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PubMed1985

Platelet-aggregating activities of metastasizing tumor cells. III. Platelet aggregation as resulting from thrombin generation by tumor cells.

Thrombin generated in the process of platelet aggregation induced by three metastasizing murine tumors was measured using a chromogenic substrate specific for thrombin. Addition of B16 cells or 3LL cells to the platelet-rich plasma induced the generation of a significant amount of thrombin during the lag period preceding aggregation, while that of MH134 cells did not. Thrombin generation was observed in both the presence and the absence of platelets, indicating that platelets are not necessarily required for thrombin generation by these tumor cells. This suggests that the adherence of platelets to tumor cells is not an essential step for the initiation of thrombin-mediated aggregation induced by B16 and 3LL cells. Furthermore, the results of a one-stage clotting assay using plasma deficient in coagulation factors indicated that B16 and 3LL cells generated thrombin through direct activation of factor X.

Animals↗
PubMed2002

Effect of UV-modified fibrinogen on platelet aggregation in platelet-rich plasma.

Oxidized UV-modified fibrinogen activates platelets in platelet-rich plasma. Kinetic turbidimetry showed that addition of oxidized fibrinogen to platelet-rich plasma led to platelet aggregation. Reversible aggregation is recorded starting from the 30th second and then constantly grows with the same rate. Nonoxidized fibrinogen produced no such effect. The relationship between aggregation intensity and rate and the degree of fibrinogen oxidation was described by a bell-shaped curve with a peak corresponding to 24% fibrinogen oxidation. The amplitude of aggregation increased with increasing the concentration of irradiated fibrinogen from 0.1 to 1.0 mg/ml and then plateaued. The rate of aggregation little depended on fibrinogen concentration.

Dose-Response Relationship, Radiation↗
PubMed1975

The effect of non-steroid anti-inflammatory drugs, dibutyryl cyclic 3',5'-adenosine monophosphate and phosphodiesterase inhibitors on platelet aggregation and the platelet release reaction in normal and essential fatty acid deficient rats.

A comparison was made of the action of three classes of substances with platelet aggregation inhibiting effect in normal and essential fatty acid deficient rats. In the latter group, the effect of indomethacin was considerably reduced, whereas the difference was smaller with aspirin. Dibutyryl cyclic AMP had the same inhibiting effect in both groups. Of the phosphodiesterase inhibitors tested, dipyridamole was inactive, whereas the inhibiting effects of caffeine and papaverine are slightly reduced in the deficient animals. The same differences between the two groups were seen in the magnitude of the release reaction after 14C-serotonin labelling. These data support the idea that the non-steroid anti-inflammatory drugs act by inhibiting the formation of an aggregation-inducing substance from arachidonic acid.

Animals↗
PubMed1987

Platelet aggregation and platelet-inhibiting drugs.

Platelet function may cause a progression of central gray matter damage after cerebrospinal hemorrhage or trauma because of the thrombotic occlusion of injured vessels or a vasospasm induced by extravasated blood. It has therefore been suggested that antiplatelet drugs could limit the extent of the neurological lesions produced by a spinal trauma. In view of this possibility, the hemostatic functions of platelets and the mechanism of action of antiplatelet drugs are briefly reviewed.

Humans↗
PubMed1988

Effect of a moderate fish intake on platelet aggregation in human platelet-rich plasma.

This paper describes the results of an international study to investigate the effect of a reasonable amount of dietary fish on platelet aggregation in platelet-rich plasma (PRP) induced by collagen and thrombin. In Maastricht, Tromsø, and Zeist two groups of healthy male volunteers were given a daily dietary supplement consisting of 135 g of canned mackerel paste (experimental group, n = 40) or meat paste (control group, n = 42) for a 6-week period. Compliance, calculated on the basis of the urinary excretion of lithium, added to the supplements, was about 80%. Platelet number in PRP decreased significantly in the fish group. Collagen-induced platelet aggregation in PRP differed widely between the three centres despite the attempt to use exactly the same conditions. Nonetheless, aggregation decreased significantly in the fish group. The mackerel effect on thrombin-induced aggregation was inconsistent.

Adolescent↗
PubMed2002

Effects of red wine and wine polyphenol resveratrol on platelet aggregation in vivo and in vitro.

