to become more important after leukocyte infiltration of the arterial wall, as it may contribute to initiating enough platelet activation to lead to cyclic flow variations at sites of arterial stenosis and endothelial injury. Data from the present study suggest that PAF antagonists may be used as antiplatelet agents.

Animals↗
PubMed2000

Effects of endothelial cells and mononuclear leukocytes on platelet aggregation.

Although normal vascular endothelium prevents adhesion and aggregation of platelets by the release of nitric oxide (NO) and prostacyclin, the endothelium exposed to oxidized low density lipoprotein (LDL) may be damaged, damage that may include a reduction in its secretory capacity. On the other hand, mononuclear leukocytes (ML) can also release NO to inhibit platelet aggregation. Platelet aggregation was measured with a Chrono-Log aggregometer (USA) in the presence of cultured endothelial cells (EC) or isolated ML, stimulated by collagen. Platelet aggregation was markedly inhibited (28.5 +/- 5.0 versus control 92.2 +/- 1.7%), when EC were added to platelets. Pre-incubation of the EC with 10 micromol/l of indomethacin or 300 micromol/l of L-NG-monomethyl-arginine (L-NMMA) for 6 h substantially reduced their anti-aggregating activity (72.8 +/- 5.1 and 76.6 +/- 7.7%, respectively). However, incubation of the EC in culture with 10 micromol/l of lysophosphatidyl choline (LPC) for 6 h did not affect the anti-aggregating capacity of EC (LPC 28.1 +/- 5.5 vs. EC 28.5 +/- 5.0%). Non-stimulated ML also inhibited (43.2 + 5.9 vs. control 69.2 3.2%) the platelet aggregation induced by collagen. The inhibition was dependent on the number of ML added. In addition, it was enhanced by increasing the concentration of collagen from 2.5 to 10 microg/ml. Platelet aggregation is inhibited mainly by the EC, however, blood ML also inhibit platelet aggregation. Incubation of the EC in culture with LPC did not affect the anti-aggregating capacity of the EC.

Animals↗
PubMed1998

Heparin-bonded grafts induce platelet aggregation in the presence of heparin-associated antiplatelet antibodies.

PURPOSE: Thromboresistant synthetic grafts should decrease the frequency of graft thromboses and could be useful in bypasses to small arteries and to arteries with compromised flow. Heparin-bonded grafts (HBG) have been developed. Studies were done to determine whether the heparin bond is permanent and whether the HBG would aggregate platelets in the presence of heparin-associated antiplatelet antibodies (HAAbs). METHODS: We studied an 8 mm HBG from company A (HBGA) and 8 mm and 6 mm HBGs from company B (HBGB-8 and HBGB-6), none of which is available for clinical use in the United States. Five 1 cm long segments of HBGA, HBGB-8, and HBGB-6 were incubated for 24 hours in 5 ml of plasma, 10 ml of saline, or 10 ml of Ringer's lactate. After incubation, 1 ml was obtained from each solution and assayed for heparin. Segments of each graft that leached off an equivalent of 1 U of heparin/ml (i.e., 1 mm2 of HBGA, 5 mm2 of HBGB-8, and 20 mm2 of HBGB-6) were incubated with 0.15 ml of plasma with HAAbs (six samples per graft) for 30 minutes at 25 degrees C. The grafts were removed, and 0.1 ml of normal-donor, platelet-rich plasma was added. The samples were placed in an aggregometer and allowed to react until positive aggregation occurred or 27 minutes had elapsed. Segments of non-heparin-bonded polyester grafts served as controls. RESULTS: Heparin leached off all grafts in plasma (mean values: HBGA, 83.4 U of heparin/ml; HBGB-8, 4 U of heparin/ml; HBGB-6, 6.2 U of heparin/ml). In normal saline, the mean heparin concentrations were lower (HBGA, 10.8 U of heparin/ml; HBGB-8, 0 U of heparin/ml; HBGB-6, 0.01 U of heparin/ml. The mean heparin concentration after incubation in Ringer's lactate were 10 U of heparin/ml for HBGA, 0 U of heparin/ml HBGB-8, and 0.22 U of heparin/ml HBGB-6. All of the HBGs induced platelet aggregation inHAAb-positive plasma. None of the control grafts induced platelet aggregation in HAAb-positive plasma. CONCLUSIONS: All HBGs leached heparin into plasma, and all induced platelet aggregation in the presence of HAAbs. The possibility of sensitizing patients to heparin leeching from a HBG with the activation of platelets and secondary thrombosis strongly suggests that HBG be used with great caution. Other methods for inducing graft thromboresistance should be developed.

