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 487 records · Page 27Linked to original sources
PubMed1987

Effects of novel aggregation inhibitors on serotonin uptake by human blood platelets.

Novel aggregation inhibitors blocked serotonin uptake by human blood platelets in concentrations ranging from 0.7 +/- 0.1 microM to 237.5 +/- 35.7 microM; a modified procedure, validated by kinetic analysis, was employed in which pH drift was minimized to 0.03 during the active assay period. Structural features in carbamoylpiperidine and nipecotoylpiperazine derivatives which actually constitute molecular probes, and show remarkable specificity for aggregation-inhibitory target sites, disclosed striking differences between the latter and serotonin receptors or other loci affecting serotonin uptake.

Adult↗
PubMed1982

Transient kinetics of the rapid shape change of unstirred human blood platelets stimulated with ADP.

Unstirred (isotropic) suspensions of human blood platelets stimulated with ADP in a stopped-flow laser turbidimeter exhibit a distinct extinction maximum during the course of the classical rapid conversion of initially smooth flat discoid cells to smaller-body spiny spheres. This implies the existence of a transient intermediate having a larger average light scattering cross section (extinction coefficient) than either the disc or the spiny sphere. Monophasic extinction increases reaching the same final value were observed when either discoid or spiny sphere platelets were converted to smooth spheres by treatment with chlorpromazine, and sphering of discoid cells was accompanied by a larger total extinction change than the retraction of pseudopods by already spherical cells. These and other results suggest that the ADP-induced transient state represents platelets that are approximately as "spherical" as the irregular spiny sphere but lack the characteristic long pseudopods and as a consequence are larger bodied. Fitting the ADP progress curves to the series reaction A leads to B leads to C by means of the light scattering equivalent of the Beer-Lambert law yielded scattering cross sections that are consistent with this explanation. The rate constants for the two reaction steps were identical, indicating that ADP activation corresponds to a continuous random (Poisson) process with successive apparent states "disc," "sphere," and "spiny sphere," whose individual probabilities are determined by a single rate-limiting step.

Adenosine Diphosphate↗
PubMed1975

Blood platelet response to plasma from patients with ischemic heart disease.

Blood platelets change shape (from small round spheres to larger spread forms) as they participate in thrombosis. Using an electron microscopic technique, we surveyed 14 patients with both acute and chronic ischemic heart disease; each had increased spread platelet forms (69 plus and minus 22.2 [standard deviation] percent) when compared with 14 asymptomatic control subjects (P less than 0.001). When platelets from these 14 control subjects were exposed to plasma from the patients with ischemic heart disease, spread forms increased from 13.4 plus and minus 9.1 to 44.5 plus and minus 15.5 percent (P less than 0.001). There was no significant increase in spread platelets in these control subjects when their blood was mixed with plasma from another control group. Similar studies were performed in seriously ill noncardiac patients: 9 of 13 had increased spread platelet forms when compared with control subjects, but plasma from only 5 of these 9 subjects caused increased spread forms when mixed with platelets from normal subjects (P less than 0.05). Thus a factor existed in the plasma of these patients with ischemic heart disease that caused normal platelets to become spread. Similarly the plasma of some patients with serious noncardiac disease had a comparable effect on normal platelets. Although the identity of this factor is unknown, it is probably unrelated to hormonal or therapeutic influences occurring either during acute infarction or during the stress of serious illness because (1) the effect of the plasma from patients with acute ischemic heart disease was identical to that of patients with chronic ischemic heart disease, and (2) the effect was not present in all patients with serious noncardiac disease.

Acidosis↗
PubMed1991

Effect of concanavalin A on intracellular calcium concentration in single blood platelets.