Low to moderate consumption of red wine reportedly has a relatively greater benefit than other alcoholic beverages in the prevention of atherosclerosis and coronary heart disease (CHD). This beneficial effect is increasingly attributed to the polyphenol resveratrol, present in red wine. In the present study, we investigated the effects of resveratrol and red wine on aggregation of platelets isolated from healthy, normotensive male volunteers and in rabbits with experimental hypercholesterolemia. Platelet aggregation rate (PAR) was measured using Born's method. The results showed that aggregation of platelets from healthy subjects induced in vitro by collagen (5 microg/ml), thrombin (0.33 units/ml), and ADP (4 microM) was significantly inhibited by 10-1000 microM resveratrol, in a concentration-dependent manner. Hypercholesterolemic rabbits showed enhanced ADP-induced platelet aggregation; the average PAR increased from 39.5+/-5.9% in normal animals to 61.0+/-7.0% in the high-cholesterol fed group (n=8, p<0.001). Resveratrol (4 mg/kg/day) inhibited ADP-induced platelet aggregation in vivo by maintaining the PAR at 35.7+/-6.3% (vs. 39.5+/-5.9% for control rabbits, n=8, p=0.228), but had no effect on serum lipid levels. Similarly platelet aggregation in hypercholesterolemic rabbits was also inhibited when animals received intragastrically Chinese red wine (with or without alcohol, 4 ml/kg/day). These results suggest that resveratrol can inhibit platelet aggregation both in vitro and in vivo, which conceivably could be one of the mechanisms by which this red wine polyphenol exerts its cardioprotective effects.

Animals↗
PubMed1994

Platelet-aggregating effects of platelet-activating factor-like phospholipids formed by oxidation of phosphatidylcholines containing an sn-2-polyunsaturated fatty acyl group.

Previously, we reported the formation of four kinds of phosphatidylcholines (PC) with a short-chain monocarboxylate, dicarboxylate, dicarboxylate semialdehyde or omega-hydroxymonocarboxylate group by oxidation of PCs containing polyunsaturated fatty acid (PUFA) in an FeSO4/ascorbate/EDTA system. In this study, we identified these novel phospholipids by GC-MS as oxidation products of two alkyl ether-linked PCs, 1-O-hexadecyl-2-docosahexaenoyl and 1-O-hexadecyl-2-arachidonoyl-sn-glycero-3- phosphocholine (GPC). The sn-2-acyl moieties of oxidatively fragmented PCs derived from PCs containing docosahexaenoate were one methylene unit shorter than those detected as major oxidation products of PCs containing arachidonate. The platelet-aggregations induced by the oxidized PCs were all inhibited by FR-900452, an antagonist of platelet activating factor (PAF). The PAF-like activity of oxidized 1-O-hexadecyl-2-docosahexaenoyl-GPC, which was equivalent of 1372 +/- 262 pmol 16:0-PAF/mumol starting PC, was 5 times that of oxidized 1-O-hexadecyl-2-arachidonoyl-GPC and 150 times that of oxidized 1-palmitoyl-2-docosahexaenoyl-GPC, suggesting that both an sn-1-alkyl ether linkage and an sn-2-acyl group with a short chain length are important structural requirements for induction of platelet aggregation. These possibilities were confirmed by experiments on the platelet-aggregating activities of synthetic PAF-like compounds. Quantitative measurements by GC-MS of PAF-like phospholipids formed by lipid peroxidation and the activities of synthetic PAF-like phospholipids, suggested that the activities of most oxidized PCs containing PUFA were ascribable to those of PCs with an sn-2-short-chain monocarboxylate group.

Animals↗
PubMed1989

Suppression by tetrandrine of human platelet aggregation induced by platelet-activating factor and other stimulants.

Tetrandrine was found to have inhibitory effects on platelet-activating factor induced platelet aggregation in a dose-dependent manner. There was preferential inhibition of platelet aggregation induced by agents such as collagen, thrombin, adrenaline, and adenosine diphosphate. No inhibitory effect of tetrandrine was observed on platelet aggregation induced by adenosine diphosphate, arachidonic acid, and the calcium ionophore A23187. These results support our previous findings of interference with the phosphatidylinositol second-messenger system as one of the sites of action of tetrandrine. Since platelets may have an important role in the pathogenesis of asthma and other allergic diseases, these findings suggest that tetrandrine may have clinical application as a non-steroidal broad-spectrum anti-allergic drug.

Adenosine Diphosphate↗
PubMed1986

Dextran 40 reduces heparin-mediated platelet aggregation.