Antibodies↗
PubMed1986

The effect of AD6 (8-monochloro-3-beta-diethylamino-ethyl-4-methyl-7-ethoxy- carbonylmethoxycoumarin) on washed human platelet aggregation induced by platelet activating factor (PAF) and epinephrine.

The effect of AD6 (8-monochloro-3-beta-diethylamino-ethyl-4-methyl-7- ethoxycarbonylmethoxycoumarin) was studied in vitro on washed human platelet aggregation and beta-thromboglobulin (beta TG) release induced by PAF alone or in combination with epinephrine. AD6 caused concentration-dependent inhibition of aggregation and beta TG release. Acetylsalicylic acid and the ADP scavenger apyrase were ineffective on the same parameters, while the specific PAF antagonist CV 3988, the Ca2+ antagonist diltiazem and the cyclo-oxygenase-lipoxygenase inhibitors nordihydroguaiaretic acid and BW 755C inhibited aggregation. The results indicate that AD6 is an inhibitor of platelet aggregation in vitro with a mode of action different from cyclo-oxygenase blockade.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed2005

Enhanced expression of Aggrus (T1alpha/podoplanin), a platelet-aggregation-inducing factor in lung squamous cell carcinoma.

Aggrus (T1alpha/podoplanin, known as a specific marker for type I alveolar cells or lymphatic endothelial cells) is a transmembrane sialoglycoprotein that aggregates platelets. Previously, we showed that upregulated expression of Aggrus occurs in colorectal tumors or testicular tumors and could be associated with platelet-aggregating activity and metastatic ability. In testicular tumors, Aggrus is specifically expressed in seminoma. The present study investigates Aggrus expression in human primary lung cancer tissues of different types. Microarray analysis demonstrated that aggrus was significantly expressed in squamous cell carcinoma (10/15; 66.7%). Immunohistochemical analysis also showed that the incidence of positive staining in sections of squamous cell carcinoma (7/8; 87.5%) was higher than that in adenocarcinoma (2/13; 15.4%). Furthermore, Aggrus expression was detected in a squamous cell carcinoma cell line, NCI-H226, by real-time PCR. These findings indicated that overexpression of Aggrus occurred in squamous cell carcinoma of the lung. Therefore, Aggrus could be a useful diagnostic marker for squamous cell carcinoma of the lung.

Biomarkers, Tumor↗
PubMedDate not supplied

Synergistic interaction of epinephrine and calcium ionophore in platelet aggregation.

BACKGROUND: Platelets play a key role in haemostasis. Human Platelets contain alpha2 adrenergic receptors, which are coupled with guanine nucleotide proteins (G proteins). The platelet activation involves a number of receptors for agonists. It has also been shown that most of the agonists act in synergy and potentiate the effects of each other. The present experimental study was designed to study the potentiation of epinephrine on human platelets by calcium ionophore A23187 and the possible role of calcium in platelet aggregation as a second messenger. METHODS: Study was carried out at Department of Biological Sciences Aga Khan University, Karachi. Blood samples from healthy volunteers were collected; Platelet aggregation was measured using Dual channel Lumi Aggregometer. The chemicals used include epinephrine, calcium ionophore A23187, yohimbine, diltiazem, verapamil and S Nitrosoacetylpenicillamin (SNAP). RESULTS: Epinephrine at low concentrations (0.01-0.2 microM) and/or A23187 (0.1-0.5 microM) itself did not produce platelet aggregation. However, when added together, a marked potentiation of platelet aggregation was observed. This synergistic effect was inhibited by alpha2-receptor blocker yohimbine; (IC50 = 0.05 microM) showing that the response is receptor mediated. To find out the molecular basis of this potentiation, we used SNAP, a nitric oxide donor and Ca++ channel blockers, i.e. diltiazem and verapamil. The SNAP, diltiazem and verapamil inhibited the platelet aggregation induced by A23187 and epinephrine with IC50 value of 0.5 microM, 50 microM and 22 microM respectively. CONCLUSION: The results of the study suggest that epinephrine and calcium ionophore act synergistically and Ca++ plays an important role in this synergistic interaction. While calcium channels blocking drugs diltiazem and verapamil inhibit this synergism.

