[Investigation on the central regulation of blood platelet count in peripheral blood].
Explore the source record for details and available documents.
Blood Platelets↗
SEARCH · PubMed Health
Results for “BLOOD PLATELETS”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Carvedilol--a beta-blocker with considerable antiaggregatory effect on human blood platelets.
BACKGROUND: Activated blood platelets play a key role in the genesis of many pathological states. Several studies have documented that beta-blockers can influence platelet aggregation. Carvedilol, a third generation non-selective agent with vasodilatory properties, is successfully used in pathological states accompanied with platelet hyperreactivity, however information on its antiplatelet activity is lacking. OBJECTIVES: The aim of this study was to analyse the in vitro effect of carvedilol on aggregation of human blood platelets, to compare this effect with the effect of propranolol and atenolol, and to determine whether its suggested antiaggregatory effect was accompanied with reduced thromboxane B2 formation. Moreover, some physico-chemical parameters of the drugs tested were calculated and compared. METHODS: Platelets were isolated by differential centrifugation and platelet aggregation was measured by the turbidimetric method. The amount of thromboxane B2 was measured by the radioimmunoassay method. Physico-chemical parameters of the drugs tested were calculated using the computer programme Hyperchem. RESULTS: Carvedilol and propranolol inhibited platelet aggregation in the rank order of stimuli: PMA > thrombin > A23187 > epinephrine. The reduction was accompanied by inhibition of thromboxane B2 formation. In comparison to propranolol, carvedilol was more effective, with the exception for aggregation stimulated with ADP. Atenolol did not affect any platelet function tested. From the drugs studied, the molecule of carvedilol was found to possess the highest partition coefficient, the highest index of molar refractivity, and the lowest dipole moment. CONCLUSION: Our study found carvedilol to be more potent than propranolol and atenolol in inhibiting platelet aggregation and thromboxane B2 production. This may be due to the different structure and more convenient physico-chemical parameters of the carvedilol molecule.
Adrenergic beta-Antagonists↗
Glycosylation restores survival of chilled blood platelets.
Cooling of blood platelets clusters the von Willebrand factor receptor complex. Macrophage alphaMbeta2 integrins bind to the GPIbalpha subunit of the clustered complex, resulting in rapid clearance of transfused, cooled platelets. This precludes refrigeration of platelets for transfusion, but the current practice of room temperature storage has major drawbacks. We document that alphaMbeta2 is a lectin that recognizes exposed beta-N-acetylglucosamine residues of N-linked glycans on GPIbalpha. Enzymatic galactosylation of chilled platelets blocks alphaMbeta2 recognition, prolonging the circulation of functional cooled platelets. Platelet-associated galactosyltransferase produces efficient galactosylation when uridine diphosphate-galactose is added, affording a potentially simple method for storing platelets in the cold.
Acetylglucosamine↗
The influence of novel platelet aggregation inhibitors on human blood platelet clustering and retention effected by some polymer materials, in vitro.
Human blood platelet clustering and retention in vitro induced by medical grade Cuprophane and Silastic and by non-medical grade polyethylene and Mylar, are discussed. The influence of synthetic compounds on polymer-induced platelet clustering and retention has been evaluated, interpreted in terms of physicochemical parameters, and correlated with ADP- and human alpha-trombin-stimulated aggregation; the Pearson product-moment correlation coefficient for a series of bis (alkylnipecotoylamino) alkanes was computed at r = 0.98 between (i) mylar-induced cluster formation and (ii) ADP-effected aggregation, and at r = 0.94 in corresponding correlations with thrombin as an inducing agent. All experiments were carried out in vitro. Due to the paucity of polymer specimens meeting the stipulated specifications, several evaluations had to be limited to triplicate and duplicate determinations.
Blood Platelets↗
In vitro aggregation of canine blood platelets and liquefaction of blood clots by leptospires.
Explore the source record for details and available documents.
Animals↗
[Role of blood platelets in parasitic diseases].
Blood platelet are of crucial importance in hemostasis. Little attention has been paid to their bacteriocidal activity and their potential role in parasitic infections. Activation of blood platelets may result from direct contact with a parasite or IgE, IgG, complement factors, lymphokines, CRP. Blood platelets reveale cytotoxic activity through release various inflamatory mediators, phagocitic activity and cooperation with other cells of immunologic system. The precise mechanism of all platelet cytotoxic effects remains unclear.
Animals↗
The separation and preservation of blood platelets with the Cohn blood fractionator.
Explore the source record for details and available documents.
Blood Banks↗
Preactivation and deactivation of blood platelets.
Human blood anticoagulated with a serine protease inhibitor was centrifuged with an erythrocyte agglutinating agent in the bottom of the tube. Platelet rich plasma (PRP) obtained in this manner contained platelets with different ability to aggregate with ADP located in the various layers of the tube. Platelets in the midportion of the tube were most extensively aggregated by a standard dose of ADP (1.6 micro M) and mechanical stirring. Platelets in the lowest portion aggregated least, but still showed normal "shape change" when they were stimulated. The uppermost platelets in the tube also showed somewhat reduced aggregation compared with the midportion. These observations could not be explained by differences in platelet concentrations. On a descriptive basis the platelets in the midportion of the tube are designated preactivated and the lowermost platelets deactivated.
