ISSN:0953-7104    

DOI:10.3109/09537109509078462

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

Platelet activity has been widely recognised to be governed by various agonists through their specific receptors responsible for the initiation of signal transduction pathways. Keeping in view the paradoxical role of lipoproteins in platelet activation, various investigations were directed to explore the possibility that platelets, like other cells, may possess functional receptors specific for the apoprotein moiety in lipoproteins. These investigations led to the discovery of a novel platelet lipoprotein receptor-Ckwhich not only has a high affinity for the cholesterol moiety in lipoproteins but also has the ability to initiate a phospholipase D - dependent signalling pathway which may be responsible for the lipoprotein-dependent platelet activation-response coupling.

ISSN:0953-7104    

DOI:10.3109/09537109509078463

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

ISSN:0953-7104    

DOI:10.3109/09537109509078464

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

Both inhibition and enhancement of platelet aggregation have been observed after exposure to streptokinase (SK) in vitro. Recently we have shown that inhibition of aggregation appears to be related to the fraction containing the fibrinogen degradation product, fragment E. In addition, SK may initiate platelet aggregation by a mechanism involving specific anti-SK antibodies and plasminogen. Two monoclonal antibodies (MoAbs) (PL2-49 and LeoA1) were used to assess the immunological activation of platelets in SK-induced platelet aggregation and in SK-enhanced ADP-induced platelet aggregation. The anti-SK titers in healthy volunteers' and patients' (previously treated with SK for acute myocardial infarction) plasma, were measured using a one-site non-competitive ELISA. Serum from patients was used for the purification of IgG anti-SK by affinity chromatography.We confirmed that the degree of fibrinogen degradation is a major determinant of the aggregation inhibition induced by SK. SK-induced platelet aggregation and SK-enhanced ADP-induced platelet aggregation require the interaction of the Fc domain of the anti-SK antibodies with the FcyRII located on the platelet membrane, since they are blocked by the MoAb IV-3 directed against FcyRII. Classification of the subjects according to their responses to specific MoAbs (PL2-49 and LeoA1) supports the essential role played by immunological activation of platelets in SK-induced platelet aggregation and in SK-enhanced ADP-induced platelet aggregation. The ability of anti-SK antibodies to promote SK-induced platelet aggregation and SK-enhanced ADP-induced platelet aggregation, seems to result from the interaction between two separate mechanisms: the fist mechanism is based on immunological activation of platelets and the second is related to the intervention of a defined subset of anti-SK antibodies.

ISSN:0953-7104    

DOI:10.3109/09537109509078465

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

Platelets play a major role in the development of patency complications in vascular grafts. The aim of this study was to evaluate changes in platelet count and function, and also in factor VIII:C (FVIII:C) and von Willebrand factor (vWF) plasma levels, induced by aorto-bifemoral by-pass with Dacron grafts in seven patients. Platelet count, platelet aggregate ratio (PAR), and platelet aggregability induced by several stimuli, as well as FVIII:C and vWF plasma levels were evaluated before and on days 1,4,9 and 11 after surgery. We observed a mild thrombocytopenia on day 1, followed by a progressive increase in platelet count, which attained a relative thrombocytosis on the 11th day. PAR did not vary significantly during the whole observation period. Platelet aggregation, assayed by the optical method using ADP, epinephrine, arachidonic acid, collagen and ristocetin, (decreased on days 1 and 4). Thereafter, an increase in aggregation was observed until day 11 when hyperaggregability was verified. FVIII:C and vWF peaked on the 4th day, decreasing progressively to pre-surgery values on day 11.

ISSN:0953-7104    

DOI:10.3109/09537109509078466

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

In previous studies we have shown that relaxin (RLX), a peptide hormone produced predominantly during pregnancy, is a powerful inhibitor of platelet aggregation. The current study shows that RLX, given systemically to rats, also affects the number of circulating platelets and their release by spleen megakaryocytes. Male albino rats were treated acutely or chronically with RLX, and the effects of the peptide evaluated by platelet count and morphological analysis of spleen megakaryocytes. The results obtained show that RLX causes a decrease of circulating platelets, which is already appreciable 1 h after a single administration and becomes significant upon a May treatment with the peptide (790000±18000/ml in the RLX-treated rats versus 865 000±23 000/ml in the controls; P<0.01). Coincidentally, spleen megakaryocytes show clearcut changes consistent with a depression of platelet release, namely the appearance of a thick peripheral cytoplasmic halo, filled with actin microfilaments and without platelet territories, and a virtual absence of images of thrombocytopoiesis. Based on the properties of RLX in inhibiting hemostasis, recognized in previous investigations and further proved by the present study, a role of the peptide is proposed in counteracting the hypercoagulable state which currently takes place during normal pregnancy.

