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At least 145 records · Page 8Linked to original sources
PubMed1987

Platelet aggregation induced by ether-linked phospholipids. 2. Mechanism of desensitization of rabbit platelets by platelet activating factor and reversibility of inhibitory actions of its antagonists.

Rabbit platelets pretreated with CV-3988 had reduced responsiveness to platelet activating factor(PAF) even after the platelets had been washed with a buffer. This was due to its tight binding to receptor sites for PAF, but not conformational changes of the receptor, because the platelets that were pretreated with CV-3988 and then washed with buffer containing 0.5% bovine serum albumin showed full responsiveness to PAF. In contrast, the reduced responsiveness of PAF-pretreated rabbit platelets was not reversed by washing with buffer containing 0.5% BSA. The PAF-pretreated platelets showed significantly lower responsiveness to 1-O-hexadecyl-2-O-monomethylaminocarbonyl-sn-glycero-3-phosphochol ine (MC-PAF) than to PAF, although MC-PAF had the same potency as PAF on inducing aggregation of normal rabbit platelets by interacting with receptor sites for PAF. These results suggest that the desensitization is accompanied by a decreased affinity of receptor sites for PAF or reduced efficiency in coupling of activated receptor to regulatory protein in plasma membranes rather than loss of receptor sites.

Animals↗
PubMed1983

Comparison of platelet-derived growth factor prepared from release products of fresh platelets and from outdated platelet concentrates.

Platelet-derived growth factor was isolated from the release products of washed, human platelets and from freeze-thawed outdated platelet concentrates. On the basis of sodium dodecyl sulphate polyacrylamide gel electrophoresis and amino acid sequence determination we conclude that platelet derived growth factor released from platelets by the agonist thrombin (EC 3.4.4.13) is structurally similar to that isolated from lysed platelets and from platelet concentrates stored for more than 72 hr at room temperature.

Amino Acid Sequence↗
PubMed2001

Platelet-reactive HLA antibodies associated with low posttransfusion platelet increments:a comparison between the monoclonal antibody-specific immobilization of platelet antigens assay and the lymphocytotoxicity test.

BACKGROUND: Platelet-reactive HLA antibodies are a major reason for low posttransfusion platelet increments. The clinical importance and value of the test systems for their in vitro determination is still controversial. STUDY DESIGN AND METHODS: A prospective analysis of HLA antibodies was performed in sera obtained once a week for at least 4 consecutive weeks from 55 patients (female/male, 28/27; age: median, 49 years; range, 18-69) undergoing intensive chemotherapy and in need of prophylactic platelet transfusions. All sera (n = 330) were analyzed by the monoclonal antibody-specific immobilization of platelet antigens (MAIPA) assay and by the standard lymphocytotoxicity test (LCT). RESULTS: In the MAIPA, 24.5 percent of sera (81/330) obtained from 22 patients contained HLA antibodies. These were detected significantly more often by the MAIPA assay than by the LCT (24.5% vs. 8.2%). Fifty-five sera (20 patients) were positive in the MAIPA assay only. In 15 patients, HLA antibodies were transient. In 3 patients, HLA antibodies were detected earlier by the MAIPA assay than by the LCT. Significantly more sera obtained at the time of low posttransfusion platelet increments were positive in MAIPA alone, rather than in both MAIPA and the LCT (44% vs. 17%). CONCLUSION: The MAIPA assay is more sensitive than the standard LCT in detecting platelet-reactive HLA antibodies. These MAIPA-positive/LCT-negative HLA antibodies affect the posttransfusion platelet increment.

Adolescent↗
PubMed1988

The effect of a dietary supplement of n-3 polyunsaturated fat on platelet lipid composition, platelet function and platelet plasma membrane fluidity in healthy volunteers.

1. Eight healthy male volunteers (aged 22-39 years) supplemented their normal daily diet with 15 g encapsulated fish oil (MaxEPA) for a 6 week period. Fasting blood samples were taken before, at the completion of and 3 months after the period of supplementation. 2. Evaluation of nutrient intakes showed that the intake of n-3 polyunsaturated fatty acids rose significantly (P less than 0.01) during supplementation. This was reflected in changes in the fatty acid composition of platelet phosphatidyl choline (PC) and phosphatidyl ethanolamine (PE) without any changes in phosphatidyl serine, phosphatidyl inositol or sphingomyelin. 3. In both PC and PE there were significant (P less than 0.05) increases in the levels of 18:1n-9 and 20:5n-3 fatty acids and a significant (P less than 0.05) decrease in 20:4n-6 during supplementation. 16:0 rose significantly in PC (P less than 0.05) while in PE, 18:0 fell and both 22:5n-3 and 22:6n-3 rose significantly (P less than 0.05). 4. There were no significant effects of fish-oil supplementation on serum lipids, platelet cholesterol: phospholipid, collagen-induced platelet aggregation or collagen-induced platelet thromboxane B2 production. However, there was a significant correlation (P less than 0.001; r + 0.63) between total phospholipid arachidonic acid and platelet thromboxane production. 5. The fluorescent probe 1,6-diphenyl-1,3,5-hexatriene was used to determine whether fish-oil supplementation altered fluorescence polarization of isolated platelet plasma membrane and, by inference, platelet plasma membrane fluidity. No significant effect of fish-oil supplementation on fluorescence polarization was seen.