Using platelet aggregometry, we investigated the in vitro efficacy of dextran, mean MW 40,000, in reducing the heparin-mediated platelet aggregation seen with the syndrome of heparin-associated thrombocytopenia (HAT). Six patients with the clinical syndrome of HAT were studied who had a plasma factor which induced aggregation of normal platelets in the presence of heparin. At a final concentration of 2% (20 mg/ml) Dextran 40 reduced heparin-stimulated aggregation by 60.5 +/- 36% (SD) in mixtures of normal platelet-rich plasma/HAT patient plasma. In contrast, the same dextran concentration reduced ADP-stimulated aggregation of normal platelet-rich plasma by only 18.6 +/- 12%. This selective inhibition of heparin-mediated aggregation by dextran was highly significant (P less than 0.005, Wilcoxon rank sum). Whereas protamine abolished heparin's anticoagulant and platelet aggregating activity, dextran had no effect on heparin's anticoagulant properties. These data show that Dextran 40 selectively blocks heparin-mediated aggregation in vitro, perhaps by blocking heparin binding to the platelet membrane. This study suggests that dextran may be a clinically useful adjunct in the treatment of HAT, and describes a simple method for testing the efficacy of drugs in the treatment of HAT.

Adenosine Diphosphate↗
PubMed1989

Platelet aggregation induced by type IIb platelet von Willebrand factor.

Platelet lysates from five patients with a form of type IIb von Willebrand's disease (vWd), associated with spontaneous platelet aggregation and thrombocytopenia, induced platelet aggregation of normal and other vWd's platelet-rich plasma (PRP). Platelet lysate from normals, type I or type IIa vWd did not cause platelet aggregation of normal PRP. When polyclonal monospecific antibodies directed against plasma von Willebrand factor (vWf) were incubated with the type IIb platelet lysate, they inhibited the platelet aggregation. Monoclonal antibodies directed against the glycoprotein (GP) Ib binding domain of plasma vWf incubated with the type IIb platelet lysate did not inhibit the platelet aggregation. Normal platelets suspended in afibrinogenaemic plasma did not aggregate when type IIb vWd platelet lysate was added. Normal platelets incubated with monoclonal antibodies directed against the fibrinogen and vWf binding site(s) on the GPIIb/IIIa were not aggregated by the type IIb platelet lysate. Bernard-Soulier PRP aggregated when type IIb vWd platelet lysate was added, while Glanzmann's thrombasthenic platelets did not. Peptides containing the RGDS sequence or the sequence of the carboxy terminal 15 amino acids of the gamma chain of fibrinogen inhibited the type IIb vWd platelet lysate-induced platelet aggregation. These data suggest that type IIb platelet vWf can cause platelet aggregation of PRP without the addition of any agonist. This interaction is different from that observed with the plasma vWf from these patients.

Antibodies, Monoclonal↗
PubMed1985

Role of myosin phosphorylation in contractility of a platelet aggregate.

The relationship between tension and myosin 20,000-Da light chain phosphorylation in intact nonmuscle cells was investigated using a preparation of thrombin-activated, irreversibly aggregated platelets known as the platelet strip. Steady-state levels of tension generated by the platelet strip were found to be linearly related to the level of myosin phosphorylation. This relationship was observed during dose-dependent relaxation induced by the adenylate cyclase activators prostaglandin (PG) E1 and PGI2, and during contraction induced by ADP, epinephrine, and the prostaglandin endoperoxide analogue U-46619, which did not appreciably alter the basal level of adenosine 3',5'-cyclic monophosphate in the preparation. The fully relaxed platelet strip, in the absence of external Ca2+, was associated with a level of 12% light chain phosphorylation, which increased to 72% on maximal contraction. During both relaxation and contraction, changes in myosin phosphorylation were also found to precede or coincide with tension changes. Furthermore, steady-state contraction induced by ADP was associated with a maintained elevation in the level of myosin phosphorylation. These results support the concept that myosin phosphorylation is an important regulatory mechanism for contractility in platelets.

Adenosine Diphosphate↗
PubMed1991

Relationship of intraglomerular coagulation and platelet aggregation to glomerular sclerosis.

In order to investigate the relationship between intraglomerular coagulation and glomerular sclerosis, the distribution of fibrin-related antigen (FRA) in glomeruli without extracapillary lesions was examined by immunoperoxidase microscopy in 80 patients with IgA nephropathy (IgA-N). A total of 302 glomeruli were examined, including 20 with global sclerosis, 31 with segmental sclerosis (SS glomeruli), and 251 nonsclerosed glomeruli. In the nonsclerotic areas of SS glomeruli, the deposition of FRA was significantly greater than in the nonsclerosed glomeruli. In the nonsclerosed glomeruli FRA was mainly found in the mesangium, while in the nonsclerotic areas of SS glomeruli FRA was not only present in the mesangium but also in the endothelium of the glomerular capillary loops. FRA-positive microclots were also often observed attached to the endothelium of the capillaries of the nonsclerotic areas of SS glomeruli. Cross-linked FRA was also observed in the endothelium of the same capillaries using the monoclonal antibody DD3B6/22. Deposition of von Willebrand factor (vWF) was greater in the endothelium than in the mesangium in the same areas. Aggregated platelets adhering to the glomerular capillary walls in these areas were frequently detected using the monoclonal antibody P2. Such distribution of platelets and vWF showed that the endothelium of the nonsclerotic areas of SS glomeruli was more severely damaged than that of nonsclerosed glomeruli. These findings suggest that endothelial cell damage might activate the intraglomerular coagulation, which might be one of the factors in the development of global glomerular sclerosis.