Calcium↗
PubMed1970

Effet of prostaglandin E1 alone and in combination with theophylline or aspirin on collagen-induced platelet aggregation and on platelet nucleotides including adenosine 3':5'-cyclic monophosphate.

1. Human platelet nucleotides were labelled by incubating platelet-rich plasma with [U-(14)C]adenine. With such platelets, the effects of prostaglandin E1, theophylline and aspirin were determined on collagen-induced platelet aggregation and release of platelet ATP and ADP. Intracellular changes of platelet radioactive nucleotides, particularly 3':5'-cyclic AMP, were also determined both with and without collagen treatment. 2. Prostaglandin E1, theophylline and aspirin inhibited collagen-induced aggregation of platelets in a dose-dependent manner. Collagen-induced release of ATP and ADP and breakdown of radioactive ATP were also inhibited in a dose-dependent manner. 3. Prostaglandin E1 stimulated the formation of platelet radioactive 3':5'-cyclic AMP in a dose-dependent manner. With a given dose of prostaglandin E1, maximum formation of radioactive 3':5'-cyclic AMP occurred by 10-30s and thereafter the concentrations declined. The degree of inhibition of aggregation produced by prostaglandin E1, however, increased with its time of incubation in platelet-rich plasma before addition of collagen, so that there was an inverse relationship between the radioactive 3':5'-cyclic AMP concentration measured at the time of collagen addition and the subsequent degree of inhibition of aggregation obtained. 4. Neither theophylline nor aspirin at a concentration in platelet-rich plasma of 1.7mm altered platelet radioactive 3':5'-cyclic AMP contents. In the presence of prostaglandin E1, theophylline increased the concentration of radioactive 3':5'-cyclic AMP over that noted with prostaglandin E1 alone, but aspirin did not. 5. Mixtures of prostaglandin E1 and theophylline had a synergistic effect on inhibition of platelet aggregation. The same was true to a lesser extent with mixtures of prostaglandin E1 and aspirin. Such mixtures also inhibited collagen-induced release of platelet ATP and ADP and breakdown of platelet radioactive ATP. 6. Certain concentrations of either theophylline or aspirin and mixtures of small concentrations of prostaglandin E1 with either theophylline or aspirin caused little or no increase of radioactive 3':5'-cyclic AMP at the time of collagen addition, but inhibited aggregation to a marked degree, whereas higher concentrations of prostaglandin E1 alone caused a much greater increase of radioactive 3':5'-cyclic AMP at the time of collagen addition but inhibited aggregation to a lesser extent. With these compounds there does not appear to be a correlation between these parameters.

Adenine Nucleotides↗
PubMed1992

Membrane fluidity and platelet aggregation: dibucaine permits ristocetin-induced platelet aggregation with low-molecular-weight von Willebrand multimers.

The effects of brief incubation of platelets with dibucaine were studied. Membrane fluidity was increased after incubation with 1 mM dibucaine for 1 min as determined by fluorescence polarization. Platelet aggregation was increased when ristocetin was employed as modulator and normal plasma used as a source of von Willebrand factor (vWF). In contrast, aggregation was decreased with botrocetin. After cryoprecipitation the supernatant, which contained predominantly low-molecular-weight vWF multimers, was effective with ristocetin only after prior incubation of the platelets with dibucaine. This indicates that low-molecular-weight vWF multimers can also support ristocetin-induced aggregation when the membrane fluidity is increased. This idea was supported by the use of plasma from a patient with von Willebrand disease type IIa. Being a multimeric protein, von Willebrand factor contains multiple binding sites for glycoprotein Ib (GP Ib). GP Ib-dependent aggregation by agents that do not contain multiple binding sites, i.e. wheat germ agglutinin or polyclonal antibodies to GP Ib, was decreased after brief incubation with dibucaine. These observations are discussed in relation to the hypothesis that the increased membrane fluidity allows an increased number of GP Ib molecules to bind to each vWF multimer.