ISSN:0953-7104    

DOI:10.3109/09537109509078467

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

Platelet volume is a measure of platelet function. An increased platelet volume is found in acute vascular syndromes and may have a causative role and predict outcome. Patients with autosomal dominant polycystic kidney disease (APKD) are at increased risk of developing, and dying from, premature vascular disease. We hypothesized that platelet volume might be altered in patients with APKD. Platelet volume was measured in 16 normotensive APKD patients with normal renal function and 16 normal volunteers pair-matched for age, gender, race and body mass index.Mean platelet volume was increased by 0.4 fl (95% confidence limits 0.1 to 0.9, 2P=0.017) in patients with APKD as compared with normal subjects: median 8.4 fl (0.7) versus 8.0 fl (0.3) respectively. In contrast, platelet count was lower by 63×109/1 (−5 to -108, 2P = 0.031): 225 (40)×109/1 versus 280 (35)×109/1 while the platelet mass was not different, -0.36 ml/l (−0.81 to 0.02, 2P=0.070): 1.82 (0.30) ml/l versus 2.28 (0.38) ml/l. Platelet volume and count were inversely correlated across the two groups, rs= -0.342 (2P=0.055). Serum levels of erythropoietin, a hormone that contributes to the regulation of thrombopoeisis, were not different between the APKD patients and normal controls, 35 U/1 (−71 to 120, 2P=0.42): 107 U/I (53) versus 84 U/I (57). Although erythropoietin did not correlate with platelet volume, R., = -0.185 (2P =0.36), it was positively associated with platelet count, R., = 0.465 (2P=0.029) and platelet mass, rs= 0.466 (2P= 0.028).Since an increased platelet volume is associated with platelet hyperactivity, the increased platelet volume in APKD may be a marker, or even contribute to the development, of premature vascular disease and sudden cardiac death in patients with APKD.

ISSN:0953-7104    

DOI:10.3109/09537109509078468

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

Rapid and relevant evaluation of platelet function is often clinically important. By means of fluorescent labelled chicken antibodies (which do not bind to Fc-receptors) against fibrinogen and von Willebrand factor and flow cytometry, we have determined the time course of ligand association to platelets after stimulation with adenosine 5′-diphosphate and ristocetin respectively. The expression of guanosine 5′-phosphate (GMP)-140 was also measured. We have applied this technique to evaluate platelet function during platelet storage and cardiopulmonary bypass. There was a significant reduction of the binding of fibrinogen and von Willebrand factor and significantly increased expression of GMP-140 after 9 days of storage. Changes in metabolic variables such as lactate accumulation, glucose consumption and decrease in pH confirm that the functional impairment is due to a large extent to a deteriorated platelet metabolism. No significant differences were found between samples taken before and during cardiopulmonary bypass, but there was a tendency towards increased ligand binding as well as increased expression of GMP-140 at the end of cardiopulmonary bypass. The flow cytometric technique that is described may be useful for evaluation of platelet function and platelet activation in vivo.

ISSN:0953-7104    

DOI:10.3109/09537109509078469

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

The inhibitory effects on platelet reactivity of increased extracellular magnesium were investigated. Wherever possible, experiments were performed in hirudinized whole blood. Concentration dependent inhibition of platelet aggregation and dense granule release were observed with MgSO4. Antiaggregatory effects were identical with MgCl2, indicating that the effects are due to the Mg2+ion. Antiaggregatory effects of CaCl2, differed from those of MgCl2, indicating that this is not a non-specific divalent cation effect. MgSO4also caused concentration-dependent inhibition of platelet thromboxane production. Experiments in the presence of apyrase and indomethacin showed that complex formation with ADP and inhibition of cyclo-oxygenase do not entirely account for the inhibitory effect of magnesium on platelet activation. Studies with an anti-GPIIb/IIIa antibody showed that the inhibitory effects on the release reaction and thromboxane synthesis are independent of those on aggregation.The results are consistent with magnesium modifying an intracellular signal transduction pathway common to several agonists, rather than the effects of magnesium being specific for one agonist. This study also shows that MgSO4inhibits agonist-induced increases in intracellular free calcium. Increasing the extracellular concentration of magnesium up to 10 mM had no effect on agonist-induced increments in intraplatelet free Mg2+concentration.

ISSN:0953-7104    

DOI:10.3109/09537109509078470

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

At fixed pH and ionic environment platelet net charge depends on the composition of surface glycoproteins and phospholipids. It is believed that this composition changes, becoming more negative in the course of activation, and that certain thrombotic disorders such as transient ischemic attacks (TIA) may be associated with platelet activation. To investigate this hypothesis we measured the electrophoretic mobility (U) of normal platelets, activated normal platelets and platelets from patients with TIA and immune thrombocytopenic purpura (ITP). Normal platelets gave U = -0.91±0.05 pm cmh, while normal platelets activated by ADP gave -1.25 and by collagen -1.70. TIA patients (n = 22) had mean U = -1.14±0.10 and the ITP patients (n = 37) had U= -1.07±0.13. The U of both patient groups differed significantly from normal controls,P<0.001. Indeed, only 2 of the 22 TIA cases had U within 2 SD of the control value. The ITP group included 10 patients with TIA-Like symptoms; the mean U of this subgroup was identical to that of the TIA group without ITP. We conclude that U is a useful measure for research on platelet abnormalities and may even be useful as a routine clinical tool. This work was greatly facilitated by the use of an automated instrument, the DELSA 440, allowing determination of U of a given sample in as little as 5 min.

ISSN:0953-7104    

DOI:10.3109/09537109509078471

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor