Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Platelets”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,387 records · Page 77Linked to original sources
PubMed1987

A monoclonal antibody to the surface membrane of human platelets which inhibits ristocetin- and collagen-induced platelet aggregation reacts with H1 histones of cell nuclei.

A murine monoclonal antibody HuPIA3, produced by immunization with human platelet membranes, reacted by radioimmunoassay with platelets, and inhibited ristocetin- and collagen-induced platelet aggregation and release of 14C-serotonin. The antibody also inhibited ristocetin-induced aggregation of washed, formaldehyde-fixed platelets by von Willebrand factor. On cultures of human and rodent fibroblasts, and on frozen sections of rabbit liver and rat kidney, the antibody gave a diffuse, homogenous immunofluorescence staining of cell nuclei which could be abolished by treatment with 0.1 M HC1 or 2 M NaCl and restored by reconstitution with histones, suggesting a reaction with nuclear histones. Absorption of the antibody with histones abolished nuclear staining and abrogated the inhibitory effect of the antibody on ristocetin- and collagen-induced platelet aggregation and 14C-serotonin release. Conversely, absorption with platelets removed antibody reactivity for platelets and for cell nuclei. In addition, the antibody reacted with H1 histones by radioimmunoassay, and immunoblotting studies showed that the antibody reacted with a protein of 199,000 daltons on platelets and with H1 histones (31,000 dalton and 32,000 dalton). These observations suggest that the antibody recognizes epitopes found on surface molecules of platelets as well as on H1 histones of cell nuclei.

Antibodies, Antinuclear↗
PubMed1988

Platelet parameters. Part II. Platelet volume-number relationships in various normal and disease states.

The relationship between mean platelet volume (MPV) and platelet count was evaluated in 259 patients with rheumatoid arthritis and 311 patients with various haematological disorders. Platelet volume-number relationships determined in a previous study on normal subjects were used as a reference range. There was a significant inverse relationship between MPV and platelet count in patients with rheumatoid arthritis (r = -0.49; P less than 0.0001), which by interval analysis was shown to be non-linear. In the patients with haematological disorders, the platelets were found to be disproportionately small for number in patients with aplastic anaemia, chemotherapy-induced marrow suppression and some cases of acute idiopathic thrombocytopenic purpura (ITP). In subjects with chronic ITP followed longitudinally, the inverse platelet volume-number relationship was retained. MPV was appropriate for platelet number in myelodysplastic syndromes, variable in iron deficiency anaemia and disproportionately large in myeloproliferative syndromes, most notably in agnogenic myeloid metaplasia. The observation that the MPV was disproportionately large in comparison with the platelet count was used in establishing the diagnosis of an hereditary giant platelet syndrome in a family of British origin.

Adult↗
PubMed1987

Shortening of bleeding time by 1-deamino-8-arginine vasopressin (DDAVP) in the absence of platelet von Willebrand factor in Gray platelet syndrome.

The Gray platelet syndrome is a rare disorder characterised by the absence of platelet alpha-granules and their contents. We describe a new patient and the effects of infusions of 1-deamino-8-arginine vasopressin (DDAVP). The patient had a prolonged skin bleeding time and his platelets had reduced numbers of alpha-granules, increased vacuolation and reduced retention on glass beads. Platelet von Willebrand factor antigen (vWf:Ag) was undetectable and levels of platelet fibrinogen, beta-thromboglobulin, platelet factor 4 and thrombospondin were reduced. All tests of plasma coagulation factors were normal, including Factor VIII (F.VIII:C), vWf:Ag, ristocetin cofactor (R:CoF) and botrocetin cofactor. Platelet ATP, ADP, platelet albumin, surface membrane glycoproteins and 14C-serotonin uptake were also normal. Infusions of DDAVP increased plasma F.VIII:C, vWf:Ag and R:CoF and shortened the bleeding time on two occasions. This suggests that DDAVP shortens the bleeding time by releasing vWf:Ag and/or other proteins from cellular storage sites other than the platelet.

Adult↗
PubMed1985

Gray platelet syndrome: immunoelectron microscopic localization of fibrinogen and von Willebrand factor in platelets and megakaryocytes.

