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Biomedical subjects

K Zawilska

Publications and source records attributed to K Zawilska.

At least 19 recordsLinked to original sources
PubMed1995

On the action of a heparan-like glycosaminoglycan (Hemovasal) on the mechanism of haemostasis and fibrinolysis.

Hemovasal produced by Manetti-Roberts, Florence, Italy, is a glycosaminoglycan obtained from porcine intestinal mucosa which belongs to the family of heparan sulfates. The substance was examined On 36 male survivors of myocardial infarction with an interval of at least 6 months after the acute event. No anticoagulants were given and ASA was withdrawn at least 2 weeks before the trial. Hemovasal was administered in 3 different i.m. doses as single injections. A further group received a daily oral dose of 300 mg for one week. A comparable placebo group of patients as well as a group of healthy volunteers was run in parallel. The coagulation profile showed only a slight prolongation of the aPTT, a trace of diminution of Antithrombin III and no activation of Heparin cofactor II. The fibrinolytic system showed an enhancement of the diurnal increase of t-PA without an alteration of the total increase of this activity. There was a considerable and highly significant diminution of the PAI-1 activity. This was dose dependent and could be found after i.m. as well as after oral administration. It was assumed that the thrombolytic effect which was repeatedly described was a consequence of the diminution of PAI-1.

Administration, Oral↗
PubMed1995

[Progress in the detection of intravascular activation of fibrinolysis].

Methods for measuring antigen and activity of plasminogen activators (t-PA, u-PA), plasminogen activator inhibitors (PAI-1, PAI-2) and their complex have been improved in the past few years, but few comparative data are available and they should be standardized. In particular the commercial kits for determination of PAI-1 activity seem to be not accurate for the measurement of PAI-1 in plasma. The amount of generated plasmin can be measured as plasmin-alpha-2-antiplasmin complex (PAP). There are also some new tests which could differentiate between fibrinogenolysis (FgDP) and fibrinolysis (FnDP, D-dimer) as between primary and secondary activation of fibrinolysis (B beta 15-42 peptide). Normal D-dimer plasma concentration allows for the ruling out of venous thromboembolism with high probability, but the specificity of this tests is poor.

Enzyme-Linked Immunosorbent Assay↗
PubMed1994

[Markers of intravascular activation of coagulation].

New markers of intravascular activation of coagulation have been developed, based on advance in our understanding of the biochemistry of the haemostatic mechanism. These are sensitive methods for measuring of peptides liberated with the generation of thrombin (factor IX activation peptide, factor X activation peptide, peptide F1 + 2), for measuring concentration of enzyme-inhibitor complexes (eg. thrombin-antithrombin III-TAT complexes), as well as for investigating the effect of thrombin on fibrinogen (fibrinopeptide A-FPA) or on protein C (protein C activation peptide). Studies employing these markers indicate that a state of hypercoagulability can be detected in the blood of humans prior to the appearance of thrombotic phenomena. However, further studies will be required to determine whether these methods can identify individuals who are entering a clinically relevant hypercoagulable state as well as to monitor an antithrombotic treatment.

Animals↗
PubMed1992

Subcutaneous low molecular weight heparin versus subcutaneous unfractionated heparin in the treatment of deep vein thrombosis: a Polish multicenter trial.

In a prospective multicenter trial, 149 consecutive patients with phlebographically proven proximal and/or distal deep vein thrombosis of the leg were randomly allocated to receive subcutaneously for 10 days either low molecular weight heparin CY 216 (Fraxiparine) in a fixed dose or unfractionated heparin (UFH) in doses adjusted according to the activated partial thromboplastin time. Pre- and post-treatment phlebograms were assessed blindly using the Arnesen's score system in 134 patients available for analysis of the treatment efficacy. The mean phlebographic score after 10 days of treatment was significantly decreased in both groups (p less than 0.001) in comparison with the baseline score but the difference in score changes between the two groups was not statistically significant. There was an improvement in 45/68 patients (66%) in the Fraxiparine group and in 32/66 patients (48%) in the UFH group, and an increase in the thrombus size in 10/68 (15%) and 12/66 (18%), respectively. One symptomatic non-fatal pulmonary embolism and one major bleeding episode were observed in the UFH group. During a follow-up period of 3 months, two rethromboses had occurred in the UFH group and none in the Fraxiparine group. It is concluded that subcutaneous fixed dose Fraxiparine is safe and at least as effective as subcutaneous adjusted UFH in the treatment of deep vein thrombosis.

Adult↗
PubMed1992

[Evaluation of thrombotic risk in young men after myocardial infarction during a period of clinical stability].

