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At least 19 recordsLinked to original sources
PubMed1992

[Effect of different vascular prosthesis materials on blood platelets, blood clotting and fibrinolysis].

Studies were performed on Dacron vascular prostheses (USA), Gore-Tex (Germany), polyester prostheses (Czechoslovakia), Lawsan (Russia), as well as on DALLON-standard and DALLON-double velour prostheses (Poland), non-impregnated or impregnated with collagen, with heparin and albumin, with antithrombotic and antibacterial preparation, and with antibacterial preparation. In vitro, all the materials of vascular prostheses cause an adhesion of platelets in different degree, increase the availability of platelet factor 3, release platelet factor 4, reduce the blood clot retraction, shorten clotting time of the whole blood as well as recalcination time of intact plasma and increase the prothrombin consumption. None of the materials induced platelet aggregation nor influenced the activity of fibrinolytic system. Prostheses impregnated with collagen or with heparin and albumin were the most thrombogenic. Those impregnated with antibacterial preparation or with antibacterial and antithrombotic preparations, and Gore-Tex prostheses showed the lowest thrombogenicity. Thrombogenicity of vascular prostheses not only depends on chemical structure of the material, but on the method of fibre manufacturing by individual producers as well.

Animals↗
PubMed1989

Immunoelectron microscopic localization of actin, alpha-actinin, actin-binding protein and myosin in resting and activated human blood platelets.

Blood platelets are particularly rich in cytoskeletal proteins and respond to stimulation and activation by changes in shape. We examined the effect of blood platelet activation on the subcellular distribution of the cytoskeletal proteins, actin, myosin, alpha-actinin and actin-binding protein. These studies were performed with immunofluorescent staining on thin cryosections of paraformaldehyde-fixed platelets and by immunogold labeling of ultrathin cryosections of glutaraldehyde-fixed blood platelets. Platelets were studied immediately at blood collection (resting platelets), in platelet-rich plasma and after gel filtration (partially activated platelets), and after gel filtration and thrombin activation (0.5 U/ml, 10 min, 37 degrees C) (activated platelets). Resting platelets were disk-shaped and showed homogeneous distribution of cytoskeletal proteins. Partially activated platelets were more spherical and showed at least one protrusion. Immunofluorescence and immunogold labeling showed a more intense staining of the peripheral 0.2 to 0.3 micron of cytoplasm of these platelets. In the immunofluorescence photographs this resulted in the appearance of small fluorescent rings with staining at the periphery of cross-sectioned cells. Activated platelets showed an irregular outline composed of broad based pseudopods. Cell centers were composed of poorly delineated electron-dense material, interspersed with profiles of surface-connected tubules. The broad based pseudopods stained uniformely for actin, alpha-actinin and actin-binding protein. The cell center stained poorly for these proteins. Myosin staining was found in the peripheral cortex, but also in the cell center. Partially activated platelets that had returned to the disk shape after incubation at 37 degrees C showed increased submembranous concentration of microfilament proteins. These data reveal the profound cytoskeletal rearrangements that already occur upon minimal platelet activation and emphasize that platelets that have returned to the disk shape are not identical to resting platelets.

Actinin↗
PubMed1982

Taurine in human auricular myocardium and blood platelets.

Blood platelets have been used as a model for the aminergic neurones. In the hypertrophied left ventriles and platelets of spontaneously hypertensive rats the taurine content increases simultaneously. The main purpose of this work was to compare the taurine contents of human platelets and heart tissue. The taurine content was estimated from blood platelets and from the right atrial appendage removed during open heart surgery in 43 patients suffering from ischaemic heart disease. The results indicate that the taurine content increases in the hypertrophied right atrium of the patients with atrial septal defect, as it had previously been shown to increase in the hypertrophied left ventricle in patients who died of congestive heart failure. No correlations were found: 1) between the heart and platelet taurine contents of different groups, 2) between the atrial and platelet taurine in the pooled total results, 3) between the diastolic blood pressure and atrial or platelet taurine levels. Thus the increased taurine content of the auricular tissue is not reflected in the taurine content of the platelets.

Adult↗
PubMedDate not supplied

[Structure and function of blood platelets].