Adult↗
PubMed1998

The effects of new platelet inhibitory drug E-5510 on platelet deposition on aortic bifurcation grafts: assessment by indium-111-oxime labeled platelet imaging.

The effects of a recently synthesized anti-platelet aggregation drug (E-5510) on platelet deposition in a knitted Dacron aortic graft underwent preliminary evaluation by In-111 oxime labeled platelet imaging. Seven patients undergoing aortofemoral bypass using this graft for occlusive disease were randomized into two groups: those receiving E-5510 and those receiving no medication. This agent was administered for 17 days postoperatively, and on the 14th day In-111 platelets were injected and images were acquired at 24, 48, and 72 hours. Platelet deposits in the grafts were assessed by the ratios of graft radioactivity to that of the adjacent native iliac arteries. Platelet deposition at the sites of anastomosis and deposition along the entire graft were normalized by initial deposition at 24 hours, and had significantly decreased at 72 hours in the three treated patients, while the normalized deposition increased progressively over time in the remaining four nonmedicated patients. E-5510 seems to have the potential to inhibit excessive platelet deposition on recently implanted grafts.

Aged↗
PubMed1986

Platelet volume, platelet release reaction and platelet response to infused adrenaline are increased in essential hypertension.

Hypertensive men aged 42 (n = 35) were compared to normotensive men of similar age (n = 44). Platelet numbers were similar in the two groups, but hypertensive men had larger venous platelets than the normotensive (7.46 versus 7.12 femtoliter, p = 0.01). Plasma concentration of beta-thromboglobulin (BTG), a marker of platelet release reaction, was increased in arterial blood in hypertension (40 versus 21 micrograms/l, p = 0.02). The normotensive subjects had markedly higher BTG concentration in venous compared to arterial blood (p less than 0.01), but this arterio-venous difference was not present in the hypertensive group. Twelve normotensive subjects received infused saline, which did not induce changes in platelet variables. Adrenaline was infused to 13 hypertensive and 12 normotensive subjects, with dose gradually increasing to 0.04 microgram/kg/min. Platelet count increased in both groups, but significantly more in the hypertensive group. Platelet volume and BTG both increased markedly in the hypertensive group, but not in the normotensive men. Thus, young men with hypertension have increased platelet activity and increased sensitivity to exogenous adrenaline.

Adult↗
PubMed1988

Characterization of a monoclonal antibody ITI-Pl 1 directed against human platelet membrane glycoprotein IIb using extracts of whole platelets and platelet surface and intracellular membranes.

A monoclonal antibody (mAb) termed ITI-Pl 1 has been prepared by the hybridoma procedure. Using immuno-absorption and crossed immunoelectrophoresis of Triton X-100 extracts of untreated and EDTA-treated human platelets it was shown to be directed against the surface membrane glycoprotein IIb (GP IIb). This mAb binds to whole platelets independently of ADP-stimulation and the presence of Ca2+-ions. It saturates at around 870 ng/10(8) cells corresponding to approximately 35,800 molecules/platelet. ITI-Pl 1 did not significantly inhibit GP IIb-IIIa dependent functions such as platelet aggregation or fibrinogen binding. Immunofluorescence could be demonstrated using ITI-Pl 1 and intact normal platelets, but not with platelets from a Glanzmann's thrombasthenia patient. Crossed immuno-electrophoresis with platelet extracts from four different thrombasthenic patients gave a line precipitate in the intermediate gel with 125I-labelled ITI-Pl 1 and autoradiography indicating trace amounts of free GP IIb or the GP IIb-IIIa complex. The epitope on GP IIb detected by ITI-Pl 1 is not destroyed by neuraminidase treatment. Thus the mAb also interacts with neuraminidase-treated GP IIb-IIIa complex in highly purified platelet surface membrane fractions as well as with GP IIb-IIIa from untreated internal membranes isolated by continuous flow electrophoresis.

Animals↗
PubMed1994

Diminished platelet yield and enhanced platelet aggregability in platelet-rich plasma of peripheral vascular disease patients.