Mobilization of Ca++ was estimated in single rabbit blood platelets with digital imaging microscopy. Concanavalin A (Con A) caused a rapid initial increase in intracellular concentration of Ca++ ([Ca++]i) with a latent time of about 20 sec, followed by a sustained increase in [Ca++]i. This effect of Con A was antagonized by alpha-methyl-D-mannose, which already was shown to antagonize the inhibitory effect of Con A on 5-HT transport, indicating that this effect of Con A was also derived from its binding to cell surface glycoproteins. The presence of EGTA in the medium did not affect the initial rise, but inhibited the latter phase of sustained rise. Thus, Con A induced elevation of [Ca++]i was suggested to consist of two different processes: mobilization of Ca++ from the intracellular storage sites and successive Ca++ influx through Ca++ channels. The effect of Con A on the 5-HT transport was tested in the presence of EGTA, a condition where no Ca++ influx occurs. The results indicate that Con A induced inhibition of 5-HT transport was not influenced by EGTA in the medium. It is suggested that the effect of Con A on 5-HT transport might be exerted through the Ca++ mobilization from its intracellular storage sites.

Animals↗
PubMed1976

The effect of phospholipase C on human blood platelets.

The effect of phospholipase C (EC 3.1.4.3) on human blood platelets has been studied. Phospholipase C from Bacillus cereus was purified to homogeneity as judged by analytical and sodium dodecyl sulphate disc gel electrophoresis and by immunoelectrophoresis. Human platelets isolated from platelet-rich plasma by gel filtration or by centrifugation and washing were incubated with phospholipase C. A loss of 20-45% of the total platelet phospholipid was observed, whereas 88% was hydrolyzed when platelet homogenates were submitted to identical enzyme treatment. Intact platelets lost 50-75% phosphatidylethanolamine, 20-50% phosphatidylcholine, and 20-25% phosphatidylserine. Sphingomyelin was not a substrate for the enzyme under the conditions used. The platelets contained no detectable endogenous phospholipase C activity. The loss of phospholipid was not accompanied by aggregation of the platelets, nor did the platelets lose their ability to aggregate with ADP or thrombin. Total platelet factor 3 releasable by freezing and thawing was reduced. Measurements of releasable platelet factor 4 and the efflux of serotonin showed that no release reaction was triggered even when up to 45% of the total phospholipid in the platelets was hydrolyzed. When sphingomyelinase was added together with, before, or after phospholipase C, aggregation occurred. Sphingomyelinase alone gave no aggregation. The gel-filtered platelets also aggregated upon addition of purified phospholipase C from Clostridium perfringens. The distribution of phospholipids in the platelet membrane is discussed.

Bacillus cereus↗
PubMed2003

[Blood platelets: biochemistry and physiology].

This article reviews the roles of blood platelets in different physiologic and pathologic processes in the human body. Besides the basic processes in primary haemostasis, platelet adhesion, platelet secretion, platelet aggregation, clot retraction, the new model of thrombin formation on the platelet surface is presented. The different signal transduction pathways in platelets are a main focus of this review.

Blood Platelets↗
PubMed1975

[Ultrastructure of the blood platelets in the newborn infant and in the young mongolian child. Study of 13 cases].

Blood platelets from infant and new born mongolians were examined and compared taking into consideration existing or non existing haematologic anomalies, such as transitory leucoblastosis with or without hyperthrombocytosis and acute leucosis without thrombopenia. These abnormalities were correlated with the analysis of control samples from haematologically normal new-born and premature children as well as samples from adult mongolian, patients with other chromosomal alterations (13-15, phi) and new-born or adults with thrombocytosis. The presence of dysmorphic platelets could be observed in variable degrees and numbers in all the mongolian samples. The characters of the morphologic abnormalities, constantly observed with variations due to pathological causes, denote either metabolic or structural thrombopathy.

Acute Disease↗
PubMed1989

Human rhabdosarcoma cell-induced aggregation of blood platelets.

