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Biomedical subjects

K Zawilska

Publications and source records attributed to K Zawilska.

At least 55 records · Page 3Linked to original sources
PubMed1989

Low-dose heparin in the prevention of thrombotic complications following acute myocardial infarction.

103 patients with acute myocardial infarction (AMI), disqualified for thrombolytic treatment, were randomized into two groups. Group I received 5000 IU of heparin (subcutaneously, twice daily) for 14 to 21 days. Group II was without anticoagulant prophylaxis. Patients were evaluated for deep vein thrombosis (DVT) using radiofibrinogen uptake test and for the presence of intracardiac mural thrombus (ICT) by two-dimensional echocardiography (50 patients). The incidence of DVT was 4% in group I and 19% in group II. ICT was diagnosed in three patients (13%) of group I and in 10 patients (45%) of group II. Five patients under heparin prophylaxis and 6 non-anticoagulant patients died in the hospital of cardiac causes. There were no bleeding complications. Low-dose heparin seems to be an effective prophylaxis of thrombotic complications in patients with AMI.

Adult↗
PubMed1987

Binding of heparin to human endothelial cell monolayer and extracellular matrix in culture.

Endothelial binding of heparin contributes to its local antithrombotic action and catabolism. However, it is uncertain whether heparin may be bound to a damaged or even de-endothelialized vessel surface. Therefore, the binding of 3H-heparin to cultured endothelial cell monolayer and extracellular matrix was studied. The binding reached equilibrium after 4 h. 3H-heparin bound to endothelium could be displaced by unlabelled heparin which competed for about 80% of binding. The binding became saturable when the concentration of heparin exceeded 30-times the therapeutical value. Approximately 6 X 10(11) binding sites for heparin per cm2 of endothelium were calculated. Heparin was bound not only to endothelial cells but also to extracellular matrix, even when it was exposed in the absence of cells. About 40% of binding sites were localized in the extracellular matrix fraction. A similar affinity of binding of 3H-heparin to complete endothelium, endothelial cells and extracellular matrix was estimated /Kd of almost 1 microM/. The binding of heparin to extracellular matrix should be considered in the interpretation of heparin interaction with endothelium.

Cells, Cultured↗
PubMed1987

The binding of 125I-fibrinogen to blood platelets in patients with chronic uraemia.

The binding of 125I-fibrinogen to blood platelets was assessed in 41 patients with chronic uraemia. The study was performed in three groups of subjects: treated conservatively, with haemodialysis and with peritoneal dialysis. Platelets from uraemic patients were shown to be more susceptible to fibrinogen binding than platelets from healthy subjects.

Adult↗
PubMed1981

The effect of isolated leukaemic blasts on platelet aggregation.

The effect of blastic cells isolated by Böyum's method from the blood of 20 nontreated patients with acute myelogenous leukaemia on normal platelet aggregation has been studied. The isolated blasts in concentration of 2,000/microliter and higher, inhibit normal platelet aggregation induced by ADP or collagen, but have no influence on aggregation initiated by epinephrine. This effect is unaffected by the presence of metabolic poisons or by the disruption of the blastic cell membrane. Our results seem to exclude interference of blastic cells with platelet prostaglandin biosynthesis. In patients with acute leukaemia and an increased leukocyte count the preparation of platelet suspension free of blastic cells is not possible, even by the albumin gradient method or by gel filtration. The leukaemic blast content in platelet-rich suspensions may account for the variations in the aggregation behaviour which are found in these patients. The influence of blastic cells may be an important factor in the bleeding tendency in myelogenous leukaemia

Adenosine Diphosphate↗