Centrifugation of citrated whole blood (cit-WB) for platelet rich plasma (PRP) preparation resulted in a significantly diminished platelet yield compared to when blood was collected in citrate + aspirin (acetylsalicylic acid; ASA) or EDTA anticoagulants in both apparently healthy young subjects and peripheral vascular disease (PVD) patients. The loss in platelets was significantly greater in PVD patients than in young apparently healthy subjects when using cit-WB. Median platelet volume (MePV) of PRP preparations was not different between PVD patients and apparently healthy subjects. The MePV of EDTA-PRP preparations was significantly bigger than cit-PRP and cit + ASA-PRP in both PVD patients and apparently healthy subjects. Citrate and citrate + ASA-PRP of patients was significantly more aggregable to adrenaline. In EDTA-PRP, adrenaline-induced aggregation did not occur. These findings indicate that platelet hyperactivity occurs in PVD even in the presence of ASA. Furthermore, studies involving the use of PRP may not be representative in PVD due to the significant loss of platelets during centrifugation. The methodology described here can be used by those who do not have facilities designed specifically for platelet research.

Aged↗
PubMed1982

Platelet to leukocyte adherence phenomena. (Platelet satellitism) and phagocytosis by neutrophils associated with in vitro platelet dysfunction.

Platelet to leukocyte adhesion phenomena (PLAP) and the phagocytosis of platelets by neutrophils from the EDTA anticoagulated blood samples are described. PLAP was transferable to a normal blood specimen by patient's plasma or serum with or without complement. Further studies revealed in vitro evidence of hereditary platelet dysfunction. In vivo study of platelet survival and in vitro analysis of platelet membrane glycoproteins were normal. We conclude that PLAP can be seen in an asymptomatic individual with in vitro evidence of hereditary platelet dysfunction.

Adolescent↗
PubMed1998

Changes of platelet cytoskeletal proteins following platelet aggregation induced by collagen and platelet membrane glycoprotein in Japanese black cattle with delta-storage pool deficiency.

Five Japanese Black cattle showing the tendency of persistent hemorrhage were diagnosed as delta-storage pool deficiency because of lack of dense bodies in platelets. There was no significant difference in the platelet count, fibrinogen concentration, prothrombin time and activated partial thromboplastin time between the cases and normal control cattle. However, the maximum platelet aggregation rate and the values of myosin in the cytoskeletons during platelet aggregation induced by collagen were significantly lower in the cases compared with those in normal control cattle. The quantities of platelet membrane glycoprotein were in the range of 94-160 kDa and were not different between the cases and control cattle. However, a decrease of thrombospondin in alpha-granules in platelet cytoplasm were suspected in two of the 5 cases.

Animals↗
PubMed1976

Ultrastructure of platelet aggregation in refractory anemia and myelomonocytic leukemia. II. Individual platelet abnormalities: thrombasthenia-like platelets, surface defects, and dissociation phenomena.

Studies of in vitro platelet aggregation were done in five patients with refractory anemia and two with acute myelomonocytic leukemia. The macroscopic results as well as the general ultrastructural findings were reviewed in a companion paper. Electron microscopic analysis of changes in the individual platelets within aggregates revealed a striking heterogeneity, both in the degree of response of each platelet are in the ultrastructural characteristics of the platelet population. Many of the unaggregated platelets had reacted individually, resembling the platelets of patients with Glanzmann's thrombasthenia. There were other abnormalities suggesting the presence of surface defects, such as the presence of areas of obliteration of the interplatelet space (so-called tight connections). One of the most striking findings was a peculiar dissociation between the different components of the aggregation sequence.

Anemia, Aplastic↗
PubMed1990

Filtration of platelet-poor plasma specimens yields platelet-free plasma. Application for batch analysis of beta-thromboglobulin and platelet factor 4.

The authors investigated filtration of platelet-poor plasma through a 0.2-micron filter for the analysis of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) in frozen specimens. Platelets were detected by electron micrograph in the platelet-poor plasma preparation without filtration. No platelets or platelet fragments were seen after filtration. Freezing the unfiltered specimens resulted in a significant increase in the beta-TG and PF4 concentrations, presumably because of release of these proteins from the platelet alpha-granules during freezing and thawing. There was no change in the PF4 levels and only a slight decrease in beta-TG levels after freezing of the filtered specimens. The filtered samples could be frozen for later batch analysis, resulting in considerable cost savings to the laboratory.

Blood Platelets↗
PubMed1982

Comparison between induced platelet aggregation and circulating platelet aggregates as platelet function tests in patients with transient ischemic attacks.

Routine blood analysis, platelet counts, number of circulating platelet aggregates (CPA) and platelet aggregation in vitro against adenosine-diphosphate (ADP), epinephrine and collagene were studied in 45 healthy controls, in 10 hospitalized patients with other neurological diseases than stroke and in 12 patients with transient ischemic attacks (TIA) before and after prophylactive treatment with anticoagulants (AC) or antiplatelet drugs (APD). Except for lower hemoglobin and hematocrit levels in women, sex, smoking, oral contraceptives of pregnancy did not significantly influence the routine blood parameter. Smoking females taking oral contraceptive had an increased number of CPA and the most easily induced aggregation in vitro. Patients with TIA had no significant differences in blood or platelet findings versus the healthy controls (except smoking females on oral contraceptives) or the non-stroke patients, even though individual patients could have high numbers of CPA and an easily induced platelet aggregation in vitro. Treatment with AC did not influence platelet function, whereas APD therapy decreased the number of CPA and inhibited the secondary platelet aggregation in vitro.