An immunogold method was used for investigating the subcellular localization of von Willebrand factor (vWF) and fibrinogen (Fg) in platelets and cultured megakaryocytes from normal subjects and from three patients with the gray platelet syndrome (GPS), a rare congenital disorder characterized by the absence of alpha-granules. In normal platelets at rest, vWF was detected exclusively in alpha-granules, with a characteristic distribution: gold particles were localized at one pole of each labeled granule, outlining the inner face of its membrane. vWF was distributed similarly in the alpha-granules of megakaryocytes at day 12 of culture, where it was also found in small vesicles near the Golgi complex. In contrast, Fg was observed in the whole matrix of all platelet alpha-granules but not in the nucleoids. In platelets from three patients with GPS, vWF and Fg were distributed homogeneously in the rare normal alpha-granules, which could be recognized by their size, and also in small granules identified as abnormal alpha-granules, which were similar in size to the small, possibly immature granules present in normal megakaryocytes. In addition, in some unstimulated platelets, Fg labeling was associated with dense material in the lumen of the surface-connected canalicular system (SCCS). At day 12 of culture, megakaryocytes from the patients with GPS contained some small alpha-granules labeled for Fg and vWF identical to those found in mature platelets. The majority of alpha-granules of normal size appeared partially or completely empty. Thus, we conclude that vWF is distributed differently from Fg in normal alpha-granules, and that unstimulated platelets from patients with GPS contain Fg and vWF in a population of small granules identifiable as abnormal alpha-granules only by immunoelectron microscopy. In addition, the presence of Fg in the SCCS of gray platelets suggests a spontaneous release of the alpha-granule content.

Adult↗
PubMed1985

A monoclonal anti-human platelet antibody: a new platelet aggregating substance.

A monoclonal anti-human platelet antibody, TP82, is described, which caused irreversible aggregation of platelets in association with the release of adenosine triphosphate or [14C] serotonin, and which inhibited ristocetin-induced agglutination. Immunofluorescence assay showed that the antibody binds to platelets, megakaryocytes, and common acute lymphoblastic leukemia cells. The antibody (IgG1) immunoprecipitated a polypeptide of 23,000 daltons with an isoelectric point of about 7.0. The aggregation induced by the purified antibody and/or F(ab')2 fragments occurred in platelet-rich plasma and with washed platelets, but not with formalin-fixed washed platelets. TP82-induced aggregation was completely inhibited by disodium ethylendiaminotetraacetate, diltiazem, W-7, PGE1, and several metabolic inhibitors. At a concentration of apyrase or CP/CPK, which inhibited adenosine 5-diphosphate-induced aggregation. TP82-induced aggregation was only partially affected. Thrombin was not required for the antibody-mediated effects, since two thrombin inhibitors failed to block the reaction. The antibody, at least at a high concentration, induced platelet aggregation by a mechanism almost independent of thromboxane A2 formation, since cyclooxygenase inhibitors had little inhibitory effect on aggregation. TP82 monoclonal antibody is a new platelet-aggregating substance that interacts with a low-molecular-weight binding site on the platelet membrane.

Adenosine Triphosphate↗
PubMed1985

Kinetics of In-111-platelets in the baboon: I. Isolation and labelling of a viable and representative platelet population.

A fully representative and viable platelet population was isolated from the blood of 15 baboons by a multiwash procedure, and labelled with In-111-oxine. The recovery of the total platelet population in the circulation was 85% +/- 9. Mean platelet life span was 146 hr +/- 13. Correcting for plasma radioactivity (always less than 3.5%) did not significantly affect the estimate of platelet life span (145 hr +/- 16) or recovery (85% +/- 12). Platelet survival estimates, repeated at different times, were reproducible. In 5 baboons, platelets were also harvested by a single step differential centrifugation. The mean life span of a representative platelet population was significantly longer than that of platelets harvested by a single step. Recovery values of the representative and non-representative population were similar. We conclude that it may be important to harvest and label a fully representative platelet population for kinetic studies. The proposed method is simple and reproducible, and may be applied in studies in humans.