Blood platelets are discoid cellular fragments without nucleus originating from megakaryocytes. Platelets are able to respond to a great variety of agonists which bind to specific receptors localized on the plasma membrane. This process takes place when blood vessels are cut. Platelets then change their shape, adhere to newly exposed subendothelial tissues, release the content of numerous secretory granules and aggregate together. During this process, a great numbers of biochemical reactions are triggered such as phospholipases activation, synthesis of mediators and protein phosphorylation. These events result from increased cytoplasmic free calcium originating through calcium channels from the extracellular medium and from internal stores. Involvement of blood platelets in cardiovascular diseases may result from an exaggeration of these mechanisms by risk factors and are also discussed.

Animals↗
PubMed1976

Effects of sex steroids on serotonin uptake in blood platelets.

Blood platelets have been suggested as amodel for serotonin uptake and storage in the brain. To examine possible effects of se- steroids, platelets from human volunteers were incugated for 15 min with oestradiol, testosterone, and dihydrotestosterone, and then incubated fro 1 min with radioactive serotonin. The effects of the various steroids on serotonin uptake were measured. At 10(-3) M, oestradiol decreased serotonin uptake by 70%, testosterone by 49%, and dihydrotestosterone by 25%. Both oestradiol and testosterone showed maximal enhancement of uptake at 10(-6) M; oestradiol increased serotonin uptake by 41%, and testosterone by 60%. Dihydrotestosterone maximally facilitated uptake by 40% at a concentration of 10(-4) M. No sex differences were found in either direction or in magnitude of change in uptake due to any hormone. It is suggested that the effects of oestradiol are of physiological significance and that the site of action of the sterioid effect on serotonin uptake is the cell membrane of the platelets.

Blood Platelets↗
PubMed1994

Daily variations of functional parameters and density distribution in human blood platelets.

Blood platelets play a critical role in the onset of myocardial infarction, which has been shown to have a circadian rhythmicity with a peak incidence in the morning. In an attempt to correlate platelet parameters with the outcome of cardiovascular diseases, we studied the daily (24-h) variation of the following platelet parameters: distribution pattern of functional heterogeneous platelet subpopulations; serotonin uptake; ketanserin binding; aggregation upon thrombin, serotonin, and ADP stimulation; and platelet count. Furthermore, we analyzed the tryptophan and serotonin concentrations in the blood samples. The percentage of less dense platelets, which represent the subpopulation with the highest preactivation, showed a rhythmicity period of 24 h and an acrophase at 21:18 h. The time course of intermediate and high density platelets was inverse to that of low density platelets. The serotonin uptake exhibited also a rhythmicity with a 24-h period. The acrophase was at 13:50 h. The aggregation curves were inverse to the ketanserin binding curves. The serotonin concentration exhibited a 12-h rhythmicity. The results obtained suggest that (a) changes in platelet activity are reflected by several parameters of platelet function that underlie daily variations; (b) the aggregation curves show a peak in the morning, with an additional peak in the afternoon; and (c) changes in the distribution pattern occur independently from variations in platelet functions like aggregation and serotonin binding.

Adenosine Triphosphate↗
PubMed1987

[Adrenergic receptors of blood platelets].

Blood platelets possess adrenergic receptors and are stimulated by adrenaline in the circulation. This review summarizes the state of knowledge of the pharmacology of adrenergic receptors and the biochemical mechanisms of platelet activation by adrenaline in various physiological and pathological conditions.

Blood Platelets↗
PubMed1983

The 5-hydroxytryptamine receptor of blood platelets.

Blood platelets show specific, high affinity binding of 3H-5-hydroxytryptamine, 3H-ketanserin and 3H-D-lysergic acid diethylamide. 5-HT-antagonists are considerably more potent than agonists regarding both the displacement of specifically bound 3H-ketanserin and the shape change reaction mediated by the 5-HT-receptor. The latter depends on a rise of free intracellular Ca2+. The binding site for 3H-ketanserin and the site at which the 5-HT-induced shape change is triggered show the characteristics of a 5-HT2-receptor whose intracellular mediator seems to be Ca2+. The 5-HT2-receptor of platelets may be used as a partial model for that in neurons; however, it remains to be elucidated whether Ca2% is a mediator of the latter.

Animals↗
PubMed1980

Nuclear magnetic resonance studies of blood platelets.

