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At least 19 recordsLinked to original sources
PubMed1989

[Relation of the level of platelet membrane glycoproteins, platelet adhesion, platelet aggregation and traditional Chinese medicine syndrome patterns of coronary heart disease].

This experiment made quantitative analysis of platelet GPlb of 56 patients with coronary heart disease and with McAb SZ-2 resisting to human being platelet GP by using the method of indirect immunity fluorescence saturation, observed the changes of coronary heart patients' platelet GPlb based on TCM differentiation of the pattern, and determined the level of PAdT, PAgT. The results showed that the level of platelet GPlb of coronary heart disease was higher than normal. Among them, the acute myocardiac infarction group was the most obvious, followed by the unstable angina pectoris group and the stable angina pectoris group. The level of PAdT, PAgT of coronary heart patients was higher than those of the normal group (P less than 0.005, 0.05); the level of platelet GPlb in blood stasis syndrome group was higher remarkably than the group of having no blood stasis syndrome and the normal (P less than 0.001). These results suggested that it played an important part in the occurrence and development of coronary heart disease as manifested by abnormal increase of platelet GPlb, and enhancement of platelet's adherence and aggregation. The abnormal increase of platelet GPlb is due to pathological mechanism of blood stasis syndrome of coronary heart disease. This experiment also provided a fresh evidence to TCM differentiation of the pattern and treatment of coronary heart disease.

Adult↗
PubMed1989

Alpha-tocopherol, an effective inhibitor of platelet adhesion.

Platelet adhesiveness was tested ex vivo in a group of six normal individuals receiving varying doses of alpha-tocopherol. Adhesion to glass slides coated with fibronectin, collagen, fibrinogen, or plasma proteins was studied by perfusing platelet-rich plasma through a flow chamber that allowed time- and space-resolved observations of platelet adhesion. Platelet adherence was measured in an area of parallel flow lines and low shear rate under standardized conditions before and after dietary supplementation with vitamin E at doses of 200 and 400 IU/d. Platelet adherence differed in magnitude depending on the adhesive surface. There was a distinct preference of platelets to adhere to sites that had been previously occupied. A remarkable decrease in platelet adherence was observed after vitamin E supplementation. The average decrease in adhesion after 2 weeks of 200 IU vitamin E was 75%. After 2 weeks of 400 IU vitamin E, platelet adhesion was reduced by 82%. The inhibitory activity of alpha-tocopherol was dose dependent and correlated well with the increase in alpha-tocopherol concentration in platelets after supplementation. Scanning electron microscopy revealed a striking decrease of pseudopodium formation in alpha-tocopherol-enriched platelets. Our results suggest that vitamin E may also be an effective antiadhesive agent in vivo.

Blood Platelets↗
PubMed1990

Plasma lipoproteins mediate platelet adhesion.

Platelet adhesion to VLDL, LDL, HDL, and to a mixture of purified apolipoproteins was examined. Platelets adhered to all the classes of lipoproteins tested. VLDL and the apolipoprotein mixture promoted the greatest degree of adhesion. Platelet adhesion was inhibited by addition of EDTA, RGD-containing peptides and anti-GPIIb-IIIa, monoclonal antibodies. Platelets from patients with Glanzmann's Thrombasthenia which lack the GPIIb-IIIa receptor adhered to VLDL less than half as well as did normal platelets. These results demonstrate that the major circulating lipoproteins can mediate in vitro platelet adhesion and that this adhesion occurs via platelet integrin receptors. We postulate that lipoprotein mediated platelet adhesion may play an important role in the progression of atherosclerosis.

Antibodies, Monoclonal↗
PubMed1984

Platelet adhesion.

Platelets do not adhere to surfaces to which flowing blood is normally exposed in vivo. When the lining of a blood vessel is altered or damaged, however, platelets do adhere to the injured site. Platelet adhesion is one of the first events in the formation of hemostatic plugs and thrombi, and plays a part in the development of atherosclerotic lesions. Other surfaces to which platelets adhere include particulate matter in the blood stream, bacteria and other microorganisms, the artificial surfaces of prosthetic devices, and some altered cells in the blood, particularly macrophages. The majority of investigators have studied the interaction of platelets with the subendothelium of normal vessels of young animals, or with isolated vessel wall constituents such as collagen. There are very few studies of platelet adhesion to repeatedly damaged or diseased blood vessels, although it is generally assumed that platelets interact with the connective tissue, fibrin, and cholesterol crystals in atherosclerotic lesions. Underlying the endothelium of blood vessel is the basement membrane, which has been shown to contain type IV collagen, elastin with its associated microfibrils, von Willebrand Factor, fibronectin, thrombospondin, laminin, and heparan sulfate. If only the endothelium is removed, the main structure exposed is the basement membrane with its associated proteins, but deeper injuries expose fibrillar type III collagen and microfibrils. In most studies in which large arteries have been injured by passage of a balloon catheter, basement membrane, type III collagen and the microfibrils around elastin have been exposed. Platelets do not react strongly with basement membrane and the type IV collagen in it is relatively inert. In contrast, platelets adhere firmly to type III (and type I) collagen and spread on it. Although in vitro studies have shown that platelets can interact with collagen in artificial media without plasma proteins, investigations of platelet adhesion at high shear rates indicate that von Willebrand Factor is necessary for firm platelet adhesion under these conditions. Fibronectin and thrombospondin may also have a role in platelet adhesion. However, platelets do not bind von Willebrand Factor or fibronectin until the platelets have been stimulated to release their granule contents, so these binding sites probably do not become available until the platelets have interacted with collagen or another release-inducing agent such as thrombin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Role of plasma viscosity in platelet adhesion.

