Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “BLOOD 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 559 records · Page 31Linked to original sources
PubMed2001

The generation of superoxide anion in blood platelets in response to different forms of Proteus mirabilis lipopolysaccharide: effects of staurosporin, wortmannin, and indomethacin.

Lipopolysaccharide (LPS), the major component of the outer membrane of Gram-negative bacteria may activate blood platelets. The aim of our study was to evaluate the effects of different forms of Proteus mirabilis LPS and isolated lipid A and polysaccharide part on the production of superoxide radicals in blood platelets and to estimate the role staurosporin, wortmannin and indomethacin on this process. We compared the generation of superoxide radicals in platelets treated with LPS after preincubation with inhibitors of the signal transduction pathways, namely staurosporin (inhibitor of protein kinase C), wortmannin (inhibitor of phosphoinositide 3-kinase), and indomethacin (inhibitor of cycloxygenase). Our results demonstrate that all LPS molecules and their fragments caused a stimulation of O2- generation in platelets (P<.5). LPSS1959 had the strongest stimulatory effect. Straurosporin and wortmannin, but not indomethacin inhibited O2- production in LPS-stimulated platelets. Staurosporin (8 nM) and wortmannin (50 nM) caused about 50% inhibition of thrombin-induced O2- generation in platelets, while indomethacin (10 microM) had only a slight inhibitory effect on this process. Our results provide support that in LPS- and thrombin-activated platelets, at least part of O2- generation in platelets, while indomethacin (10 microM) had only a slight inhibitory effect on this process. Our results provide support that in LPS- and thrombin-activated platelets, at least part of O2- is generated due to the activation of the enzymes (protein kinase C and phosphoinositide 3-kinase) involved in signal transduction pathway. Cycloxygenase seems to be not involved in this process.

Androstadienes↗
PubMed1988

Changes in blood platelet function, coagulation, and fibrinolytic activity in response to moderate, exhaustive, and prolonged exercise.

In a group of 47 healthy men aged 25-55, the influence of moderate, exhaustive, and prolonged exercise on blood platelet function, coagulation, and fibrinolytic activity was evaluated. Static exertion of short duration and moderate intensity did not cause significant alterations in any of the indices analyzed. Prolonged exercise (60 min) performed on a bicycle ergometer in aerobic conditions led to strong activation of the fibrinolytic system [euglobulin lysis time (ELT) fell from 208 to 88 min] and a slight increase in platelet count (PC) but did not cause significant changes in platelet factor 4 (PF 4) and platelet aggregate ratio, recalcification (RT), and prothrombin time (PT). Repeated bouts of maximum exercise leading to considerable acidosis (pH = 7.22; BE = -13.3) caused a significant increase in blood platelet count and an increase in PF 4 release. These changes were accompanied by strong intensification in fibrinolytic activity (over 63% reduction of ELT and a marked increase of fibrin/fibrinogen degradation products). In some individuals, unfavorable hemostatic changes were observed following intensive exercise. It is concluded that more attention should be given in future to the problem of verification of preventive and rehabilitative training programs from the point of view of exercise-induced hemostatic changes.

Adult↗
PubMed1990

Effects of exercise and exercise conditioning on blood platelet function.

The effects of exercise and exercise conditioning on blood platelet function were investigated in six healthy individuals who had not engaged in regular exercise for at least 1 yr prior to the study. The subjects (three men and three women) had a mean age of 28 (range 23-32) and participated in a supervised program of treadmill exercise. Subjects exercised for 20 min, three times weekly, for 12 wk at 70-80% of estimated maximum heart rate. Samples for platelet counts, platelet aggregation, and plasma beta-thromboglobulin (beta-TG) were obtained prior to training and after 6 and 12 wk of training. All subjects responded with an increase in aerobic capacity during training. Resting mean systolic and diastolic blood pressures decreased after training (P less than 0.05). Platelet counts increased after exercise, and the increment in week 12 exceeded that in the 1st wk by 57%. Platelet aggregation studies in platelet rich plasma (PRP) showed an increase in slope after exercise (week 1, P less than 0.05) which decreased with training (week 1 vs week 12, P less than 0.01). Aggregation studies utilizing impedance aggregometry in diluted native whole blood showed an acceleration of both spontaneous aggregation (P less than 0.01 weeks 6 and 12) and aggregation using epinephrine as an agonist (P less than 0.05) following exercise. Plasma beta-TG levels did not increase significantly after exercise; however, resting concentrations of beta-TG decreased with training (P less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Coated membranes in blood platelets.