Crotalid Venoms↗
PubMed1980

Correlation between fibrinogen binding to human platelets and platelet aggregability.

Fibrinogen is essential for aggregating platelets with adenosine diphosphate (ADP) and was recently shown to bind to platelets stimulated with ADP. The present work confirms the specific and saturable nature of the platelet-fibrinogen interaction. Binding of 125iodine-labeled fibrinogen to human gel-filtered platelts was maximal at 1 min, and the receptors were saturated when the fibrinogen concentration in the suspending medium approached 0.8 mg/ml. Assuming that one fibrinogen molecule interacts with a single receptor, experiments with 9 normal donors revealed the presence of 12,896 +/- 2456 receptors per platelet. Much of the bound material dissociated from platelets after incubation with apyrase or EDTA. Binding was markedly inhibited at pH 6.5, in the presence of EDTA, and with platelets from 3 thrombasthenic patients but not with those from a patient with the Bernard-Soulier syndrome. Fibrinogen binding was also virtually absent with platelets that had been incubated with EDTA for 8 min at 37 degrees C and pH 7.8. These platelets could not aggregate when mixed with ADP and adequate CaCl2 and fibrinogen, although they could still change their shape. Thus, ADP-induced binding of fibrinogen correlates with platelet aggregability.

Adenosine Diphosphate↗
PubMed1980

Circulating platelet aggregates: a chronic platelet activation in patients with transient ischaemic attacks.

Platelet hyperaggregability was tested in 62 TIA patients by means of the formalin fixing principle of Wu and Hoak. Compared to age-matched controls, the platelet aggregates ratio (PAR) was reduced from 0.99 +/- 0.04 SD to 0.807 +/- 0.14 SD. This means a highly significant increase of circulating platelet aggregates (CPA) in untreated TIA patients, regardless of the interval sinche the last attack (from 2 days to 1 year). PAR was especially reduced in patients with abnormal angiography (expressing pronounced cerebral or diffuse ATS) and it was possibly affected by previous antiplatelet treatment with ASA.

Aspirin↗
PubMed1999

Platelet aggregation and platelet-derived growth factor inhibition for prevention of insufficiency of the transjugular intrahepatic portosystemic shunt: a randomized study comparing trapidil plus ticlopidine with heparin treatment.

Intimal proliferation at the interface between prosthetic material and tissue is an intrinsic phenomenon of stenting and the major cause of insufficiency of the transjugular intrahepatic portosystemic shunt (TIPS). For its prevention, a randomized study was performed comparing standard heparin treatment with a combination of trapidil, a drug with anti-platelet-derived growth factor (PDGF) activity, and ticlopidine, a platelet aggregation inhibitor. Ninety patients with cirrhosis who received a transjugular shunt were randomized, and 84 patients completed the trial. Group 1 (n = 42) received a bolus of heparin (12 to 24 U/kg) at shunt placement, followed by 1 week of intravenous and 4 weeks of subcutaneous heparin treatment. Group 2 (n = 42) received the same heparin bolus, followed by a 1-day intravenous heparin treatment and a 6-month treatment with trapidil (400 mg/d) and ticlopidine (250 mg/d). Shunt function was assessed by duplex-sonography and angiography. Stenoses were classified according to their location as type 1 (within the stent) and type 2 (in the draining hepatic vein). The estimated rate of overall stenoses (intention-to-treat analysis) at 1 year showed a significant reduction in patients receiving trapidil and ticlopidine (group 2) as compared with heparin (33 vs. 57%; P =.047). There was no difference in the estimated 1-year rate of type 1 stenoses between the two groups, but there was a significant reduction in type 2 stenoses (group 1: 58%, group 2: 19%; P =.016). The treatment effect continued after withdrawal of the drugs and was accompanied by a decreased incidence of rebleeding. The study demonstrates that the incidence of type 2 stenosis of the transjugular shunt can be reduced by combined inhibition of platelet aggregation and PDGF activity. The findings may be of relevance not only for the transjugular shunt, but also for other stent applications, e.g., vascular and biliary, as well as for bypass and shunt surgery.