Platelet adhesion to the vessel wall is initiated by transport of blood platelets from the bulk flow to the wall. The process of diffusion and convection of the platelets is affected by rheological conditions such as well shear rate, red blood cell (RBC) deformability, and viscosity of the medium. To study the effect of plasma viscosity on platelet adhesion, perfusion experiments with a rectangular perfusion chamber were performed. Reconstituted blood, consisting of washed platelets and washed RBCs, was circulated through this chamber for 5 minutes at a wall shear rate of 300 s-1. Different albumin concentrations were made, to obtain different medium viscosities (0.89 to 1.85 mPa.s). Platelet adhesion decreased with increasing medium viscosity up to viscosities of 0.95 mPa.s, but increased with medium viscosity above this value. Instead of human albumin solution, different plasma viscosities were obtained by dilution of Waldenström plasma with buffer. Plasma was depleted of fibronectin, which gave a final plasma viscosity of 2.0 mPa.s, and was dialyzed against HEPES buffer and subsequently diluted with the dialysis buffer in different fractions (0.89 to 2.00 mPa.s). Perfusions were performed over a purified von Willebrand factor coating on glass, or over an endothelial cell matrix, preincubated with von Willebrand factor. With both surfaces, platelet adhesion was dependent on the plasma viscosity in a similar way: at low plasma viscosities, adhesion was decreased with increasing plasma viscosity, while at higher plasma viscosities, adhesion increased with plasma viscosity. Adhesion values at higher plasma viscosity or at higher human albumin concentrations could be explained by effects of the medium on the rigidity of the RBCs, since platelet adhesion is known to be increased by enhanced RBC rigidity. Effects of the medium on the deformability of the RBCs were measured separately with the laser diffraction method. These experiments confirmed that presence of human albumin or plasma in the measuring suspension increased the rigidity of RBCs. To prevent influence of the medium on the RBCs in perfusion experiments, the RBCs were fixated with glutaraldehyde. Perfusion experiments with fixated RBCs in plasma over a von Willebrand factor preincubated endothelial cell matrix, showed a consequent decrease in adhesion with increasing plasma viscosity, according to the diffusion theories, whereas the increase of adhesion at high plasma viscosities was lacking. This suggests that the latter effect was entirely due to increased transport of platelets by more rigid RBCs.

Blood Viscosity↗
PubMed1993

SIN-1 reduces platelet adhesion and platelet thrombus formation in a porcine model of balloon angioplasty.

BACKGROUND: Nitric oxide inhibits platelet adhesion and platelet aggregation in vivo. In this study, we investigated the effects of the nitric oxide donor SIN-1 on platelet adhesion and platelet-thrombus formation following experimental angioplasty. METHODS AND RESULTS: Bilateral carotid angioplasty was performed in 20 anesthetized pigs. Animals received either SIN-1 (3-morpholino-sydnonimine; 10 micrograms/kg/min; n = 8) or placebo (n = 8) before and during angioplasty. An additional control group of pigs received trimetaphan (n = 4), which induced hemodynamic changes similar to those that followed treatment with SIN-1. Platelet deposition was quantified by the injection of autologous 111In-labeled platelets. SIN-1 reduced platelet deposition after deep arterial injury compared with placebo (mean +/- SEM, 10.870 +/- 2.415 versus 40.326 +/- 9.889 platelets x 10(6)/cm2, p < 0.05). SIN-1 reduced platelet adhesion after superficial injury compared with both placebo and trimetaphan (2.231 +/- 0.333 versus 5.278 +/- 0.606 versus 5.022 +/- 1.136 platelets x 10(6)/cm2, respectively; p < 0.005). Scanning electron microscopy confirmed that platelets were deposited in the form of an adherent monolayer following superficial endothelial denudation and were reduced in number following treatment with SIN-1. The effects of SIN-1 on platelet function were associated with a significant increase in platelet cyclic GMP concentration from baseline (3.15 +/- 0.88 versus 1.58 +/- 0.73 pmol/10(9) platelets, p < 0.005). CONCLUSIONS: SIN-1 reduces platelet adhesion and platelet-thrombus formation following experimental angioplasty. The antiadhesive effects of SIN-1 are independent of changes in systemic hemodynamics. These results imply that the administration of a nitric oxide donor may prove effective in modifying the pathophysiological response to angioplasty injury.