Adenosine Diphosphate↗
Image analysis of blood platelets adhesion.
Adhesion of blood platelets is one of the major events in haemostatic and thrombotic processes. We studied adhesion of blood platelets on fibrinogen and fibrin dimer sorbed on solid support material (glass, polystyrene). Adhesion was carried on under static and dynamic conditions and measured as percentage of the surface covered with platelets. Within a range of platelet counts in normal and in thrombocytopenic blood we observed a very significant decrease in platelet adhesion on fibrin dimer with bounded active thrombin with decreasing platelet count. Our results show the imperative use of platelet poor blood preparations as control samples in experiments with thrombocytopenic blood. Experiments carried on adhesive surfaces sorbed on polystyrene showed lower relative inaccuracy than on glass. Markedly different behaviour of platelets adhered on the same adhesive surface, which differed only in support material (glass or polystyrene) suggest that adhesion and mainly spreading of platelets depends on physical quality of the surface. While on polystyrene there were no significant differences between fibrin dimer and fibrinogen, adhesion measured on glass support material markedly differed between fibrin dimer and fibrinogen. We compared two methods of thresholding in image analysis of adhered platelets. Results obtained by image analysis of spreaded platelets showed higher relative inaccuracy than results obtained by image analysis of platelets centres and aggregates.
Blood Platelets↗
The receptor for IgE on blood platelets.
Highly purified blood platelets from man and rat could be induced into cytotoxic effectors against schistosome larvae by an IgE-dependent mechanism. Such a process implied the existence of a receptor for the Fc part of IgE on the surface of these blood elements. Normal platelets, incubated in the serum of infected individuals as well as in the IgE-rich serum from asthmatic patients, showed similar capabilities. Flow cytofluorometric analysis evidenced that the platelets bearing IgE receptors represented a subpopulation (20%), the percentage of which was significantly increased (up to 50%) in rats or patients with high levels of circulating IgE. Radiolabeled IgE, whose binding was specifically inhibited by an excess of unlabeled IgE or by anti-Fc epsilon receptor antibody, allowed the demonstration that the receptor for this isotype on the platelet surface was saturable. The binding of increasing amounts of IgE followed a bimodal curve, with less than 1000 sites per platelet showing an affinity coefficient of 3.3 X 10(7) M-1 at low concentrations, and a Ka of 7.8 X 10(5) M-1 for higher concentrations. Beyond their interest in the demonstration of cytotoxic properties of thrombocytes, these observations place emphasis on the potential role of the platelets in immediate-type allergic reactions by their direct interaction with IgE antibody molecules, through a specific receptor.
Animals↗
[Effects of platelet activating factor on blood platelets].
Explore the source record for details and available documents.
Blood Platelets↗
Pathological changes in cerebral arteries following experimental subarachnoid hemorrhage: role of blood platelets.
The role of blood platelets in producing early intimal changes in cerebral arteries following subarachnoid hemorrhage (SAH) was examined by using 18 cats. Experimental SAH was produced by a rupture of the proximal portion of the right middle cerebral artery. Following SAH, the scanning electron microscope revealed that structural alterations in the intimal layer of major cerebral arteries occurred as early as 2 hours and became more severe by 48 hours. Vascular alterations, which were predominantly detected in the ruptured vessel, consisted of endothelial cell corrugation, detachment, crater formation, intimal adhesion of platelets and red blood cells, intimal thrombi, and reendothelialization. When cats were pretreated prior to SAH with an anti-platelet-aggregating agent, OKY-1581, the intimal blood elements and thrombi were clearly reduced, and reendothelialization was not observed. However, endothelial cell changes in the OKY-1581-treated group were very similar to those occurring in the nontreated group. While these results suggest that bioactive substances contained within blood platelets, such as growth factors, serotonin, and norepinephrine, have little effect on producing endothelial cell injury, platelets may be important in the initiation of reendothelialization following vessel injury.
Animals↗
Localization of phosphatidylethanolamine in the plasma membrane of diamide-treated human blood platelets.
In human blood platelet plasma membranes phosphatidylethanolamine (PE) is asymmetrically distributed between the two leaflets. The main part of this phospholipid is localized at the inner half of the lipid bilayer. Upon stimulation of the cell a substantial transbilayer movement of PE as well as phosphatidylserine occurs and the outer leaflet then provides a procoagulant surface. The thrombin-induced PE flip-flop is inhibited by pretreatment of platelets with diamide, whereas pretreatment of platelets with diamide alone up to 5 mM did not change considerably the localization of PE in the platelet membrane. Thus, cytoskeletal proteins, which are modified by diamide, are not involved in the maintenance of the PE asymmetry but are important for the realization of the agonist-induced events in the platelets.
Adenosine Diphosphate↗
Methylene blue inhibits the arachidonic acid metabolism in human blood platelets.
When human blood platelets are incubated with methylene blue (MB) that oxidizes cellular NADPH, a marked inhibition of platelet aggregation and of the metabolism of arachidonic acid (AA) in both the cyclooxygenase and lipoxygenase pathway is found. The inhibition of aggregation and AA metabolism is prevented, at least partially, by the thiol-oxidizing agent diamide. The results indicate an involvement of the reduced coenzymes NADPH and glutathione (GSH) in the regulation of cyclooxygenase and lipoxygenase activity in platelets.
Arachidonic Acids↗
Rheological behavior of blood platelets in vivo.
Blood platelets labeled in vivo with the fluorochrome acridine red can be localized objectively within a thin optical section, using fluorescence microscopy. This allows the study of the rheological behavior of platelets in vivo as exemplified by the assessment of the concentration distribution and the orientation of platelets flowing in small arterioles of the rabbit mesentery.
Animals↗
Pharmacological manipulation of the thromboxane pathway in blood platelets.
Interference with blood platelet thromboxane A2 (TxA2)-formation using aspirin has proven to be clinically efficient in the prevention of arterial thrombosis. The protection, however, is far from absolute and during recent years we have witnessed the development of new classes of drugs with more specific impact on TxA2-dependent pathways of platelet activation. Thromboxane synthase inhibitors (TSI) act on the thromboxane synthase, thus preventing the formation of TxA2, and causing a shunting of the prostaglandin cyclic endoperoxide metabolism towards other prostanoids, such as the platelet inhibitory PGD2 and PGI2, the latter when endothelial cells are present that can 'steal' platelet derived cyclic endoperoxides. TSI, however, do not block the formation of the cyclic endoperoxides. Since those products themselves can also act on the TxA2-receptor, the net effect of a TSI will be the result of a complex balance of pro- and anti-aggregatory prostanoids. Known thromboxane receptor antagonists (TRA) inhibit the interaction of both TxA2 and the cyclic endoperoxides with the receptor in a competitive way, but do not change the relative levels of the different prostaglandins formed. The combination of the two actions leads to a stronger influence on in vivo, ex vivo and in vitro laboratory tests as can be seen when a TSI and TRA are used in combination, or when a drug is studied that has both characteristics. Additional data show that such a double-action drug is able to quickly reduce levels of beta-thromboglobulin, a marker for ongoing in vivo platelet activation, in patients with obstructive arterial disease.
Animals↗
Glycogen distribution in rat blood platelets.
In rat blood platelets, glycogen particles have been observed in masses contiguous to the open channel system as well as in masses or individual particles scattered throughout platelet hyaloplasm. Rat platelets showed a glycogen distribution in relation to the open channel system in approximately one-third of all platelets seen in randomly selected photomicrographs. The glycogen particles had a mean diameter of 256 A, and the density of glycogen deposits was similar to that observed in human platelets. Glycogen related to the open channel system was seen in proximity to granular structures and frequently was membrane bound. Addition of thrombin, ADP or collagen to platelet-rich plasma, as well as storage of platelets at 21 C, was associated with a loss of glycogen in sites adjacent to the open channel system, but many dispersed glycogen particles appeared to be preserved. The collection of platelets in ethylenediamine tetracetic acid and chilling of platelets reduced the number of glycogen particles contiguous to the open channel system but did not entirely eliminate those glycogen deposits. Glycogen in human platelets apparently has not been observed in a similar relationship to granules and the open channel system. The observations were consistent with the hypothesis that open channel system-related glycogen is more labile in the presence of stimuli for the release reaction and glycogenolysis than is diffusely distributed glycogen.
Adenosine Diphosphate↗
Surface movements during the spreading of blood platelets.
When human blood platelets spread on a substratum they increase their surface area as much as 4-fold. We investigated the mechanism of spreading by light microscopy and by scanning and transmission electron microscopy. Contact of a platelet with a glass surface induces formation of thin extensions which spread out over the substratum. These extensions resemble the actin-containing microspikes and lammelipodia of tissue cells in culture and appear to be drawn from the peripheral cortical layer associated with the plasma membrane. If platelets are initially labeled on their external surface with cationic ferritin or lentil-conjugated gold particles and then allowed to spread, the labels are retained in the central region, or granulomere. Proteins released by the spreading platelet--fibronectin and fibrinogen--also remain in this central unspread region. Peripheral regions of spread platelet surface (hyalomere) were unlabeled following the above procedures but could be labeled with cationic ferritin or lentil-conjugated gold provided these were applied after spreading was completed. These markers are cleared with time from the periphery, moving centripetally to accumulate at the granulomere. We suggest, on the basis of these observations, that platelets spread onto a substratum by a closely similar mechanism to that used by cells such as fibroblasts. In both cases the spreading involves the peripheral actin cortex and is accompanied by a continual centripetal movement of surface components--a "membrane flow"--which continues even after spreading is completed.
Actins↗