Animals↗
PubMed1985

Platelet aggregation in Finnish men and its relation to fatty acids in platelets, plasma and adipose tissue.

Platelet aggregation and its relation to fatty acid composition of platelets, plasma and adipose tissue was determined in 196 randomly selected, free-living, 40-49-year-old men in two regions of Finland (east and southwest) with a nearly twofold difference in the IHD rate. There were no significant east-southwest differences in platelet aggregation induced with ADP, thrombin or epinephrine. ADP-induced platelet secondary aggregation showed significant negative associations with all C20-C22 omega 3-fatty acids in platelets (r = -0.26- -0.40) and with the platelet 20: 5 omega 3/20: 4 omega 6 and omega 3/omega 6 ratios, but significant positive correlations with the contents of 18:2 in adipose tissue (r = 0.20) and plasma triglycerides (TG) (r = 0.29). Epinephrine-induced aggregation correlated negatively with 20: 5 omega 3 in plasma cholesteryl esters (CE) (r = -0.23) and TG (r = -0.29), and positively with the total percentage of saturated fatty acids in platelets (r = 0.33), but had no significant correlations with any of the omega 6-fatty acids. Thrombin-induced aggregation correlated negatively with the omega 3/6 omega ratio in adipose tissue (r = -0.25) and the 20: 3 omega 6/20: 4 omega 6 ratio in plasma CE (r = -0.27) and free fatty acids (FFA) (r = -0.23), and positively with adipose tissue 18:2 (r = 0.23) and 20:4 omega 6 (r = 0.22) in plasma phospholipids (PL). The percentages of prostanoid precursors in platelet lipids, i.e. 20:3 omega 6, 20:4 omega 6 and 20:5 omega 3, correlated best with the same fatty acids in plasma CE (r = 0.32 - 0.77) and PL (r = 0.28 - 0.74). Platelet 20:5 omega 3 had highly significant negative correlations with the percentage of 18:2 in adipose tissue and all plasma lipid fractions (r = -0.35 - -0.44).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1985

The effect of lanosterol on platelet aggregation in human platelets.

It has been reported that lanosterol can sensitize isolated rat platelets to agonists such as ADP and thrombin (4). The purpose of this paper was to determine whether lanosterol had similar effects on human platelets and whether this was achieved by changes in membrane fluidity. Lanosterol did increase the sensitivity of human platelets, particularly to adrenaline and ADP at concentrations as low as 5 mg.L-1 when added from solutions in ethanol. At similar concentrations cholesterol, 4-cholesten-3-one or ethynyloestradiol had either no effect or were inhibitory. Measurement of membrane fluidity with diphenylhexatriene indicated that lanosterol did not affect membrane fluidity. Incubation of platelets with [4C]-mevalonic acid gave rise to a very small incorporation into lanosterol, squalene and farnesol. Sudden activation of the platelets did not accelerate lanosterol synthesis during or after platelet aggregation. It was concluded that lanosterol could only influence platelet behaviour if it came from the plasma. However the concentration of the steroid in both platelets and plasma is ten fold less than that required to sensitise the platelets.

Blood Platelets↗
PubMed1978

Platelets from "giant platelet syndrome (BSS)" are discocytes and normal sized.

A comparison is made between the shape of human platelets obtained from nine normal donors and two BSS donors. Sizes are evaluated from a cinematographic analysis of freely rotating, unfixed, and glutaraldehyde-hardened platelets in citrated PRP and of platelets on blood smear. On blood smeae, the mean diameters of BSS platelets are 1.7 to 1.8 times larger than those of normal platelets, with a major fraction having a diameter greater than 2.5 micrometer. As for normal donors, 80% to 90% BSS platelets in PRP are in the disc form (discocyte). In addition, they are essentially indistinguishable from a normal discocyte. Echinocytes (spherical forms with pseudopods) for BSS have a main body diameter (i.e., excluding pseudopods) 1.6 times larger than normal and in addition a reduced number of pseudopods. The results demonstrate that the giant size of BSS platelets results from abnormal behavior of these platelets during the preparation of the blood smear. It is suggested that this disorder is associated with a defect in the mechanism of platelet shape change.