The study was aimed at an evaluation of individualized indications for antithrombotic therapy for secondary prevention in a group of 40 young survivors (aged 30-40 years) of myocardial infarction, presenting a stable phase of coronary disease. The control group consisted of 19 healthy men, of approximately similar age distribution. The determinations concerned the following: in vitro ADP and collagen induced platelet aggregation, plasma fibrinogen concentration, factor VII, VIII and antithrombin III activity, protein C concentration, spontaneous fibrinolytic activity and fibrinolytic activity after venostasis, plasminogen and alpha-2 antiplasmin activity. Moreover, to determine correlations with hemostatic parameters lipids, apolipoproteins, glucose, uric acid plasma concentration as well as percentages of lipoproteins and glycolyzed hemoglobin were also studied. In the study group various hemostasis disturbances were found: an increased platelet aggregation induced by low concentrations of ADP, increased plasma fibrinogen concentration and factor VII activity, decreased protein C concentration and impaired plasma fibrinolytic activity after venostasis. Some correlations between hemostatic and lipids parameters were also observed. Results of the study have suggested necessity for the individualized antithrombotic prevention in young survivors of myocardial infarction with antiplatelet and/or anticoagulant drugs.

Adult↗
PubMed1992

[Platelet activation in young men after myocardial infarction: its relation to metabolic coronary risk factors].

Selected parameters of platelet function as well as their relationship with metabolic coronary risk factors are studied in a group of 40 young survivors (aged 30-40 years) of myocardial infarction, now presenting stable coronary disease. Nineteen healthy men, of approximately similar age-span, constituted the control group. The following parameters were determined: platelet survival half-time (via non-isotope method), intraplatelet activity of cyclooxygenase and lipoxygenase pathway of arachidonic acid (by measurements of malondialdehyde concentration before and after incubation with acetylsalicylic acid acid) and 125-I-fibrinogen binding to platelets. Moreover, the plasmatic concentration of total cholesterol, HDL-cholesterol, triglycerides, phospholipids, Apo A and B, total beta lipoproteins, glucose, uric acid as well as percentages of beta, prebeta, alpha lipoproteins and glycosylated hemoglobin were also studied. Platelet survival half-time in patients was significantly shortened (3.64 +/- 1.37 days) when compared with the control group (4.97 +/- 1.7 days). A higher intraplatelet activity of lipoxygenase pathway (2.02 +/- 0.62 and 1.49 +/- 0.54 nmol MDA/10(9) platelets, respectively) was also found. However, activity of cyclooxygenase pathway of arachidonic acid and 125-I-fibrinogen binding to platelets remained unchanged. Shortened platelet survival half-time and the hyperactivity of intraplatelet lipoxygenase pathway correlated with a reduced plasmatic concentration of HDL-cholesterol (r = 0.323, p less than 0.05 and r = -0.451, p less than 0.05, respectively). The remaining parameters of platelet function were not statistically related to metabolic risk factors. The values of platelet function indicators in subgroups of patients divided according to family history of coronary heart disease, oral glucose load test result, and submaximal exercise test result did not differ significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[Acquired platelet storage pool deficiency in rheumatoid arthritis].

A 64-year-old woman with a 15-years-history of rheumatoid arthritis developed generalized hemorrhagic diathesis. Routine coagulation tests revealed a slightly diminished platelet count only. Platelet aggregation in vitro induced by ADP, collagen, thrombin, arachidonic acid and ristocetin were reduced. The patient's plasma aggregating activity was significantly diminished which was due to a decrease of the intraplatelet nucleotide pool. The number of mepacrine labelled bodies as well as dense bodies in electron microscopy was below the normal values as well. Moreover, the intraplatelet concentration of cyclooxygenase--malonylodialdehyde (MDA) and lipoxygenase pathway products were lowered. Total platelet immunoglobulin G and M contents were significantly increased. The platelet survival time (in vitro aspirin method) was slightly shortened. Finally the diagnosis of delta-acquired platelet storage pool deficiency (delta-SPD) was established and possibilities of treatment were discussed.

Arthritis, Rheumatoid↗
PubMed1991

[Evaluation of platelet malondialdehyde and 12-hydroperoxyeicosatetraenoic acid in type I and II diabetic patients with ketoacidosis and after clinical complications].

In 33 insulin-dependent, I and II type diabetic patients the authors evaluated the intraplatelet concentration of 12-hydroperoxyeicozatetraenoic acid (12-HPETE) and malonylodialdehyde (MDA) which are the products of lipoxygenase (LO) and cyclooxygenase (CO) metabolism of arachidonic acid (AA) in blood platelets. Moreover, in all patients, determinations of cholesterol total lipids, phospholipids, triacylglycerols were performed as well as serum lipoproteinogram. The studies were done in diabetic ketoacidosis and 2 weeks after compensation of diabetes was attained. Sixty healthy persons, with no changes in the coagulation system, constituted the control group. In patients with diabetic ketoacidosis a higher intraplatelet concentration of 12-HPETE (7.2 +/- 4.0 nmol/10(9) platelets) was found as compared with the values observed in the control group (4.7 +/- 2.1 nmol MDA/10(9) platelets); p less than 0.01. Intraplatelet MDA concentration did not, however, show a statistically significant difference. When compensation of diabetes was obtained the mean intraplatelet 12-HPETE concentration fell to values close the normal ones (5.5 +/- 3.4 nmol MDA/10(9) platelets). Nevertheless, the results of comparative determinations of mean values of both 12-HPETE and MDA concentrations in ketoacidosis as well as in compensated diabetes did not show statistically significant difference. High intraplatelet 12-HPETE concentration in diabetic ketoacidosis may be a cause of the formation or intensification of atherosclerotic changes, typical of this group of patients. The studies did not prove any correlation between the intraplatelet concentration of AA metabolism products and blood glucose concentration and lipid metabolism products. Neither was there any correlation between 12-HPETE and MDA concentration and the duration of clinically symptomatic diabetes.