The simultaneous addition of alcian blue and tannic acid to human blood platelets during glutaraldehyde fixation leads to an excellent representation of coated membranes (CM). Coated membrane segments can be found (1) in plasmalemma, in vesicle system and lysosomal granules, or (2) as coated pits or coated vesicles. They possess the same morphological properties as in other animal cells. An increased number of coated membranes is observed in platelets which have been stimulated with ADP. The role played by coated membranes remains unsolved in contrast to the role of other endomembranes in platelets for instance the vesicle system.

Blood Platelets↗
PubMed1989

Regulatory control of complement on blood platelets. Modulation of platelet procoagulant responses by a membrane inhibitor of the C5b-9 complex.

Antibody against a membrane inhibitor of the C5b-9 complex has been used to investigate regulatory control of the terminal complement proteins on blood platelets. Monospecific rabbit antibody (alpha-P18) was raised against the purified 18-kDa erythrocyte membrane inhibitor of C5b-9 (Sugita, Y., Nakano, Y., and Tomita, M. (1988) J. Biochem. (Tokyo) 104, 633-637). In addition to its interaction with erythrocytes, this antibody (and its Fab) bound specifically to platelet membranes. In immunoblots of cell membrane proteins prepared under non-reducing conditions, alpha-P18 bound specifically to an 18-kDa erythrocyte membrane protein and to a 37-kDa platelet membrane protein. Absorption of this antibody by platelet membranes competed its binding to the purified 18-kDa erythrocyte protein, suggesting that epitopes expressed by the erythrocyte 18-kDa C5b-9 inhibitor are common to the platelet. When bound to the platelet surface, the Fab of alpha-P18 increased C9 activation by membrane C5b-8, monitored by exposure of a complex-dependent C9 neo-epitope. Although alpha-P18 caused little increase in the cytolysis of platelets treated with C5b-9 (total release of lactate dehydrogenase less than 5%), it markedly increased the cell stimulatory responses induced by these complement proteins, including, secretion from platelet alpha- and dense granules, conformational activation of cell surface GP IIb-IIIa, release of membrane microparticles from the platelet surface, and exposure of new membrane binding sites for components of the prothrombinase enzyme complex. Prior incubation of C5b67 platelets with 100 micrograms/ml alpha-P18 (Fab) lowered by approximately 10-fold the half-maximal concentration of C8 required to elicit each of these responses (in the presence of excess C9). Incubation with alpha-P18 (Fab) alone did not activate platelets, nor did incubation with this antibody potentiate the stimulatory responses of platelets exposed to other agonists. These data indicate that a membrane inhibitor of the C5b-9 complex normally serves to attenuate the procoagulant responses of blood platelets exposed to activated complement proteins, and suggest the mechanism by which a deletion or inactivation of this cell surface component would increase the risk of vascular thrombosis.

Blood Platelets↗
PubMed1992

Generation of active oxygen species in blood platelets--spin trapping analysis.

Generation of active oxygen species by bovine blood platelets was examined by the electron spin resonance (ESR) spin trapping technique with 5,5-dimethyl-1-pyroline-1-oxide (DMPO). The hydroxyl spin-trapped adduct 5,5-dimethyl-2-hydroxyl-1-pyrolidinyloxy (DMPO-OH) was formed in the presence of platelets, indicating the generation of hydroxyl radicals (.OH) by the platelets. Generation of .OH was observed even with platelets in the resting state, but was markedly enhanced when the platelets were activated with stimulants. Stronger stimulants such as the calcium ionophore ionomycin, induced greater radical generation than the weaker stimulant ADP. When the platelets were stimulated by thrombin, generation of .OH was greatest after 1.5 min, and depended on the dose of the stimulant. It was inhibited by inhibitors of platelet activation such as forskolin and phenolic antioxidants.

