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At least 271 records · Page 15Linked to original sources
PubMed1986

Beta-transforming growth factor is stored in human blood platelets as a latent high molecular weight complex.

Human blood platelets, the richest known source of beta-transforming Growth Factor extractable under acid conditions, release in neutral extracts (pH 7.2) a latent form of this growth factor with an apparent molecular weight of 400 Kd. This latent form, poorly active on rat NRK-49F indicator cells in soft agar assays can be activated by exposure to acid pH or 8 molar urea. The acid activated beta-Transforming Growth Factor from neutral extracts elutes on Biogel P60, in 1 molar acetic acid, as a broad peak of apparent molecular weight 15-30 Kd, like when this factor is extracted from platelets by the usual acid-ethanol procedure. Moreover, beta-Transforming Growth Factor from both acid activated neutral extracts and from acid-ethanol extracts elutes on reverse phase at 30% acetonitrile. We suggest that beta-Transforming Growth Factor is stored in human blood platelets as a poorly active high molecular weight complex which may be dissociated and activated in appropriate in vivo microenvironments.

Animals↗
PubMed1980

Uptake of 5-HT by blood platelets of patients with myoclonus epilepsy.

5-HT uptake by blood platelets was tested in patients with PME with no Lafora bodies. Blood platelets from patients with myoclonus epilepsy and those from healthy sex and age matched controls were incubated for 5 min with 0.1 microM 3H-5-HT in Krebs-Henseleit buffer at 37 degrees C. The radioactivity taken up by platelets was assayed by liquid scintillation counting. 5-HT uptake in platelets from patients tended to be slightly higher (19%, n = 18, P greater than 0.05). The kinetic pattern as revealed by the Lineweaver-Burk plot, was very similar in the two groups. All patients were on antiepileptic drugs (sodium valproate, clonazepam and phenobarbital), but no evidence was found in vitro that these drugs would have any direct effect on the uptake.

Adolescent↗
PubMed1973

Effect of cations on the blood platelet release reaction.

1. Stimulus-secretion phenomena in blood platelets incubated with trypsin or thrombin have been investigated.2. Secretion occurs in at least two stages: (a) induction, obtained when the platelets are incubated with proteolytic enzymes in the presence of the chelating agent EDTA, and (b) release, which occurs with the subsequent addition of Ca(2+) to the incubation medium.3. Ca(2+) was the only essential divalent cation required for release. Ba(2+) and Mg(2+) inhibited release and Sr(2+) could only partially substitute for Ca(2+).4. Blood platelets exhibited recovery from enzymic perturbation by trypsin or thrombin by a mechanism that was temperature dependent, but did not require the synthesis of new protein.5. The results are discussed in relationship to stimulus-secretion in other cells.

Adenine Nucleotides↗
PubMed1977

Mepacrine, a tool for investigating the 5-hydroxytryptamine organelles of blood platelets by fluorescence microscopy.

In the blood platelets of various species exposed to mepacrine, the average number of green-yellow fluorescent granules (probably identical with the 5-hydroxytryptamine [5-HT] storage organelles) corresponded to that of flashes emitted by the platelets on prolonged irradiation with violet-blue light. In platelets of fawn-hooded rats the number of granules did not markedly differ from that of normal rat platelets, but the fluorescence intensity and the uptake of mepacrine in vitro showed a marked decrease and the flashes were less numerous. The heavy population of human platelets exhibited considerably more granular structures than the light population. The data suggest that (1) in normal, mepacrine-loaded platelets one flash corresponds to one 5-HT organelle and (2) mepacrine is a useful tool for investigating the number and function of the 5-HT organelles in live platelets and possibly for studying platelet age.

Animals↗
PubMedDate not supplied

[Comparative effect of chlorpromazine, imipramine and papaverine on the blood platelet function].

With a view of decoding the mechanisms of their action the effect of papaverine, chlorpromazine and imipramine produced on a number of blood platelets hemostatic functions was studied. All the three drugs suppress in a characteristic fashion the aggregation on blood platelets caused by thrombin in the Tyrode solution and in a plasma defibrilated by heating, as well as by collogen and ADP in the citrated plasma. Unlike chlorpromazine and imipramine papaverine exerts a strong inhibiting action on the phosphodiesterase activity. Chlorpromazine and imipramine suppress the absorption of serotonin and retraction more intensively than this is done by papaverine and call forth morphological changes in the blood platelets that proceed parallel with changes in the intensity of the photodiffusion and liberation of endogenous serotonin. It is postulated that chlorpromazine and imipramine manifest their inhibitory effect through nonspecific damage of the blood platelets membranes, whereas papaverine does this through exchange of adenine-nucleotides and, especially, of 3',5'-AMP.