Blood platelets contain membrane-enclosed granules which have inside them high concentrations of 5-hydroxytryptamine (serotonin) along with adenine nucleotides and divalent metal ions. 19F n.m.r. of fluorinated serotonin incorporated into the granules of both human and pig intact platelets has shown that the motional state of the serotonin is restricted. Comparison with 31P n.m.r. experiments indicates that this restriction of motion is a consequence of high molecular weight aggregates formed by the adenine nucleotides and metal ions, and that it varies with the species from which the platelets are obtained. In the case of human platelet granules, at least, these high molecular weight aggregates are present in the absence as well as in the presence of serotonin. The biological significance of these data is briefly discussed.

Adenine Nucleotides↗
PubMed1976

On the significance of the influx of calcium ions into stimulated human blood platelets.

Blood platelets, upon stimulation with various substances, take up calcium ions from the suspending medium. This influx occurs simultaneously with the release reaction, i.e. the specific secretion of a variety of substances from storage organelles and the second wave of aggregation. Various inhibitors of the release reaction inhibit this Ca2+ influx. Platelets previously loaded with 45Ca show an increased efflux of the cation upon stimulation by thrombin. These results suggest that the plasma membrane acquires an increased permeability to Ca2+ only in a later phase of platelet activation, in most cases after the earlier release of Ca2+ into the cytoplasm from Castoring organelles. Rapid shape change and release proceed independently of external calcium, whereas clot retraction depends upon a prolonged increased permeability of the plasma membrane to this cation.

Adenosine Diphosphate↗
PubMed1980

Activation time of blood platelets.

Blood platelets react rapidly in their hemostatic function. Determination of the reaction or activation time of individual platelets is difficult because it requires that physical and/or chemical effectors of activation are nonlimiting. Analysis of experimental conditions shows that the best estimate of mean activation time comes from in vivo measurements. Thus, the constancy of height-to-length ratio of a growing thrombus, and its change with flow rate, provide additional evidence for the activation time hypothesis.

Animals↗
PubMed1980

Binding of adenosine diphosphate to human blood platelets and to isolated blood platelet membranes.

The equilibrium binding of 14C-labeled ADP to intact washed human blood platelets and to platelet membranes was investigated. With both intact platelets and platelet membranes a similar concentration dependence curve was found. It consisted of a curvilinear part below 20 microM and a rectilinear part above this concentration. At high ADP concentrations, the rectilinear part appeared to be saturable. Because of this, two classes of saturable ADP binding sites were proposed. ADP was partly converted to ATP and AMP with intact platelets while this conversion was virtually absent in isolated platelet membranes. ADP was bound to platelet membranes with the same type of curves found for intact platelets. The ADP binding to the high affinity system, which was stimulated by calcium ions, was nearly independent of temperature and had a pH optimum at 7.8. A number of agents were investigated for inhibiting properties. Of the sulfhydryl reagents only p-chloromercuribenzene sulfonate inhibited both high and low affinity binding systems while iodoacetamide and N-ethylmaleimide were without effect. Compounds acting via cyclic AMP on platelet aggregation, such as adenosine and cyclic AMP itself, had no influence on binding. Some nucleosidediphosphates and nucleotide analogs at a concentration of 100 microM had no, or only a slight, effect on high affinity ADP binding. For some other nucleotides inhibitor constants were determined for both platelet ADP aggregation and ADP binding. The inhibitor constants of ATP, adenyl-5'-yl-(beta,gamma-methylene)diphosphate, IDP, adenosine-5'(2-O-thio)diphosphate, for aggregation and high affinity binding were in good correlation with each other. Exceptions formed fluorosulfonylbenzoyl adenosine and AMP. The ATP formation found with intact platelets could be attributed to a nucleosidediphosphate kinase. It was investigated in some detail. The enzyme was magnesium dependent, had a Q10 value of 1.41, a pH optimum at 8.0, was competitively inhibited by AMP and reacted via a ping pong mechanism. All findings described in this paper indicate that platelets as well as platelet membranes bind ADP with the same characteristics and they suggest that the high affinity binding of ADP is involved in platelet aggregation induced by ADP. The results on nucleosidediphosphate kinase did not permit a firm conclusion about the role of the enzyme in induction of platelet aggregation by ADP.

Adenosine Diphosphate↗