Antigens, Human Platelet↗
PubMed1981

Platelet aggregation and coagulation in the pathogenesis of diabetic retinopathy in rats.

Fifty male rats were made diabetic by a single injection of streptozotocin and were killed at periods varying from 1 to 12 mo. Ten saline-injected rats and three rats treated with 3-O-methylglucose and streptozotocin served as controls. Intraluminal changes in retinal vessels were studied by electron microscopy. In diabetic rats maintained for 9-12 mo, microthrombus formation was observed in the various sized retinal vessels at the histologic and ultrastructural level. The microthrombi were mainly composed of aggregated platelets and fibrin strands. However, there was no definite evidence of detachment or loss of the endothelial cells. This microthrombus formation may play an important role in the development of diabetic retinopathy.

Animals↗
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↗
PubMedDate not supplied

Dipyridamole potentiates the inhibition of platelet aggregation by aspirin (in human platelet rich plasma and whole blood).

This study investigates the influence of dipyridamole on platelet aggregation as evaluated by a single agonist or a pair of agonists in human platelet rich plasma and whole blood. Dipyridamole up to 30 microM was not found to influence the platelet aggregation of platelet rich plasma or whole blood; aspirin (100 microM), on the contrary, did inhibit platelet aggregation. The inhibition of platelet aggregation by aspirin could be reversed by using high concentrations of agonists or pairs of agonists. In this model dipyridamole inhibited platelet aggregation in both platelet rich plasma and whole blood in a dose-dependent fashion. Thromboxane A2 was less than 10% of controls in aspirin-treated PRP stimulated with low or high concentrations of collagen or with a pair of agonists. This study suggests that dipyridamole has direct antiplatelet activity in platelet rich plasma and whole blood when the cyclooxygenase pathway is blocked by aspirin.

Adult↗
PubMed1986

The influence of glutathione and other thiols on human platelet aggregation.

The platelet membrane contains sulfhydryl groups which are essential for normal platelet function. Reduced glutathione (GSH) and other thiols such as cysteine and 6-mercaptopurine were found to inhibit human platelet aggregation induced by adenosine diphosphate (ADP), collagen and arachidonic acid. The inhibition of ADP-induced aggregation by GSH (IC50 = 0.61 +/- 0.05 mM) was greater than that by cysteine (IC50 = 13 +/- 1 mM) or 6-mercaptopurine (IC50 = 5.4 +/- 0.2 mM). Two other thiols, dithiothreitol and beta-mercaptoethanol were found to cause platelet aggregation instead of inhibition. The interaction of GSH with the ADP receptor was noncompetitive in nature.

Adenosine Diphosphate↗
PubMed2004

Effects of platelet inhibitors on propyl gallate-induced platelet aggregation, protein tyrosine phosphorylation, and platelet factor 3 activation.

Propyl gallate (PG) is a platelet agonist characterized by inducing platelet aggregation, protein tyrosine phosphorylation, and platelet factor 3 activity. The mechanisms of platelet activation following PG stimulation were examined by pre-incubating platelets with well-defined platelet inhibitors using platelet aggregation, protein tyrosine phosphorylation, activated plasma clotting time, and annexin V binding by flow cytometry. PG-induced platelet aggregation and tyrosine phosphorylation of multiple proteins were substantially abolished by aspirin, apyrase, and abciximab (c7E3), suggesting that PG is associated with activation of platelet cyclooxygenase 1, adenosine phosphate receptors, and glycoprotein IIb/IIIa, respectively. The phosphorylation of the cytoskeletal enzyme pp60(c-src) increased following PG stimulation, but was blunted by pre-incubation of platelets with aspirin, apyrase, and c7E3, suggesting that tyrosine kinase is important for the signal transduction of platelet aggregation. Propyl gallate also activates platelet factor 3 by decreasing the platelet coagulation time and increasing platelet annexin V binding. Platelet incubation with aspirin, apyrase, and c7E3 did not alter PG-induced platelet coagulation and annexin V binding. The results suggest that platelet factor 3 activation and membrane phosphotidylserine expression were not involved with activation of platelet cyclooxygenase, adenosine phosphate receptors, and glycoprotein IIb/IIIa. PG is unique in its ability to stimulate platelet aggregation and coagulation simultaneously, and platelet inhibitors in this study affect only platelet aggregation but not platelet coagulation.

Annexin A5↗