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PubMed2000

Comparative efficacy of different low-molecular-weight heparins (LMWHs) and drug interactions with LMWH: implications for management of vascular disorders.

The low-molecular-weight heparins (LMWHs) are more efficacious and safer than unfractionated heparin (UFH) in the prevention and treatment of venous thrombosis and to a certain extent in the treatment of acute ischemic syndromes. Because of their predictable pharmacokinetics and bioavailability after subcutaneous administration, LMWHs can be more convenient for outpatient use than UFH. Differences in the manufacturing process of LMWHs result in significant structural and molecular weight differences; thus, LMWHs have individual biochemical and pharmacological profiles and are not interchangeable on the basis of either mass or anti-Xa activity. Using thromboelastograph (TEG) and platelet aggregometry, this investigation compared the in vitro efficacy among various LMWHs and examined the interactions between LMWHs and platelet glycoprotein (GP) IIb/IIIa antagonists. TEG was used to determine the ability of platelet and fibrin interactions to augment blood clots, an effect measured under conditions of maximal platelet activation during clot formation accelerated by recombinant human tissue factor (TF). The comparative efficacy of LMWHs on different mediator-induced clot retraction in human blood was assessed by TEG, which demonstrated the potency of different LMWHs to inhibit various mediator-induced clot formations under shear. Tinzaparin was relatively more effective in inhibiting TF-, lipopolysaccharide-, factor (f) Xa-, and thrombin-induced clot formation under shear. Under these conditions, platelets significantly enhance clot strength (eightfold vs. platelet-free fibrin clots). LMWHs appear to have broader efficacy than other anticoagulants. Abciximab and roxifiban further inhibited clot strength by affecting the transmission of platelet contractile force to fibrin by platelet GPIIb/IIIa receptors. Subtherapeutic doses of tinzaparin combined with abciximab or roxifiban resulted in a distinct synergy that improved anticoagulant and antiplatelet efficacy mediated by TF, fXa, or thrombin. As these data suggest, the combination of low-dose tinzaparin with low-dose GPIIb/IIIa antagonists (abciximab, roxifiban) may be efficacious in the prevention and treatment of various thromboembolic disorders.

Amidines↗
PubMed1997

A modified thromboelastographic method for monitoring c7E3 Fab in heparinized patients.

The monoclonal antibody, c7E3 Fab, binds to the platelet surface fibrinogen receptor (GPIIb/IIIa), inhibiting platelet aggregation and clot retraction. We performed an in vitro study to assess the ability of a modification of the thromboelastograph (MTEG) to detect inhibition of clot strength by c7E3 Fab and its reversal with platelet-rich plasma (PRP). In the modified assay (MTEG), thrombin was added to whole blood (WB) and platelet-poor plasma (PPP) and the resultant maximum amplitude (MA) was measured, MAWB and MAPPP, respectively. Anticoagulated blood samples from 17 patients scheduled for cardiac surgery were collected for a dose response (Part I; n = 5) and c7E3 Fab reversal (Part II; n = 12) study. Clot strength was reduced in a dose-dependent manner by c7E3 Fab. Ecteola cellulose effectively reversed the effect of heparin on the thrombin time and the addition of PRP significantly increased the MAWB (P < 0.0001) and MAWP-PPP (P < 0.0001). Subtracting the MAPPP from MAWB significantly magnified the response of MA to the addition of c7E3 Fab (P = 0.002) and its reversal with PRP (P = 0.005). This in vitro study indicates that the MTEG is a responsive assay demonstrating that inhibition by the antiplatelet c7E3 Fab is reversible with PRP.

Abciximab↗
PubMed1982

Effects of colchicine and vinblastine on platelet contractility and release.

Pre-incubation of normal platelet-rich plasma for 30 minutes at 37 degrees C with concentrations of colchicine (2.5 x 10(-4)M) or vinblastine (1.1 x 10(-4)M) which disrupt platelet microtubles did not inhibit aggregation induced by ADP or collagen. Even following pre-incubation of platelets with a 10-fold higher concentration of colchicine (2.5 x 10(-3)M), platelets released 14C-serotonin and aggregated in response to collagen. In the presence of a 10-fold higher vinblastine concentration (1.1 x 10(-3)M), platelets lysed and released 51Cr. Dynamic viscoelastic measurements on recalcified platelet-rich plasma in a Weissenberg rheogoniometer demonstrated that neither colchicine (2.5 x 10(-4)M to 5 x 10(-3)M) nor vinblastine (1.1 x 10(-4)M) interferes with the initiation, rate of generation, or extent of contractile force produced in platelet-fibrin clots. These results indicate that polymerized tubulin is not essential for collagen-induced release of platelet dense granule contents. In addition, intact tubulin polymers are not required to support the platelet surface configuration necessary for platelet-fibrin adherence and the platelet contractile events which result in platelet-fibrin clot retraction.

Blood Platelets↗
PubMed1977

Ditazole and platelets. I. Effect of ditazole on human platelet function in vitro.

Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) has been shown to be a strong in vitro inhibitor of human platelet aggregation brought about by release reaction inducers; in contrast, it did not significantly affect primary ADP-induced aggregation. Ditazole strongly inhibited the release of platelet-bound 14C-serotonin under the influence of Thrombofax, whereas it did not interfere with the transport and storage of serotonin in nonstimulated platelets. The effect of ditazole was not potentiated by acetylsalicylic acid. Ditazole also inhibited ADP-reptilase clot retraction and modified thrombin-induced clot formation. The inhibition of platelet aggregation exerted by ditazole in plasma could be removed following gel filtration of platelets on Sepharose 2-B gel. This would indicate that ditazole does not act on platelets by a 'hit and run' mechanism.

Adenosine Diphosphate↗
PubMed2000

EDTA-induced changes in platelet structure and function: adhesion and spreading.

Ethylenediamine tetraacetic acid (EDTA) is an effective anticoagulant, but unfortunately causes structural, biochemical and functional damage to human platelets. Some of the functional injuries, such as adhesion to and spreading on surfaces, are considered irreversible. The present investigation has evaluated that hypothesis. Our findings indicate that platelets from EDTA platelet-rich plasma (PRP) or CCD PRP to which EDTA has been added do not adhere to glass or plastic surfaces. However, when platelets from EDTA PRP or CCD PRP containing added EDTA are washed and resuspended under conditions reported to cause irreversible dissociation of the fibrinogen receptor, GPIIb/IIIa, then washed and resuspended in buffer containing Ca2+ and Mg2+ ions will adhere and spread in the same manner as platelets not exposed to EDTA. The ability to recover adhesive function may explain why EDTA platelets are able to sustain clot retraction as well as CCD platelets.

Anticoagulants↗
PubMedDate not supplied

[Changes in the indices of apparatus coagulography in patients with viral hepatitis].

210 patients with acute viral hepatitis B (AVH) were examined by apparatus coagulography with regard to severity of the disease. Considerably prolonged start and end of coagulation, increased minimal and maximal amplitudes were established in the early period of the infection. The disorders correlated with severity of AVH. New parameter--clot retraction index (CRI)--was suggested for objective estimation of disease severity and early diagnosis of acute hepatic encephalopathy (AHE). The index provides characteristics of dynamic state of blood clot at the moment of its maximal extraction. CR1 is recommended for early diagnosis or preclinical AHE in patients with AVH.

Acute Disease↗
PubMed1983

Influence of cis-platinum on some platelet functions in vitro.

Cis-platinum added to citrated platelet rich plasma in vitro did not influence the aggregation of the platelets, their adhesion to glass, their release of platelet factor 4 or availability of platelet factor 3 and acid phosphatase. Neither any effect on the uptake of 14C-serotonin, the reptilase clot retraction or the coagulation system has been observed.

Blood Platelets↗
PubMed1999

A reconstituted dilute blood clot lysis assay for the medium throughput screening of thrombolytic compounds.

Antithrombotic and clotting factors have long been targets for drug discovery, necessitating the development of blood assays to determine the efficacy of lead compounds prior to animal testing. We have developed a reconstituted blood clot lysis assay which eliminates the need for on-site donors. The assay uses whole blood stored at 4 degrees C obtained from a local blood bank, diluted 1:10 in phosphate buffer. This blood was supplemented with 125I-labeled fibrinogen and the release of radioactive fibrinopeptides from formed clots was measured. The whole blood used in this assay, which had been stored at 4 degrees C for several days, no longer formed solid or retracting clots. Thus, platelets 5-7 days ex vivo (165 x 10(6) platelets) were added to the whole blood in the presence of thrombin (0.80 IU/ml) to form clots. Solid clots formed within 2 min of thrombin addition and began retracting shortly thereafter. In the absence of any thrombolytic agent, clots fully retracted within 2.5 h and remained stable. Thrombin-stimulated clot formation was completely inhibited by heparin. Clots could be lysed in a dose-dependent fashion in the presence of tissue-type plasminogen activator. Clot lysis could be completely inhibited in a dose-dependent fashion with plasminogen activator inhibitor type 1. To demonstrate the utility of this assay as a screen for thrombolytic agents, a 14-amino-acid PAI-1-inhibitory peptide relieved the PAI-1 effect on tPA in a dose-dependent fashion. These data describe an assay for the screening of potential pro-fibrinolytic agents that target PAI-1 inhibition in a human plasma-based system that is versatile, cost-effective, and physiologically relevant and does not rely on the availability of on-site blood donors.

Blood Coagulation Tests↗
PubMed1979

Effect of vitamin E on platelet aggregation in diabetic retinopathy.

The effect of vitamin E on platelet aggregation was investigated in a group of 10 patients with diabetic retinopathy. Adenosine diphosphate induced platelet aggregation was inhibited in the patients' group as well as in the controls in the presence of vitamin E. An increased platelet aggregation was obtained with arachidonic acid in both groups when platelet-rich plasma was incubated prior with vitamin E. The clot retraction inhibition test parallels the findings of aggregation obtained with the platelet aggregation meter.

Adenosine Diphosphate↗
PubMed1991

The role of fibroblasts in organization and degradation of a fibrin clot.

Older clots become less sensitive to fibrin degradation than newly formed ones. A possible role for fibroblasts in this defective thrombus lysis was studied. A system has been developed in which different clones of fibroblasts were incorporated into a floating whole blood clot. The effect of the incorporated fibroblasts on clot lysis has been analyzed in relation to their basic characteristics: clot retraction, production of plasminogen activators (PAs) and their inhibitors (PAIs), and secretion of collagen. In neoplastic fibroblast-enriched clots, secretion of PA was associated with spontaneous lysis of a whole blood clot. Normal fibroblasts, secreting levels of PA and PAI similar to those of the cancer cells, did not induce spontaneous lysis of the clot. Moreover, these cells protected whole blood clot from thrombolysis by added PA. Our data show that the resistance to fibrin clot degradation induced by normal fibroblasts was mainly mediated by collagen secretion and deposition rather than PAI secretion or retraction of the clot. We suggest a key role for normal fibroblasts in the acquisition of resistance to proteolytic fibrin degradation of whole blood clots through the secretion of collagen.

Collagen↗
PubMed1979

Biochemical mechanism of platelet activation. Involvement of contractile proteins.

The present state of knowledge of the biochemical mechanism of platelet activation (adhesion, shape change, microspike formation, aggregation, release reaction, clot retraction) is presented under involvement of contractile proteins. The working hypothesis on the contractile mechanism of platelet activation is explained.

Actomyosin↗
PubMed2003

[Blood platelets: biochemistry and physiology].

This article reviews the roles of blood platelets in different physiologic and pathologic processes in the human body. Besides the basic processes in primary haemostasis, platelet adhesion, platelet secretion, platelet aggregation, clot retraction, the new model of thrombin formation on the platelet surface is presented. The different signal transduction pathways in platelets are a main focus of this review.

Blood Platelets↗
PubMed1981

Human platelet aggregation tests in vitro. Effects of dilazep.

The effect of 1,4-bis-[3(3,4,,5-trimethoxybenzoyl-oxy)-propyl]-perhydro-1,4-diazepine (dilazep, Cormelian), a coronaroactive drug, was studied by various tests of hemostasis in vitro on human plasma. The antiplatelet action of the drug was clearly demonstrated: it inhibited, in appropriate concentrations, ADP, adrenaline and collagen induced aggregation platelet factor 3 (PF3) availability and clot retraction induced by ADP-reptilase. Conversely, coagulation tests as well as the lysis time of diluted whole blood were unaffected by the drug.

Adenosine Diphosphate↗
PubMed1981

Effect of ionizing radiation on platelet function in vitro.

The effect of ionizing radiation on platelet function was investigated in vitro. Platelet-rich plasma (300 x 10(9/1)) was irradiated with doses of 1, 4, 10, 20 and 50 Gy. Platelet function tests were performed on both irradiated and control (non-irradiated) platelet samples. The platelet function tests were (1) platelet aggregation by ADP (1, 2, 4 mumol final concentration), adrenaline and collagen, (2) ADP-release from platelets, (3) clot retraction and (4) platelet factor-3 availability. It was found that roentgen irradiation of platelets in vitro did not affect these platelet functions tests.

Adenosine Diphosphate↗
PubMed2003

Effect of non-heparin thrombin antagonists on thrombin generation, platelet function, and clot structure in whole blood.

Platelet contractile force (PCF), which is absent in blood obtained during cardiopulmonary bypass, significantly recovers after protamine sulfate administration. In vitro studies reveal this effect to be primarily caused by heparin. Because many of heparin's effects are mediated by suppression of thrombin generation and activity, this study assessed the influence of thrombin inhibition on PCF. The effects of natural and synthetic antithrombins were measured. Clots were formed by the addition of batroxobin (0.21 microg/mL) to whole blood (platelet count 200,000/microL). Force development was measured from the moment of batroxobin addition. After 1200 s of clotting, purified antithrombin III (22 microM) reduced PCF by 74%. Thrombomodulin (0.014 microM) reduced PCF by 60%. At 0.040 microM, PCF was reduced by 82% (6.5-1.2 Kdynes). Hirudin decreased PCF in a dose-dependent fashion, with complete suppression at concentrations > or = 0.30 microM. At concentrations between 0.04 and 0.29 microM, Lepirudin (Refludan, a recombinant therapeutic hirudin) produced dose-dependent delay and suppression of PCF. Above 0.29 microM Lepirudin, PCF was totally suppressed. At 1.60 microM, bivalirudin (a synthetic, 20 amino acid peptide) delayed and reduced PCF by 50%. At 6.40 micro;M, PCF was completely suppressed. Although 20 microM of P-PACK II (d-Phenylalanyl-L-Phenylalanylarginine- chloro-methyl ketone 2 HCl) had little effect, 40 microM delayed onset of force development from 300 to 600 s and reduced PCF at 1200 s from 5.2 to 3.3 Kdynes. At 120 microM, force development was totally suppressed. Four micromol Thromstop (BNas-Gly-(pAM)Phe-Pip) delayed force development by greater than 800 s and PCF at 1200 s was reduced by 70%. At 0.20 microM, Argatroban (a synthetic polypeptide direct thrombin antagonist) delayed onset of PCF from 300 to 540 s and decreased PCF by 40%. At a concentration of 0.40 microM and above, Argatroban totally suppressed PCF. These results indicate that some of the antiplatelet effects of heparin are the result of thrombin inhibition and that low-level thrombin generation is essential for clot retraction. The sensitivity of PCF to the presence of thrombin may permit monitoring of antithrombin agents via this assay.

Antithrombin III↗
PubMed1987

Effect of lomustin on some platelet functions in vitro.

The effect of lomustin on platelet functions was investigated in vitro using a wide battery of tests. Lomustin was found to act as a specific inhibitor of platelet aggregation, release reaction and clot retraction and to induce acquired thrombocytopathy. Thus, impairment of platelet functions might play a role in hemorrhagic complications accompanying lomustin therapy in some cases.

Adenosine Diphosphate↗
PubMed1994

Quantitative assessment of platelet function and clot structure in patients with severe coronary artery disease.

The prothrombotic state of patients with coronary artery disease (CAD) can be attributed partially to platelet activity. Management of such patients is hindered by a lack of techniques to assess hemostatic function. This study used a sensitive technique to monitor platelet function by measuring platelet force development during clot retraction. This technique allowed simultaneous measurement of clot elastic modulus on the same sample. Fibrin mass-length ratio (mu), fibrinopeptide A, D-Dimer, von Willebrand's factor, thromboxane A2, platelet aggregation studies, and bleeding times also were performed. Fourteen patients with CAD were compared with 10 healthy volunteers. Despite more than 95% suppression of thromboxane B2 and prolongation bleeding times in patients taking aspirin, force development remained significantly elevated over healthy control patients (8,279 +/- 476 dynes versus 4,857 +/- 380 dynes, p < 0.0006). Patients not taking aspirin had normal bleeding times and force development of 19,110 +/- 3,700 dynes. Clot elastic moduli were enhanced in patients with CAD whether taking or not taking aspirin. Adenosine diphosphate and ristocetin-induced platelet aggregation were insensitive to the effect of aspirin in patients with CAD. Fibrinopeptide A, von Willebrand's factor, and D-Dimer levels were significantly elevated, and fibrin mass-length ratios were significantly larger in patients with CAD. Therefore, despite aspirin therapy, patients with severe CAD have evidence of persistent platelet activation and rigid clot structure. Monitoring of platelet force development may prove useful in delineating enhanced platelet function.

Adult↗
PubMed1972

Effect in vitro on platelet function of two compounds developed from the pyrimido-pyrimidines.

VK 774 and VK 744, two new compounds developed from the pyrimido-pyrimidines, have been found to be powerful inhibitors of platelet function tested in vitro. They inhibit adenosine diphosphate (ADP)-induced platelet aggregation, and the release of platelet factor 3 by kaolin, and VK 774 also reduces platelet adhesiveness and inhibits platelet aggregation (;snowstorm' effect) in the Chandler tube system. Although measured percentage whole blood clot retraction was uninfluenced by these drugs the clot produced with VK 774 was friable and soft. VK 774 appears to be the most powerful of these compounds reported so far, being active in some test systems at 10(-6)M, and, if the results of toxicity testing are satisfactory, it should be an important agent for therapeutic trial.

Adenosine Diphosphate↗