The ability of tumor cells shed into the circulation to cause adhesion and aggregation of blood platelets may be involved in successful metastasis of primary tumors. Rhabdosarcoma is a rare, early metastasizing tumor previously uncharacterized for ability to alter platelet function. It was found that human rhabdosarcoma cells (American Type Culture Collection) dose dependently induce biphasic aggregation of human blood platelets in heparinized platelet-rich plasma; aggregation responses could also be elicited in citrated plasma. Aggregation caused by rhabdosarcoma can be inhibited by apyrase treatment of either rhabdosarcoma or platelets, and by pretreatment of platelets with prostacyclin, cilostamide, inhibitors of thromboxane A2 production, or TMB-8; only apyrase and prostacyclin inhibited both phases of aggregation. Tumor cell supernatant contained only enough ADP to cause a negligible, reversible aggregation response. Hirudin, verapamil, and triazolam do not inhibit rhabdosarcoma-induced aggregation. Aggregation of platelets by rhabdosarcoma cells thus appears to involve ADP, from tumor cells and/or platelets, and platelet calcium mobilization and thromboxane A2 synthesis and release.

Adenosine Diphosphate↗
PubMed2004

Blood platelets decrease concentration of reactive oxygen species produced by polymorphonuclear leukocytes.

BACKGROUND: Reactive oxygen species produced by polymorphonuclear leukocytes (PMNL) participate substantially in vascular injury induced by ischaemia and reperfusion. Blood platelets, accumulated simultaneously with PMNL may modulate this process. OBJECTIVE: To compare effects of resting and completely stimulated platelets on PMNL-derived oxidants. METHODS: Autologous human platelets and PMNL were co-incubated in the physiological cell ratio 50:1, and the formation of reactive oxygen species was detected by luminol- and isoluminol-enhanced chemiluminescence methods. To compare effects of platelets at different degrees of their activation, FMLP (selective PMNL stimulus) and Ca2+-ionophore A23187 (activates both PMNL and platelets) were used as chemiluminescence stimuli. The liberation of serotonin from platelets was estimated fluorometrically. RESULTS: Both stimulated and non-stimulated platelets inhibited PMNL chemiluminescence. However, while the decreasing effect of resting platelets disappeared at increased extracellular peroxidase concentration, the inhibition of chemiluminescence by activated platelets became even more pronounced after the addition of peroxidase and was accompanied by liberation of serotonin. The concentrations of serotonin released from platelets were sufficiently high to inhibit PMNL chemiluminescence. CONCLUSION: The obtained data indicate that by interference of platelets with peroxidase liberation from PMNL and the scavenging effect of platelet serotonin, resting and stimulated platelets might be respectively operative in inhibiting chemiluminescence. Since the presence of blood platelets in the proximity of PMNL effectively decreased the concentration of reactive oxygen species, platelets may represent a unique protective mechanism, active only in case of emergency and selectively at sites exposed to toxic effects of reactive oxygen species. (Tab. 1, Fig. 4, Ref. 42.).

Blood Platelets↗
PubMed2001

Neutrophils promote the release of alpha-6-fucosyltransferase from blood platelets through the action of cathepsin G and elastase.

Human blood platelets release alpha-6-fucosyltransferase during coagulation of blood or after stimulation with thrombin or other agonists that cause platelet activation (Antoniewicz et al., FEBS Lett. 244 (1989) 388-390). However, in the absence of neutrophils the thrombin-stimulated platelets release only a small fraction of alpha-6-fucosyltransferase activity (Kościelak et al., Acta Biochim. Polon. 42 (1995) 35-40). We show that the effect of neutrophils is reproduced by cathepsin G or (less efficiently) by elastase, the two enzymes that are released by neutrophils during coagulation of blood. We have also localized alpha-6-fucosyltransferase to membrane and alpha-granule fractions of platelets that had been disrupted by nitrogen cavitation. It is concluded that thrombin-activated neutrophils release cathepsin G and elastase that promote degranulation of platelets and hence the secretion of alpha-6-fucosyltransferase.

Adenosine Diphosphate↗
PubMed1987

Human blood platelets possess specific binding sites for C1q.

Although platelet interactions with C1q are implied by the inhibitory effect of C1q on collagen-induced platelet aggregation, specific receptors have not as yet been identified. To address the question of platelet receptors for free C1q, direct radioligand binding studies were performed by using human blood platelets and purified, 125I-labeled C1q, and a monoclonal antibody (II1/D1) (IgM, lambda) directed against C1q receptors on peripheral blood leukocytes. Washed platelets bound both purified 125I-labeled C1q and II1/D1 in a specific and saturable manner under physiologic ionic strength conditions. At equilibrium, approximately 4000 molecules of C1q bound per platelet with an apparent dissociation constant of 3.5 X 10(-7) M. Maximum C1q binding was achieved in 5 min and correlated well with inhibition of collagen-induced platelet aggregation. Equilibrium binding of 125I-labeled II1/D1 to washed platelets required an incubation period of 15 to 30 min and II1/D1 concentrations approaching 50 micrograms/ml. Approximately 2000 molecules of II1/D1 bound per platelet, with an apparent dissociation constant of 2.8 X 10(-8) M. II1/D1 binding could be inhibited by the collagenous tail of C1q (c-C1q), suggesting that platelet receptors for these ligands are either the same or in close proximity. The data demonstrate that human blood platelets possess specific and saturable binding sites for free C1q that may function as collagen receptors, and may antigenically resemble C1q receptors on peripheral blood leukocytes.

Antibodies, Monoclonal↗
PubMed1989

Increased serotonin2 (5-HT2) receptor binding as measured by 3H-lysergic acid diethylamide (3H-LSD) in the blood platelets of depressed patients.

3H-Lysergic acid diethylamide (3H-LSD) binding, a putative measure of 5-HT2 receptor binding, was studied in the blood platelets of 29 depressed patients and 24 normal controls. The Bmax (maximum number of 3H-LSD binding sites) in the blood platelets of depressed patients was significantly greater than that of normal volunteers. This increase in Bmax was due to an increase in female depressed patients only. Bmax was significantly lower in female compared to male normal controls but there was no difference between male and female depressed patients. There was also no difference in Kd (an inverse measure of affinity of 3H-LSD binding to its sites) between normal controls and depressed patients. The correlations between Bmax of 3H-LSD binding and the Bmax of the 3H-imipramine binding site or the Vmax of 5-HT uptake sites were not significant. The role of serotonergic processes in the psychobiology of depression is discussed.

Adult↗
PubMed1995

Inhibition and kinetic alterations by excess free ATP and ADP of the ATP diphosphohydrolase activity (EC 3.6.1.5) from rat blood platelets.

ATP diphosphohydrolase (EC 3.6.1.5) catalyzes the hydrolysis of diphospho- and triphosphonucleosides and is activated by divalent cations. The enzyme described in rat blood platelets hydrolyzes Ca(2+)-ATP and Ca(2+)-ADP with a high affinity for these Ca(2+)-nucleotide complexes as substrates. In the present paper, we demonstrate that free ATP or free ADP induces inhibition and kinetic alterations of the enzyme from rat blood platelets. From these results, we draw conclusions about the binding of free nucleotides to the enzyme and their action as inhibitors with respect to calcium-nucleotide complex.

Adenosine Diphosphate↗
PubMed1972

Uptake of latex particles by blood platelets: phagocytosis or sequestration?

The incorporation of large particulates by blood platelets is considered identical to the ingestion of bacteria by neutrophils, and is referred to as platelet phagocytosis. However, bacteria enter neutrophils in sealed vacuoles derived from the cell wall, and products deposited in the vacuoles during neutrophil degranulation are confined almost exclusively to the phagolysosomes. Products released from platelet storage organelles after uptake of foreign particles, on the other hand, are extruded to the cell exterior. The basis for this unusual difference in the phagocytic response of platelets and neutrophils has been sought in the present investigation. Combined electron microscopic and cytechemical study of platelet-latexspherule interaction revealed that platelets do not phagocytize in the usual sense. Most of the latex particles observed in platelets were lodged in channels of the open canalicular system. Channels which contained latex did not pinch off to form sealed phagocytic vacuoles, but remained open. An electron-dense tracer, lanthanum nitrate, was able to penetrate into the channels and outline the ingested latex particles. Therefore, platelets do not phagocytize latex, but sequester the spherules in preformed membranous invaginations. The persistence of open channel communication with the exterior after latex uptake may explain why platelets extrude secretory products, rather than confine them to phagolysosomes.