Adult↗
PubMed1984

Agglutination of formalin-fixed, platelet-type von Willebrand's disease platelets by human von Willebrand factor.

The interaction of platelets and von Willebrand factor (vWF) in platelet-type von Willebrand's disease (vWD) was characterized using formalin-fixed platelets from the patients. Formalin-fixed patient platelets were agglutinated directly by human vWF in normal plasma and type IIB vWD plasma, but not in type IIA vWD plasma. In the presence of a small amount of normal vWF, ristocetin-induced agglutination of patient platelets was enhanced with low concentrations of ristocetin. Wheat germ agglutinin and EDTA inhibited vWF-induced agglutination, although EDTA had no effect on ristocetin (plus vWF)-induced agglutination. These results demonstrate that vWF-induced agglutination of platelet-type vWD platelets is independent of active platelet metabolism but requires divalent cations, and suggest that platelet membrane glycoprotein I (GPI) would be involved in this agglutination.

Blood Coagulation Factors↗
PubMed1983

Purification of human platelet calcium-activated protease. Effect on platelet and endothelial function.

Calcium-activated protease (CAP) was purified from the cytosol fraction of homogenized human platelet concentrates using a combination of gel filtration chromatography and affinity chromatography on antipain aminohexyl-Sepharose and activated thiol-Sepharose 4B. Purified CAP is composed of two different polypeptides of Mr = 80,000 and 27,000. Half-maximal protease activity was observed at 0.52 mM Ca2+, and all activity was inhibited by antipain, leupeptin, and N-ethylmaleimide. Activated CAP showed a time-dependent inactivation in the presence of 1 mM Ca2+ with only 5% of the control protease activity remaining after a 1-h exposure to calcium. Preincubation of washed platelets with varying amounts of CAP (0.2-0.4 units) significantly interfered with thrombin-induced platelet aggregation. In addition, ristocetin-induced platelet agglutination in the presence of von Willebrand factor was completely inhibited by 0.4 units of CAP. Concomitant with these protease-induced changes in platelet function, a decrease was observed in a major glycoprotein band of Mr = 150,000 present in platelet membranes and presumed to be glycoprotein Ib. In addition to these effects on platelets, CAP inhibited thrombin-induced production of prostacyclin by cultured human endothelial cells in a dose-dependent manner when the cells were pretreated with CAP. Thus platelet CAP can modulate membrane functions in both platelets and endothelial cells and may thus contribute to the regulation of hemostasis.

Blood Platelets↗
PubMed1983

Platelet size as a determinant of platelet function.

The relationship between MPV and platelet function was studied in human platelet subpopulations separated on the basis of size and counterflow centrifugation. The original platelet population and five size-dependent platelet fractions were suspended in buffer or autologous PPP at a platelet count of 2 x 10(8)/ml. Collagen (10 micrograms/ml)-induced aggregation showed a significant negative correlation between MPV and onset of aggregation and positive correlations between the MPV and the rate of extent of aggregation. Thrombin stimulation (1 U/ml) demonstrated similar relationships between MPV and the rate of extent of aggregation. In contrast, ristocetin-induced platelet agglutination occurred at a similar rate and extent in all fractions. To quantitate further the differential response of the platelets, we measured the content and release of ATP and beta-TG. There was a significant correlation between MPV and both ATP and beta-TG content, and a progressive increase in the absolute release of ATP and beta-TG was associated with the increase in MPV through the fractions after stimulation. However, the percent release of total ATP and beta-TG was similar in all fractions. Our data indicate that the intrinsic function of platelets of different sizes is similar but that the absolute ability of platelets to affect their environment, as measured by aggregation and total release of granular content, correlates with their size.

Adenosine Triphosphate↗
PubMed1980

Biphasic aggregation responses to ADP and epinephrine in some storage pool deficient platelets: relationship to the role of endogenous ADP in platelet aggregation and secretion.