Adenosine Diphosphate↗
PubMed1996

The role of thromboxane A2 in increased whole blood platelet aggregation in oral contraceptive users.

Epidemiological studies have shown that oral contraceptives increase the risk of thromboembolic disease in susceptible women however the mechanisms involved are unclear. We investigated whole blood platelet aggregation in 44 women randomly allocated to 6 cycles of treatment with either gestodene (75ug) or desogestrel (150ug) combined with 30ug ethinyloestradiol (EE). The in vitro effects of aspirin and a thromboxane synthetase inhibitor, dazmegrel (UK38485) were also investigated. Oral contraceptive treatment caused a significant increase in collagen, arachidonic acid (AA) and ADP induced whole blood platelet aggregation. PAF induced aggregation was unchanged. There were no significant differences in the levels of platelet aggregation between the desogestrel/30ugEE and gestodene/30ugEE groups. In vitro incubation of platelets with aspirin and dazmegrel prevented the oral contraceptive induced increase in platelet aggregation. Dazmegrel caused an on treatment decrease in PAF induced aggregation in the desogestrel/30ugEE but not the gestodene/30ugEE group. The results of this study indicate that the use of oral contraceptives is associated with an increase in platelet aggregation that is mediated by changes in thromboxane/prostacyclin ratio(TXA2/PGI2). Although no significant differences were found between the two different progestogen combinations, the effects of dazmegrel on PAF induced aggregation suggest a possible difference in the progestogen modifying effects of desogestrel and gestodene which is unmasked when thromboxane synthetase is inhibited.

Adolescent↗
PubMed1980

[Electron-acceptor (acid) properties of the contents of blood platelet intracellular granules and their significance for the reactions of these cells].

The fluorescent marker method and measurements of aggregation were utilized to study the significance of the acidic intragranular space in blood platelets. Acridine orange is liberated from 5-HT granules after alkalinization by the ammonia ion which inhibits the induction of platelet aggregation by ADP and causes the platelet disaggregation. At low doses, ammonia ion enhances ADP-induced aggregation. The transformation kinetics of 5-HT granules was investigated in the course of clot formation with a new instrument that simultaneously monitors the light transmittance (aggregation, clot formation) and fluorescence intensity (accumulation and liberation of fluorescent marker). These experiments provide the evidence that processes of fibrin filament sedimentation and fibrin-blood platelet interaction were followed by a liberation of fluorescent marker from 5-HT granules.

Animals↗
PubMed1993

[Role of nonenzymatic glycosylation of proteins in disorders of erythrocytes and blood platelets in diabetes mellitus].

Numerous alterations in the structure and function of red blood cells and blood platelets in diabetes mellitus result from the process of nonenzymatic glycosylation of proteins. Nonenzymatic attachment of glucose to cell membrane protein amino group, for example, can accompany hypoglycaemia. Chemical modifications of membrane proteins are likely to lead to alterations in the dynamic properties of lipid bilayer and membrane fluidity in diabetic blood cells. Conformational changes of membrane and cytosol proteins glycosylation may underline changes in blood rheology and platelet hypersensitivity in diabetes mellitus.

Blood Platelet Disorders↗
PubMed2000

The effects of granulocyte colony stimulating factor on chemiluminescence and lipid peroxidation of blood platelets treated with cisplatin.