Absorption↗
PubMed1975

[Adhesion of blood platelets to electric-featuring polymers].

The authors studied the effect of electric potential arising on the plastic surface upon the blood clotting process. The study was performed according to the Breddin method. The study concerned fluorosilicone rubber, fluoroplast, polyester, polyethylene and polyvinyl chloride with various surface potentials. The authors found that the negatively charged blood platelets adhere to negatively charged plastic surfaces only to a low extent and undergo no disintegration and agglomeration. To the surfaces of the same plastics being electrically neutral, only small aggregates of blood platelets adhere. On the other hand, on the positively charged surfaces the accumulation of blood platelets takes place with concurrent aggregation and disintegration, thus initiating the thrombus formation. The authors observed the intensity of these changes using blood platelet adhesion index and fluorescence microscope.

Blood Coagulation↗
PubMed1984

Chemical modification of cytoskeletal proteins of human blood platelets by diamide.

Incubation of human blood platelets with diamide (azo-dicarboxylic acid-bis-dimethylamide, DIA) influences the aggregation behaviour considerably. Depending on concentration and incubation time DIA induces a reversible aggregation or brings about complete inhibition. The effect is reversible and may be due to the regeneration of reduced glutathione (GSH) which will be oxidized to GSSG by DIA. DIA causes disulfide-linked polymer formation of certain cytoskeletal proteins. At least three polymer families (Pa, Pb, Pc) with different molecular weights are formed depending on dosage and incubation time of DIA. The appearance of a double band in Pa correlates with reversible aggregation, the formation of Pc is always accompanied by a complete inhibition of aggregation. A disturbance of cytoskeleton-membrane interaction by polymer formation can be assumed. GSH serves as a reductant of disulfide-linked polymers whereby a direct link between the maintenance of SH/SS status of platelets and GSH can be established.

Azo Compounds↗
PubMed2002

The blood platelet as a model for regulating blood coagulation on cell surfaces and its consequences.

Platelets actively participate in regulating thrombin production following physical or chemical injury to blood vessels. Injury to blood vessels initiates activation of the large numbers of platelets that appear in the subendothelium where they become exposed to tissue factor and to molecules adhesive for platelets and normally found in the extracellular matrix. The complex of plasma factor VIIa with extravascular tissue factor both initiates and localizes thrombin production on platelets and on extravascular cells. Thrombin production at these sites in turn enhances platelet activation and the subsequent hemostatic plug formation to minimize bleeding. Thrombin production and platelet activation also initiate the process of wound healing requiring thrombin-dependent cell activation and platelet-dependent formation of new blood vessels (angiogenesis). Activated platelets release from their storage granules several proteins and other factors that regulate local thrombin formation and the responses of blood vessel cells to injury to assure hemostasis and effective wound healing. Failure to localize and adequately regulate thrombin production and/or platelet activation can have pathological consequences, including the development and propagation of atherosclerosis and enhancement of tumor development. The primary basis for the pathological consequences of the failure to adequately regulate thrombin production is that the multi-functional thrombin activates several types of cells to initiate their mitogenesis. Mitogenesis precedes many of the undesirable consequences of poorly regulated thrombin production and platelet activation. In addition, activated platelets release a variety of products which influence the functions of several cell types to the extent that inadequate regulation of platelet activation (by excessive thrombin production) could contribute to the pathogenesis of acute and chronic arterial thrombosis and to tumor development. Activated platelets participate in tumor development by releasing several factors that positively (and negatively) regulate blood vessel formation.

Blood Coagulation↗
PubMed1995

Bactericidal capability of blood platelets in eutrophic newborns.

Bactericidal activity of the blood platelets from cord blood of 69 eutrophic newborns differed in relation to sex. In female newborns we noted 8.13% killed Staphylococcus aureus ATCC 6538 P, whereas in male newborns only 2.92%. These data point to the role of platelets in unspecific defense against infections.