Angioplasty, Balloon↗
PubMed1990

Platelet adhesion to collagen. Factors affecting Mg2(+)-dependent and bivalent-cation-independent adhesion.

Platelet adhesion to collagens immobilized on plastic has been measured, with the following results. (1) Human, but not rabbit, platelets adhered readily to pepsin-extracted monomeric collagens in an Mg2(+)-dependent manner. (2) Rabbit platelets adhered to a monomeric collagen extracted without pepsin by a process that was cation-independent; human platelet adhesion to this collagen exhibited a cation-independent element. (3) Human platelet adhesion to polymeric collagens, including intact native fibres and those reconstituted from pepsin-extracted monomeric collagens, exhibited appreciable cation-independence; adhesion of rabbit platelets to these collagens occurred only by a cation-independent process; pepsin treatment of the intact fibres caused a reduction in cation-independent binding. Two mechanisms of adhesion can therefore be distinguished, one Mg2(+)-dependent, expressed by human, but not rabbit, platelets, the other cation-independent and exhibited by platelets of both species. Mg2(+)-dependent and cation-independent adhesion sites are located within the triple helix of collagen, but the latter sites are only expressed in collagen in polymeric form. In neither case is the helical conformation of the sites essential for their binding activity. Cation-independent adhesion sites are also located in the pepsin-sensitive non-helical telopeptides of collagen and can be expressed in both monomeric and polymeric collagens. Chemical modification of collagen lysine residues indicates that specific lysine residues may be involved in Mg2(+)-dependent adhesion. Adhesion using human citrated platelet-rich plasma is Mg2(+)-independent. Plasma contains factors, conceivably the adhesive proteins fibronectin and von Willebrand factor, that promote the Mg2(+)-independent mechanism.

Animals↗
PubMed1980

[Platelet changes and occupational carbon disulfide poisoning. I. Variations of platelet adhesiveness].

Platelet adhesiveness was studied in 83 workers exposed to CS2 and 47 controls. Results show an increase of platelet adhesiveness statistically significant in workers in comparison with controls and in workers with high exposure vs. workers with mild exposure. Authors suggest the usefulness of platelet adhesiveness evaluation for prevention and early diagnosis of CS2 intoxication.

Blood Platelet Disorders↗
PubMed1983

Selective inhibition of thromboxane synthetase with dazoxiben - basis of its inhibitory effect on platelet adhesion.

Platelet adhesion to rabbit aortic subendothelium or collagen-coated glass was quantitated in a rotating probe device by uptake of radio-labelled platelets. Under conditions in which aspirin had no effect, dazoxiben, a selective inhibitor of thromboxane synthetase, reduced platelet adhesion to aortic subendothelium by about 40% but did not affect adhesion to collagen-coated glass. Pre-treatment of aortic segments with 15-HPETE, a selective inhibitor of PGI2-synthetase, abolished the inhibitory effect of dazoxiben on adhesion. Concentrations of 6-oxo-PGF1 alpha in the perfusate were raised in the presence of dazoxiben alone, and following addition of thrombin (10 units/ml) there was a 2--3 fold increase in concentration. Perfusion of damaged aorta with platelets labelled with (14C)-arachidonic acid in the presence of thrombin and dazoxiben resulted in the appearance of (14C)-labelled-6-oxo-PGF1 alpha. Inhibition of thromboxane synthetase limits platelet adhesion probably by promoting vascular synthesis of PGI2 from endoperoxides liberated from adherent platelets, which subsequently promotes detachment of cells from the surface.

6-Ketoprostaglandin F1 alpha↗
PubMed2006

Effects of malondialdehyde content in low density lipoproteins on platelet adhesion.