Adult↗
PubMed1990

Fluctuation of thrombin-antithrombin III complex in patients with acute myocardial infarction: influence of low-dose heparin administration.

The haemostatic parameters were studied within 14 days of acute myocardial infarction (AMI) in 103 patients randomly allocated into a group receiving low-dose heparin or into a group treated without anticoagulants. Patients with isotopic evidence of deep vein thrombosis were excluded from the analysis. An important formation of thrombin-antithrombin III complex (TAT) in the plasma was detected in the early stage of the disease. It was accompanied by an activation of plasma intrinsic fibrinolysis (IF), an elevation of fibrinogen and its degradation products (FDP) and a reduction of extrinsic plasma fibrinolytic activity (EF) together with normal levels of factor X, antithrombin III (AT III), protein C and alpha-2-antiplasmin. Sequentially studies periods of the disease revealed a diminution of TAT complex concentration in the plasma on the seventh day of AMI together with a rise of the both plasma fibrinolytic activities (IF, EF) as well as an elevation of fibrinogen and its degradation products, returning to the initial values on the 14 day of AMI. In the patients treated with heparin the augmentation of TAT complex in the plasma was prolonged until the fifth day of AMI. Moreover, heparin administration was connected with significantly higher levels of AT III and protein C along with a lower concentration of factor X and FDP on the seventh day of the disease. The fluctuation of fibrinolytic activities (IF, EF) in the plasma was heparin-independent. The present results indicate that low-dose heparin treatment modulates the plasmatic fluctuation of TAT complex as well as factor X, AT III and protein C levels in patients with acute myocardial infarction.

Antithrombin III↗
PubMed1990

Nebulized heparin and anabolic steroid in the prevention of postoperative deep vein thrombosis following elective abdominal surgery.

One hundred eighty three patients, all over 40 years old, who underwent major abdominal surgery, were randomized into 3 groups: Group I received a single dose of nebulized heparin (800 IU per kg b.w.) administered by inhalation one day prior to surgery. Group II besides the above, also received a single injection of 50 mg of long acting anabolic steroid (nandrolone phenylpropionate) intramuscularly. Group III received 5000 IU heparin subcutaneously on hr prior to surgery as well as every 12 h for the next 5 postoperative days. Postoperatively the patients were evaluated for deep vein thrombosis (DVT) using the 125-I-fibrinogen test. The occurrence of DVT was determined as: in Group I--16%, in Group II--7.9%, in Group III--7.8%. Haemorrhagic complications (clinically important) were observed in 7.8% of patients from Group III, but only in 1.7% of patients in Group I and 1.6% in Group II. For DVT prophylaxis following abdominal surgery a single application of nebulized heparin and long acting anabolic steroid is as effective as conventional low-dose subcutaneous heparin administration, but gives less haemorrhagic complications. This method is also more advantagenous in term of acceptance by the patients and represents considerable saving of nursing time.

Abdomen↗
PubMed1990

[Assessment of hemostasis in patients with myocardial infarction complicated by deep venous thrombosis].

The study was carried out of 53 patients with acute myocardial infarction receiving no anticoagulant treatment. Changes were traced in certain indices of the blood clotting system and fibrinolysis in plasma in the first 14 days of the disease, with particular attention given to patients in whom during the hospitalization signs of deep vein thrombosis in the lower extremities appeared or a positive result was obtained of the test with 125I-fibrinogen. In a group of 9 patients with deep vein thrombosis developing during the observation, on the first day of myocardial infarction shortening of the kaolin-cephalin clotting time and considerable rise of the level of fibrinogen-fibrin (FDP) degradation products were noted in serum, and on the 14th day raised fibrinogen level and reduced exogenous fibrinolytic activity of the plasma were noted. Increased level of fibrinogen and FDP and exogenous and endogenous plasma fibrinolytic activity observed on the 7th day of the disease were not related to the development of thrombotic complications. The thrombin clotting time, platelet count, factor X level, protein C concentration and antithrombin III activity in the plasma were not significantly changed during myocardial infarction. The obtained results suggest a limited usefulness of the basic tests of the clotting and fibrinolytic systems for early diagnosis of deep vein thrombosis in acute myocardial infarction.

Blood Coagulation↗
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↗