Biphasic aggregation responses to ADP and epinephrine have been consistently observed in platelets of two patients with storage pool deficiency (SPD) despite marked reductions in platelet ADP contents. The nature of these aggregation responses was examined in relation to the role of secreted ADP as a mediator of secondary aggregation. Platelets from these patients secreted greater quantities of ADP after stimulation by epinephrine than did SPD platelets with comparable ADP deficiencies and absent second-phase aggregation, and were more sensitive than both other SPD platelets and normal platelets to the aggregating effects of low concentrations of ADP. Epinephrine-induced secondary aggregation was also associated with measurable, though less than normal, MDA formation in these patients' platelets, whereas no MDA formation occurred in SPD platelets with impaired epinephrine responses. CP/CPK did not inhibit epinephrine-induced responses in the SPD patients showing biphasic aggregation, whereas these responses in normal platelets were inhibited only with higher levels of CP/CPK than those required for inhibition of the responses to exogenous ADP. These findings suggest that secondary aggregation responses may be mediated by both prostaglandin endoperoxide production and secreted ADP, and are consistent with possibility that such mediation is primarily an intracellular process.

Adenosine Monophosphate↗
PubMed1995

Decrease in platelet survival and total platelet sialic acid concentration in rats infected with Plasmodium bergei bergei.

Suckling Wistar rats aged 3-5 weeks were infected through their dorsal tail vein with P. berghei berghei passed in Swiss albino mice. Platelet recovery and platelet survival using 51Cr-labelled heterologous platelets obtained from adult Wistar rats were determined in the infected animals on different post-infection days and on a group of non-infected rats as controls. Total platelet sialic acid was also determined in the same groups of animals. The results showed reduced platelet recovery, shortened survival and reduced total platelet sialic acid content in the infected animals compared with control values. The reduction in total platelet sialic acid content was related to the degree of parasitaemia and reached significant levels on the 5th post-infection day. It is concluded that the shortened platelet survival and reduced total platelet sialic acid content observed in the P. berghei infected rats were causally related and may account for the thrombocytopaenia reported in experimental and natural malaria infections of animals and man.

Animals↗
PubMed1995

Activity of platelet alpha-6-fucosyltransferase is inversely related to blood platelet concentration.

The activity of serum alpha-6-fucosyltransferase, a platelet derived enzyme, determined in sera of 22 normal individuals and 86 patients with various disorders was positively correlated with platelet counts. When the enzyme activity in 1 microliters serum was calculated per 1000 of platelets in blood (coefficient F/P) an inverse correlation became evident in that F/P was proportionally the higher the lower was platelet count in blood. The F/P values were in a good agreement with the results of direct assays of enzyme activities in isolated platelets. Neither granulocytes, lymphocytes nor red cells significantly contributed to serum enzyme activity though granulocytes enhanced the thrombin-induced enzyme release from platelets. In platelets separated by centrifugation in density gradients the enzyme was shown to be present in platelets of intermediate and high density but missing from the light ones. It is suggested that alpha-6-fucosyltransferase of platelets may be a marker of the ploidy level of megakaryocytes.

Blood Platelets↗
PubMed1993

Lytic solution of platelet-rich plasma clots potentiated platelet response to agonists by action on Ca2+ homeostasis.

Effects of thrombolytic agents and lytic solution of platelet-rich plasma (PRP) clots (LSPC) on platelet activation as indicated by platelet aggregation, generation of malondialdehyde (MDA), and the concentration of intracellular free calcium ([Ca2+]i) in rats were investigated. Neither urokinase nor streptokinase in vitro showed adverse effects on platelet function. The solution of PRP clots incubated either alone (as control) or with urokinase or streptokinase 2000 IU.ml-1 at 37 degrees C for 45 min potentiated the increase of platelet aggregation and MDA formation and produced a persistently high level of [Ca2+]i stimulated by thrombin, and platelet aggregation induced by ADP. But LSPC had no effects on the Ca2+ influx or the release of intracellular stored Ca2+, and no significant difference was found in the promotion of platelet response to agonists between the solution of the clots warmed in the presence or absence of thrombolytic agents. In the thrombosis model in rat abdominal aorta, both urokinase and streptokinase (40,000 IU.kg-1) slightly inhibited electrically stimulated thrombosis. In contrast, LSPC (600 microliters.kg-1) considerably enhanced the thrombosis. These findings suggested that the changes of platelet function in ischemic patients receiving thrombolytic therapy may be mediated by the proteolytic products of clots through acting on [Ca2+]i homeostasis after platelet stimulation rather than by the thrombolytic agents per se.