Platelets play a key role in thrombotic vascular occlusion at the side of an atherosclerotic plaque. Malondialdehyde (MDA) derivatives are components of oxidized LDL. Recent studies suggest enhanced adhesion of platelets on oxidized LDL, but evidence of MDA-modified LDL contribution to enhanced platelet adhesion is missing. The aim of this study was to investigate platelet adhesion on LDLs with various content of MDA and to analyze its physiological relevance. LDLs were isolated by hydroxyapatite chromatography then analyzed. MDA, vitamin E and vitamin A content was estimated by HPLC methods and adhesion of platelets on modified LDLs was assessed. Both MDA and hypochlorite reactions induced an increase of both malondialdehyde content and negative charge in LDLs preparations. In LDLs of iron-overloaded patients both MDA content and negative charge was also significantly increased. The analysis of data showed that enhanced negative charge of LDLs had only negligible influence on platelet adhesion. The binding of platelets on LDL particles modified by MDA resulted in an S-shape curve and was substantially enhanced by high levels of MDA in LDL preparations. Malondialdehyde content both in hypochlorite modified LDLs and in LDLs of iron-overloaded patient matched the lower part of the binding curve. The platelet adhesion on circulating LDLs modified in in vivo conditions of oxidation stress in blood of iron-overloaded patients depends with considerable certainty preferably on non-MDA derived changes in derivatized LDLs. On the other hand, oxidized LDLs in atherosclerotic lesions can be much more extensively modified by MDA resulting in surfaces with enhanced affinity to adhering platelets. Such LDLs may be accessible to platelets, due to endothelial denudation or plaque rupture.

Chromatography↗
PubMed1967

Postoperative changes in platelet adhesiveness.

Platelet adhesiveness was measured in patients undergoing operation. With the rotating bulb technique adhesiveness increased steadily to the sixth and ninth days following surgery. The glass bead filter technique demonstrated a marked increase in platelet adhesiveness on the day following operation.

Blood Cell Count↗
PubMed1967

Adenosine diphosphate and the measurement of platelet adhesiveness.

Platelet adhesiveness to glass beads was measured in citrated blood at intervals up to two hours after the addition of adenosine diphosphate (A.D.P.). Adhesiveness increased for 15 minutes, fell towards the original level, and then steadily increased. The initial changes were associated with the formation and subsequent dispersal of platelet clumps. The sequence of events resembled the reported platelet aggregation, the disaggregation and secondary aggregation effect of A.D.P. and emphasizes the importance of a standard technique in the measurement of A.D.P.-induced platelet adhesiveness.

Adenine Nucleotides↗
PubMed1990

Adsorption of plasma proteins and adhesion of platelets onto novel polyetherurethaneureas--relationship between denaturation of adsorbed proteins and platelet adhesion.

Novel polyetherurethaneureas which have been synthesized by the present authors were chosen for the substrate polymers, on which adhesion of platelets was investigated. The number of adhered platelets and the amount of serotonin released from platelets adhered on the polymers and the protein-coated polymers were determined by radioisotope method. Both of them were enhanced with increasing content of urea linkages in the polyetherurethaneureas. The platelet adhesion was discussed in terms of the denaturation of plasma proteins upon adsorption, which was determined by Fourier-transform infrared spectroscopy. With increasing degree of protein denaturation, the platelet adhesion and the serotonin release were enhanced. This relationship was particularly evident in the case of albumin adsorption. It was shown that the surface properties of substrate polymers affect the protein adsorption, which in turn influences the adhesion of platelets.

Adsorption↗
PubMed1985

Effect of vitamin C on platelet adhesiveness and platelet aggregation in coronary artery disease patients.

The effect of oral administration of vitamin C on platelet adhesive index (PAI), platelet aggregate ratio (PAg R) and serum ascorbic acid levels was studied. Feeding 75 g of butter to healthy males (group I, n = 10 cases), enhanced the tendency of platelet adhesiveness (PAd) and platelet aggregation (PAg) to a significant level at the end of 4 h. This was distinctly prevented when 1 g of vitamin C was added to the fatty meal. In coronary artery disease (CAD) patients (group II, n = 20 cases) 10 days of vitamin C administration at 1 g every 8 hours decreased the PAd (p less than 0.001) and PAg (p less than 0.05) significantly. There was also a significant (p less than 0.001) rise in the vitamin C levels. The study brings out a property of vitamin C which may be of considerable importance in prevention of chronic thromboatherosclerotic disease of the arteries.

Adult↗
PubMed1989

Influence of plasticised poly(vinyl chloride) on platelet adhesion and platelet aggregates.

The most widely used plasticiser for poly(vinyl chloride) (PVC) is di-(2-ethyl-hexyl) phthalate (DEHP), which is extracted in contact with blood. One approach to reducing plasticiser extraction is to incorporate the higher molecular weight plasticisers trioctyl trimellitate (TOTM) and polymeric adipate (PA). This investigation has compared the influence of these plasticisers with that of DEHP on platelet adhesion and platelet aggregate formation. PVC tubing was tested in the absence of anticoagulants and in the presence of heparin. Our results demonstrate the influence of plasticisers on platelet response and support the view that evaluation of such plasticisers should be extended from an examination of toxicological properties to a comprehensive blood compatibility assessment.

Adipates↗