Blood Platelets↗
PubMed1993

Influence of platelet membrane sialic acid and platelet-associated IgG on ageing and sequestration of blood platelets in baboons.

Platelets were isolated from blood of baboons and treated with neuraminidase to remove platelet membrane sialic acid, a process which artificially ages the platelets. The platelets were then labelled with 111In and their mean life span, in vivo distribution and sites of sequestration were measured. The effect of removal of sialic acid on the attachment of immunoglobulin to platelets were investigated and related to the sequestration of the platelets by the spleen, liver, and bone marrow. Removal of sialic acid by neuraminidase did not affect the aggregation of platelets by agonists in vitro, nor their sites of sequestration. The removal of 0.51 (median, range 0.01 to 2.10) nmol sialic acid/10(8) platelets shortened their life span by 75 h (median, range 0 to 132) h (n = 19, p < 0.001), and there was an exponential correlation between the shortening of the mean platelet life span and the amount of sialic acid removed. The increase in platelet-associated IgG was 0.112 (median, range 0.007 to 0.309) fg/platelet (n = 25, p < 0.001) after 0.79 (median, range 0.00 to 6.70) nmol sialic acid/10(8) platelets was removed (p < 0.001). There was an exponential correlation between the shortening of mean platelet life span after the removal of sialic acid and the increase in platelet-associated IgG. The results suggest that platelet membrane sialic acid influences ageing of circulating platelets, and that the loss of sialic acid may have exposed a senescent cell antigen that binds IgG on the platelet membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

The assessment of oxygen metabolism selected parameters of blood platelets exposed to low frequency magnetic radiation in cars--in vitro studies.

PURPOSE: The aim of the study was to determine how free radicals generation in blood platelets exposed to electromagnetic field (EMF) occurring in cars affects the process of these morphotic elements cell membranes phospholipid peroxidation. MATERIAL AND METHODS: The suspension of human blood platelets was exposed to EMF of proper characteristics in a specially arranged research stand. After 30, 60 and 90 min exposure of the platelet specimen to EMF, free radicals generation was measured with chemiluminescence and malondialdehyde concentration according to Placer et al. method. The obtained results were compared with the control values. RESULTS: The increase of free radicals generation was observed after 30 and 90 min exposure of platelets to magnetic field. Malondialdehyde reached the highest values also after 30 and 90 min exposure of the platelets to EMF as compared to the control. CONCLUSIONS: The increase in oxygen reactive species generation under the effect of exogenic magnetic radiation as well as proportional intensification of the peroxidation process determined on the basis of malondialdehyde concentration (the marker of this phenomenon) point to the platelet sensitivity to the investigated environmental factor.

Blood Platelets↗
PubMed1986

Effect of subchronic treatment with imipramine, chlorpromazine and the combination on 3H-imipramine binding in rat blood platelets and frontal cortex.

The effects of subchronic administration of imipramine (IMIP), chlorpromazine (CPZ) and the combination of IMIP + CPZ on 3H-IMIP binding of rat blood platelets and cortex were studied. All three treatments decreased the number of IMIP binding sites (Bmax) of rat blood platelets and cortex. The combination produced a significantly greater decrease in Bmax in platelets than either treatment alone; a similar trend in cortex was observed. The effect of some neuroleptics on 3H-IMIP binding sites may be relevant to their antidepressant action. These results, together with previous evidence that the combination has a synergistic effect on down regulation of brain serotonin-2 (5-HT2) receptors, suggest that changes in serotonergic neurotransmission may be relevant to the enhanced efficacy of the combination of tricyclic antidepressants and neuroleptics, compared to either type of drug alone, in the treatment of delusional depression.

Analysis of Variance↗