Animals↗
PubMed1976

Reactions of polylysine with human platelets in plasma and in suspensions of washed platelets.

The effects of polylysine on human platelets have been examined in citrated platelet-rich plasma (PRP) and in suspensions of washed platelets in various media. In PRP, polylysine caused aggregation after a lag phase. Heparin inhibited this completely. At certain concentrations of polylysine, two phases of aggregation occurred, the second being associated with release of 14C-serotonin from prelabelled platelets; this phase was inhibitable with prostaglandin E1, acetylsalicylic acid, sulphinpyrazone, adenosine, apyrase, or creatine phosphate/creatine phosphokinase. Polylysine-induced release also occurred in PRP with EDTA or hirudin as anticoagulant. In suspensions of washed platelets in Tyrode solution containing 0.35% or 4% albumin, or 1% gelatin, polylysine caused immediate platelet-to-platelet adherence and very little release of 14C-serotonin or platelet lysis. Heparin inhibited aggregation, but acetylsalicylic acid, prostaglandin E1, adenosine, apyrase, creatine phosphate/creatine phosphokinase or EDTA did not. In a modified Tyrode-albumin medium containing 1 mM magnesium but no calcium, polylysine-induced aggregation was associated with the release of 14C-serotonin which could be inhibited by acetylsalicylic acid or indomethacin; this is similar to the effect of ADP in this medium. In Tyrode solution without albumin or gelatin, polylysine-induced platelet aggregation was associated with release of a large percentage of 14C-serotonin, together with as much as 18% lysis; indomethacin inhibited this release reaction.

Albumins↗
PubMed1998

Recurrent arterial thrombosis linked to autoimmune antibodies enhancing von Willebrand factor binding to platelets and inducing Fc gamma RII receptor-mediated platelet activation.

A patient with a history of recurrent late fetal loss associated with multiple placental infarcts and cerebrovascular ischemia at the age of 36, followed a year later by a myocardial infarction, was referred for further investigation. Coronary angiography was normal. Antinuclear factor, lupus anticoagulant, anticardiolipin antibodies, and other thrombophilia parameters were negative, but there was moderate hyperthyroidism with positive thyroid peroxidase antibodies. Platelet numbers and von Willebrand factor (vWF) were normal. Her platelets showed spontaneous aggregation that disappeared with aspirin intake. However, aggregation still was induced by low levels of ristocetin (0.3 to 0.5 mg/mL). The low-dose ristocetin aggregation in patient platelet-rich plasma (PRP) was completely blocked by neutralizing antiglycoprotein Ib (GPIb) and anti-vWF antibodies. The monoclonal anti-Fc gamma RII receptor antibody IV.3 inhibited partly, which suggests that PRP aggregation by low-dose ristocetin was elicited by vWF-immunoglobulin (Ig) complexes. Upon addition to washed human platelets, with vWF (10 micrograms/mL), purified patient Igs dose-dependently enhanced ristocetin (0.15 mg/mL)-induced aggregation between 0 and 500 micrograms/mL, an effect that disappeared again above 1 mg/mL. Aggregation was dependent on the vWF concentration and was blocked by IV.3 or neutralizing anti-GPIb or anti-vWF antibodies. The spontaneous aggregation of normal platelets resuspended in patient plasma could be inhibited totally by IV.3 and partially by neutralizing anti-GPIb or anti-vWF antibodies. Perfusion with normal anticoagulated blood, enriched with 10% of control or patient plasma, over surfaces coated with vWF showed increased platelet adhesion and activation in the presence of patient antibodies. Treatment of the patient with the antithyroid drug thiamazol and temporary corticosteroids, aspirin, and ticlopidine did not correct the platelet hypersensitivity to ristocetin. These observations suggest that some autoantibodies to vWF may both enhance vWF binding to platelets and cause platelet activation through binding to the Fc gamma RII receptor, and thereby may be responsible for a new form of antibody-mediated thrombosis.

Adult↗