Drug Therapy, Combination↗
PubMed1978

Inhibition of platelet aggregation by protease inhibitors. Possible involvement of proteases in platelet aggregation.

The possible participation of proteases in human platelet aggregation was explored using various protease inhibitors and substrates. Protease inhibitors used included naturally occurring inhibitors of serine proteases and synthetic inhibitors that modify the active site of protease. Substrates used were synthetic substrates for the trypsin type as well as for the chymotrypsin type of protease. All these inhibitors and substrates inhibited platelet aggregation and serotonin release induced by ADP, collagen, epinephrine, or thrombin. In ADP- and epinephrine-induced platelet aggregation the second phase of aggregation was most efficiently inhibited. The inhibitors suppressed the formation of malondialdehyde during platelet aggregation. Release by aggregating agents of arachidonate and its metabolites from indomethacin-treated platelets as well as nontreated platelets was also inhibited. The inhibitors apperar to interact with stimulated platelets but not with unstimulated platelets. These observations suggest that the interaction of an aggregating agent with its platelet receptor activates a unique precursor serine protease that in turn activates platelet phospholipase to liberate arachidonic acid (the precursor of the potent platelet aggregating agent thromboxane A2) from platelet phospholipids.

Arachidonic Acids↗
PubMed1996

Purinoceptors and platelet aggregation.

1. Adenosine 5'-diphosphate (ADP) is a physiologically important mediator, being released from damaged cells and from aggregating platelets. It acts on platelets to cause aggregation via a purinoceptor ('P2T-purinoceptor') at which adenosine 5'-triphosphate (ATP) is a competitive antagonist; however, the way in which it does so is not fully understood. 2. ADP activates a G12 protein, is a weak activator of phospholipase C but causes calcium mobilization from internal stores, and also inhibits adenylate cyclase. It seems likely that these effects are mediated by a single receptor but this is still unclear. 3. ADP also causes a rapid calcium influx which has the characteristics of a receptor-operated channel, and it has been suggested that this is due to a P2X1 receptor. This suggests the presence of at least two types of receptor responding to ADP, one G protein coupled and one a cation channel, and raises questions about the role of ATP in platelet function. 4. Adenosine acts via an A2a receptor to stimulate adenylate cyclase in platelets, and this nonselectively inhibits platelet activation. As ADP released from platelets is broken down to adenosine by ectonucleotidases on endothelial cells, this may provide an important mechanism for limiting inappropriate platelet aggregation in an intact blood vessel.

Adenosine Diphosphate↗
PubMed2003

Evidence for a role for Galphai1 in mediating weak agonist-induced platelet aggregation in human platelets: reduced Galphai1 expression and defective Gi signaling in the platelets of a patient with a chronic bleeding disorder.

We have examined platelet functional responses and characterized a novel signaling defect in the platelets of a patient suffering from a chronic bleeding disorder. Platelet aggregation responses stimulated by weak agonists such as adenosine diphosphate (ADP) and adrenaline were severely impaired. In comparison, both aggregation and dense granule secretion were normal following activation with high doses of collagen, thrombin, or phorbol-12 myristate-13 acetate (PMA). ADP, thrombin, or thromboxane A2 (TxA2) signaling through their respective Gq-coupled receptors was normal as assessed by measuring either mobilization of intracellular calcium, diacylglycerol (DAG) generation, or pleckstrin phosphorylation. In comparison, Gi-mediated signaling induced by either thrombin, ADP, or adrenaline, examined by suppression of forskolin-stimulated rise in cyclic AMP (cAMP) was impaired, indicating dysfunctional Galphai signaling. Immunoblot analysis of platelet membranes with specific antiserum against different Galpha subunits indicated normal levels of Galphai2,Galphai3,Galphaz, and Galphaq in patient platelets. However, the Galphai1level was reduced to 25% of that found in normal platelets. Analysis of platelet cDNA and gDNA revealed no abnormality in either the Galphai1 or Galphai2 gene sequences. Our studies implicate the minor expressed Galphai subtype Galphai1 as having an important role in regulating signaling pathways associated with the activation of alphaIIbbeta3 and subsequent platelet aggregation by weak agonists.

Adenosine Diphosphate↗