The effects of granulocyte colony stimulation factor (G-CSF) at concentrations of 0.08, 0.8 and 8 microg/ml on reactive oxygen species (ROS) generation and lipid peroxidation induced by cisplatin in pig blood platelets were investigated. The level of reactive oxygen species (O2, H2O2, singlet oxygen and organic radicals) generated in platelets was measured by the chemiluminescence method. Lipid peroxidation was determined by the thiobarbituric acid technique and was expressed as thiobarbituric acid reactive substances. G-CSF at the concentration of 0.08 microg/ml had a strong inhibitory effect (about 60% inhibition) on the production of ROS in the isolated pig platelets. This cytokine also significantly reduced lipid peroxidation in control platelets and platelets treated with cisplatin (p<0.05). In the presence of G-CSF in the incubation medium (0.8 microg/ml) cisplatin-induced generation of ROS was also reduced (p<0.05). This study demonstrates that G-CSF has a protective effect against the oxidative stress in blood platelets caused by cisplatin.

Animals↗
PubMed1982

Stimulatory effect of blood platelet factor(s) on glycolysis in cell cultures.

The addition of bovine blood platelet homogenate to confluent cultures of three established mouse cell lines (L-929, Balb c/3T3 and SC) brings about a rapid increase of lactic acid formation. Homogenates prepared from quiescent cells previously treated with platelet breakdown products show an increased rate of glycolysis as compared with homogenates of nonstimulated cell cultures. Activities of hexokinase, pyruvate kinase and lactate dehydrogenase remained unaltered but the activity of phosphofructokinase increased by about 60 per cent. Transport of 2-deoxy-D-glucose into the cells was slightly stimulated. It is concluded that the transport of glucose was not a limiting factor in confluent 3T3 cells. The findings suggest that the increase of phosphofructokinase activity may have accounted for the changes in glycolysis seen in intact cells and cell-free homogenates prepared from cultures exposed to some unknown factor(s) present in platelet homogenate.

Animals↗
PubMed2003

Peroxynitrite-induced changes of thiol groups in human blood platelets.

In this study we investigated sulfhydryl and disulfide metabolism in blood platelets treated with peroxynitrite (ONOO-) at concentrations of 10, 100, and 1000 microM. In platelets incubated with peroxynitrite, a decrease of both protein and low molecular weight thiols (glutathione, cysteine and cysteinylglycine) was observed. The reduction of platelet free thiols caused by ONOO- was dose dependent. We found that peroxynitrite induces the oxidation of platelet free SH-groups. Platelets contain a large fraction of glutathione in reduced form (GSH). We showed that after ONOO- treatment, GSH/GSSG ratio in platelets was distinctly decreased. The presented results suggest that oxidation of thiols and depletion of GSH in platelets caused by peroxynitrite may be responsible for cytotoxic effects of this compound.

Blood Platelets↗
PubMed1976

Cyclic AMP in human blood platelets: relation to platelet prostaglandin synthesis induced by centrifugation or surface contact.

Exposure of blood platelets to physical stimuli such as centrifugation, filtration through Sepharose gel, or stirring with particulate material leads to production of prostaglandins E2 and F2alpha and to a reduction in cAMP. These effects resemble those produced by ADP, epinephrine, collagen, and thrombin in association with the platelet release reaction but are less effectively inhibited by aspirin.

Adenosine Diphosphate↗
PubMed2005

Approach to the assessment of platelet function: comparison between optical-based platelet-rich plasma and impedance-based whole blood platelet aggregation methods.

Platelet aggregation studies play an important role in the assessment of hereditary and acquired platelet function defects. The first aggregation test introduced into laboratory practice used platelet-rich plasma (PRP) where aggregation was detected by an optical method. The assessment of platelet function using whole blood (WB) aggregation by an impedance method followed up nearly 20 years later. The WB impedance aggregation assay appears to be superior to the optical method because it 1) evaluates platelets in a physiologic milieu in the presence of red and white blood cells, which are known to modulate platelet function; 2) is faster; 3) has higher sensitivity; and 4) does not require centrifugation, thus avoiding injury to platelets and loss of giant thrombocytes. These two assays were compared. Clearly, the WB impedance aggregation methodology has many advantages over the optical PRP assay for the assessment of the hyperactive platelet syndrome and the effects of anti-platelet drugs.

Adolescent↗