Blood Cell Count↗
PubMed1985

Synergistic effects of platelet-activating factor and other platelet agonists in human platelet aggregation and release: the role of ADP and products of the cyclooxygenase pathway.

The synergistic effects of platelet-activating factor (PAF) with ADP, collagen, thrombin, A23187, adrenaline, sodium arachidonate and ristocetin in human platelet aggregation and beta-thromboglobulin (beta-TG) release were investigated in citrated platelet-rich plasma (PRP). Synergism in both aggregation and release was present with all agonists except ristocetin. Upon oral intake of aspirin (ASA) the PAF-induced irreversible aggregation as well as the synergistic irreversible aggregation became reversible. Both prior to and after ASA ingestion ADP removal by creatine phosphate/creatine phosphokinase (CP/CPK) resulted in a reduced, reversible platelet aggregation induced by PAF alone or in combination with the other agonists. The ADP-removal and ASA-ingestion also strongly inhibited the beta-TG release. The synergistic aggregation and release were also inhibited by ASA and indomethacin in vitro as well as by the competitive ADP-inhibitor ATP. It is concluded that not only the activation of human platelets by low doses of PAF itself, but also the synergism of PAF and other platelet agonists is highly dependent upon ADP and products of the cyclooxygenase pathway.

Adenosine Diphosphate↗
PubMed2003

A new platelet parameter, the mean platelet component, can demonstrate abnormal platelet function and structure in myelodysplasia.

The mean platelet component (MPC) is a new platelet parameter generated by the Bayer ADVIA 120 full blood count analyser as part of the routine complete blood count (CBC) test cycle. We report a case of myelodysplasia with bleeding complications and abnormal template bleeding time in whom low mean platelet component parameters were associated with partial platelet granule deficiency, demonstrated by transmission electron microscopy. We suggest that the mean platelet component is an inexpensive and rapid test to screen for platelet dysfunction related to ultrastructural abnormalities in myelodysplasia.

Blood Platelet Disorders↗
PubMed1979

A platelet defect in a patient with eosinophilic leukaemia: absent ristocetin-induced platelet aggregation associated with a reduced platelet sialic acid content.

Platelets from a patient with eosinophilic leukaemia were not aggregated by ristocetin. The defect was not corrected by normal human plasma and was due to a platelet abnormality. The patient's platelets also showed a diminished sensitivity to aggregation by bovine factor VIIIVWF. The defect was not associated with a prolonged bleeding time. No abnormalities were detected in ADP, collagen or thrombin-induced platelet aggregation. Biochemical studies showed that the platelets were deficient in sialic acid. This deficiency was associated with a reduced staining for glycoprotein I following SDS-polyacrylamide gel electrophoresis. The results suggest an acquired platelet surface abnormality.

Adenosine Diphosphate↗
PubMed1981

Platelets in myeloproliferative disorders. III: Glycoprotein profile in relation to platelet function and platelet density.

Membrane glycoproteins (GP) are implicated in platelet functions. In myeloproliferative diseases (MD), some of these functions are known to be perturbed. 16 patients with various MD were investigated for platelet functions (retention to glass beads, epinephrine- and ristocetin-induced aggregation), platelet density distribution and PAS-staining glycoprotein profile on SDS-polyacrylamide-gel-electrophoresis. An abnormal GP pattern (moderate reduction of GP (Ib + Is) and GP IIb with corresponding increase in GP IIIb) was demonstrated but no relation to platelet dysfunction or density distribution was observed. No differences between the various types of MD were noticed although the group of polycythaemia vera was the less perturbed for platelet function, platelet density and also GP profile.

Blood Platelets↗
PubMed1987

Activity of platelet-derived growth factor (PDGF) in platelet concentrates and cryopreserved platelets determined by PDGF bioassay.

The bioassay of platelet-derived growth factor (PDGF) in platelets was established using the rat fibroblast cell line 3Y1. 3Y1 cells (5 X 10(3)/well) were cultured in 24-well microculture plates with RPMI 1640 medium using 1% of PDGF-free serum and 5% of platelet extracts for 4 days. Cell proliferation was measured by the increase of DNA content. This assay made it possible to measure the biological PDGF activity. PDGF activity of platelet concentrates kept the same level as that of fresh platelet samples during preservation for up to 120 h at 22 degrees C; cryopreserved platelets also retained PDGF activity well.

Biological Assay↗