Blood Bactericidal Activity↗
PubMed1982

[Neurotic triad and change in blood platelet number in reaction to stress].

Blood platelet count is evaluated three times in reaction to catheterization stress in a group of 21 myocardial infarction patients and a group of 21 non-coronary subjects. Coronary and non-coronary patients are divided in two groups according to their low or high results at the psychological scales (hypochondria, depression, hysteria of the M.M.P.I.). The group of non-coronary patients with low results in hypochondria, depression and in the sum of the three psychological scales presents a lower platelet count than the other groups. The non-coronary subjects with high psychological results have the same platelet count as the coronary patients with high or low values.

Blood Platelets↗
PubMed1979

High resolution two-dimensional gel electrophoresis of the proteins and glycoproteins of human blood platelets and platelet membranes.

The proteins and glycoproteins of human blood platelets and platelet membranes in both the reduced and the unreduced states have been analysed by isoelectric focusing and sodium dodecyl sulphate-discontinuosus polyacrylamide gel electrophoresis in a two-dimensional technique. Gels which had been stained with periodic acid-Schiff's reagent could be counter-stained with Coomassie Brilliant Blue, simplifying the recognition of components which stain with both reagents. The major glycoproteins and some of the proteins have been identified and the characteristics of the membrance and of the whole platelet components established in this system.

Blood Platelets↗
PubMed1985

Uptake of gamma-aminobutyric acid by human blood platelets: comparison with CNS uptake.

Human blood platelets show a sodium and temperature dependent uptake of gamma-aminobutyric acid (GABA) and other neuroactive amino acids. The most potent inhibitors tested of platelet GABA uptake were taurine and beta-alanine, while nipecotic acid and cis-3-aminocyclohexanecarboxylic acid were relatively weak inhibitors. These results suggest GABA is transported by a beta-amino acid uptake process in human platelets. Thus, platelet GABA uptake may more closely resemble glial rather than neuronal uptake.

Amino Acids↗
PubMed2004

Resveratrol reduces oxidative stress induced by platinum compounds in blood platelets.

The effects of resveratrol (trans-3,4',5-trihydroxystilbene) on the oxidative stress in blood platelets induced by platinum compounds [cisplatin and selenium-cisplatin conjugate] were studied in vitro. The production of thiobarbituric acid reactive substances (TBARS), the level of conjugate diene, the generation of superoxide anion radicals (O2-*) and other reactive oxygen species (O2-*, H2O2, singlet oxygen and organic radicals) were measured by chemiluminescence in blood platelets treated with platinum compounds. Cisplatin at the concentration of 10 microg/ml, as well as selenium-cisplatin conjugate (10 microg/ml) induced oxidative stress in blood platelets: an increase in TBARS, conjugate diene, chemiluminescence and generation of O2-*. In the presence of resveratrol (a natural compound with antioxidant activity) at the concentrations of 1-25 microg/ml, the chemiluminescence, the levels of O2-*, conjugate diene and TBARS were reduced (p < 0.05). We showed that resveratrol at different concentrations (1-25 microg/ml) had a protective effect against oxidative stress in platelets caused by platinum compounds (10 microg/ml) and it diminished platelet lipid peroxidation and reactive oxygen species generation induced by platinum compounds.

Animals↗
PubMed1984

Inhibition of 5-hydroxytryptamine-potentiated aggregation of human blood platelets by 5-hydroxytryptamine receptor-blocking agents.

Blood platelets possess specific receptors for 5-hydroxytryptamine (5-HT) which differ from the carrier for the amine uptake. Activation of 5-HT receptors causes shape change and aggregation of platelets. We studied the influence of drugs with 5-HT receptor blocking properties on 5-HT-potentiated, ADP-induced aggregation of human blood platelets. The synergistic effect of 5-HT on aggregation was inhibited by the compounds tested in the order of potency: cyproheptadine, pizotifen, spiperone, methysergide, methiothepine , mianserin, ketanserin, dihydroergotamine. The IC50 values lay in the range from 14 to 40 nmol/l. Chlorpromazine and haloperidol were less effective by more than one order of magnitude. Our results indicate a certain similarity between the 5-HT receptors on platelets and the 5-HT receptors on serotonergic neurons and vascular smooth muscle which belong to the 5-HT2 receptor type.

Adenosine Diphosphate↗