ISSN:0953-7104    

DOI:10.3109/09537109309013189

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

The influence of low density lipoprotein (LDL) on platelet aggregability was studied using filtragometry and conventional Born aggregometry in vitro. Three different concentrations of autologous LDL, obtained from 9 healthy male volunteers, were incubated for 20 min, at 37°C, with whole blood anticoagulated with low molecular weight heparin (filtragometry) or citrated platelet-rich plasma (PRP; Born aggregometry). The LDL-cholesterol concentration was increased from 1.7±0.2 mmol/1 to 2.4±0.2, 3.5±0.3 and 5.3±0.5 mmol/l, respectively. Adenosine diphospate (ADP)-induced platelet aggregation in whole blood was enhanced in a dose dependent manner by LDL, as assessed by filtragometry (ADP cone, range 0.1-0.3μM). Platelet aggregability in PRP (Born) was not affected by LDL at the ED50for ADP-induced platelet aggregation (i.e. 1-4μM ADP). The marked platelet activation caused by the high ADP concentrations used with conventional Born aggregometry may have masked a modest LDL-induced platelet activation as a slight increase in spontaneous platelet aggregation was observed in PRP at the intermediate LDL-concentration. The present findings indicate that low concentrations of LDL stimulate platelet aggregability in the physiological whole blood milieu. This adverse effect of LDL-cholesterol may be of clinical importance in patients with hypercholesterolaemia.

ISSN:0953-7104    

DOI:10.3109/09537109309013190

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

Hypothermia (24°C) was induced in 7 healthy male dogs. Hematological, hemostatic and biochemical parameters were evaluated before the onset and after 3 h of hypothermia. Following hypothermia, there was a significant increase in red cell count, hematocrit and haemoglobin concentration. The white cell and platelet counts were decreased significantly and the mean platelet volume increased significantly. The activated partial thromboplastin time was significantly prolonged whereas the prothrombin time was unchanged. Associated with these changes there was a significant increase in serum glucose and a small increase in aspartate transaminase activity probably due to muscle leakage. No change occurred in the more liver-specific alanine transaminase. The arterial pH decreased and the changes in gasses observed as a result of hypothermia were compatible with a mixed respiratory-metabolic acidosis. The mean aortic blood pressure also dropped markedly. The hematological and hemostatic changes suggest that widespread tissue 'injury' occurs even in short term hypothermia with platelet activation and accumulation in the liver and spleen. This model of hypothermia may be of use in the study of the thrombotic diathesis observed in this condition and serve as a test bed for drugs of potential use in conditions such as Raynaud's syndrome and hypothermic surgery (e.g. coronary artery bypass).

ISSN:0953-7104    

DOI:10.3109/09537109309013191

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

In aspirin-treated platelets labelled by preincubation with [3H]-choline, enhanced release of both [3H]-choline and [3H]-choline phosphate resulted from stimulation by collagen or thrombin. No such release accompanied stimulation by ADP, platelet-activating factor or adrenaline. Release of [3H]-choline phosphate was entirely dependent on aggregate formation whereas release of [3H]-choline was reduced but not eliminated, if aggregation was prevented. The properties of [3H]-choline and [3H]-choline phosphate release indicated that both collagen and thrombin induced activation of phospholipase D in the absence of aggregate formation. Such activation was augmented if aggregate formation occurred. Aggregation induced by these two agonists also caused activation of phosphatidylcholine-specific phospholipase C. These effects were prevented in the presence of staurosporine and could also be induced by addition of a synthetic 1,2-diacylglycerol indicating a role for protein kinase C.

ISSN:0953-7104    

DOI:10.3109/09537109309013192

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

To detect in vivo activated platelets in humans as well as in animal models of thrombosis, we developed a new murine monoclonal antibody, 2T60, specific for activated human and rabbit platelets by immunizing with human thronibin-activated platelets. 2T60 (IgG1subclass) showed a great difference between binding to the thrombin-activated and resting human and rabbit platelets on ELISA and flow cytometer analysis. Immunoblotting analysis revealed that 2T60 reacted with a 130 or 106 kDa protein of human or rabbit platelets, respectively, only under non-reducing conditions.125I-labeled 2T60 inserted into the intermediate gel of CIE of solubilized human platelets was incorporated into a immunoprecipitation line. 2T60 immunoprecipitated a protein of 130 or 115 kDa from human or rabbit platelets, respectively, which had been activated and125I-surface-labeled. The N-terminal sequence of the affinity purified 2T60 antigen of human platelets was identical to that of GMP 140. There were differences in the carbohydrate chain content of GMP 140 between human and rabbit platelets. In experimental cerebral thrombosis of rabbits that had been injected with 2T60, the platelets adhering to the exposed subendothelium and contained in thrombi were found to bind 2T60 prominently. These results suggest that 2T60 may be a useful tool for clinical and experimental studies of thrombotic disease.

ISSN:0953-7104    

DOI:10.3109/09537109309013193

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

The isolated low density lipoprotein (LDL) has been shown to cause shape change, granule centralization and incomplete degranulation of human blood platelets at concentrations of 50 to 300μg protein/ml in vitro. About half the number of platelets were discoid at the LDL concentration of 50μg/ml. If the platelets were pretreated with LDL at a concentration of 100μg/ml, aggregation could be induced by thrombin (0.015 U/ml) lightly. These results suggested that the LDL-incubated platelets showed a primary activation. These LDL-pretreated platelets showed enhanced sensitivity to thrombin by aggregating at a very low dosage (0.015 U/ml). The primary activation of platelets induced by LDL seemed independent of extracellular calcium when LDL concentrations were higher than 200μg/ml.

ISSN:0953-7104    

DOI:10.3109/09537109309013194

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

Compared to normal controls, platelets from myotonic dystrophy (MyD) patients, released significantly moreβ-thromboglobulin (βTG) and generated more thromboxane B2(TXB2) when platelet aggregation was induced by ADP (1.5μM) or epinephrine 1μM. TXB2generation in MyD platelets at 1 and 3 min was positively correlated (p<0.05) to platelet aggregation (PA). This suggests that, 1 min after the addition of the PA inducers, the platelets of MyD patients are already at the second (irreversible) phase of PA. Together with our previous data, these results may indicate hyperactivity of platelets caused by a membrane abnormality in MyD.

ISSN:0953-7104    

DOI:10.3109/09537109309013195

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

ISSN:0953-7104    

DOI:10.3109/09537109309013196

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor