Bilten za hematologiju i transfuziju最新文献

The congenital deficit of factor-X is extremely rare and usually goes with mild bleeding tendency. The variations of the factor-X activities are described individually and depend on the tests used, that is: activating factor-X by tissue or blood thromboplastin, Russel's Viper Venom, by neutralisation of the antibodies or immunoprecipitation. The test depends on the possibility of the specific congenital deficient plasma or on the use of the filtered bovine plasma. That's why it is rather difficult to classify the cases and order the minimum of the hemostatic level. Besides a short description of some physical, chemical and biochemical characteristics of factor-X, present the case with congenital deficit of Prower-Stuart factor discovered in our laboratory, together with the findings and procedures in identifying and confirming it.

The model of experimentally induced inflammation demand for granulocytes was used to study the changes in granulocytic cell compartments and the level of humoral regulators of granulopoiesis. The experimental inflammation in rats induced by i.p. injection of 3.5% solution of polivinylpyrrolidone (PVP) provoked during 24 hours intensive mobilisation of granulocytes into peritoneal exudate and the intensive proliferation of granulocytic cells in the bone marrow between 18-24 hours. When the bone marrow of CBA mice was cultivated in diffusion chambers implanted into rats with experimentally induced inflammation, stimulation of granulopoiesis was noted during the period of five days. The results indirectly indicate that the level of granulopoiesis stimulating factor was increased in the diffusion chambers host animals. It was demonstrated also that rat's serum obtained 20 hours after injection of PVP (leukophoretic serum) stimulates the proliferation of granulocytes in the bone marrow of normal CBA mice cultivated in diffusion chambers. The level of stimulation was confirmed to be dose dependent. Presented data indicate that in the conditions of increased demand for granulocytes, the level of humoral regulator--stimulator of proliferation of granulocytic cells--is increased in the circulation.

A monoclonal lambda IgM euglobulin with peculiar precipitable characteristics in vitro was found in the serum of a patient with Waldenström macroglobulinaemia. The precipitation was observed at room temperature only when serum was exposed to air. Covalent disulphide bonds probably contribute to the mechanism involved in the formation of precipitate in this case.

The authors present us the identification of different antibody specificities which been discovered in a woman-patient suffered from SLE. Applying the method of absorption and elution of antibodies, anti-c, anti-E, anti-Fya, anti-K and anti-S have been identified. The authors applied the method where the high percentage dextran was used in order to get blood for transfusion.

In this paper the present status of clinical usefulness of erythropoietin measurement is presented. The limitations and difficulties due to lack of the precision using current in vivo bioassay in polycythemic mouse are stated and the informations that can be obtained by determination of serum erythropoietin level in anemias and polycythemias are demonstrated.

The experiments were carried out in order to study the mechanism of thrombin--induced stimulation of glycolysis in washed human platelets. The platelets, isolated from human blood and resuspended in Krebs-Ringer-phosphate buffer (pH 7.4), were incubated in water bath (37 degrees C) either without (control) or with thrombin (1 NIH U/ml platelet suspension). Lactate, glycolytic intermediates and adenine nucleotides were measured in the neutralized perchloric acid extracts of platelets by enzymatic analysis and using the fluorimetric methods. The results of this study show that thrombin significantly increases the rate of lactate production in washed human platelets. At the same time thrombin induces the profound changes in the levels of platelet glycolytic intermediates with the "crossover" point at phosphofructokinase step of glycolysis. The results are interpreted as indicating that thrombin stimulates platelet glycolysis through allosteric phosphofructokinase activation due to the changes in adenine nucleotides energy charge.

The influence of serial, double plasmapheresis on blood coagulation was evaluated in two groups of plasma donors submitted from three up to 306 plasmapheretic sessions. An average of 375 or 660 ml of plasma respectively were weekly harvested from the donors. No statistically significant changes were observed in platelet count, activity of factor V and factor VIII, fibrinogen, plasminogen, alpha-2-macroglobulin, antithrombin III and prothrombin time, irrespectively of the frequency and the number of plasmapheresis. The concentration of alpha-1-antitrypsin was already increased after 7 plasmapheresis in both groups of donors. KCCT was progressively shortened with the increasing volume of harvested plasma (p 0.05) and thrombin time was prolonged (p 0.05).

Investigated were the behaviour of platelet aggregation and fibrinolytic activity of the blood, under the influence of different doses of Complamin, and its effect in vitro on platelet aggregation. We have shown that platelet aggregation diminished only slightly after intravenous injection of Complamin, but the ADP-and collagen-induced aggregation in vitro were inhibited. Except that, fibrinolytic activity in the blood had been induced, but the degree and continuance of fibrinolysis were limited depending on the patient. There was no significant modifications of examined tests after prolonged intravenous infusion of the drug.

The correlation between elevated serum lipids, shortened coagulation time, and the accelerated thrombosis measured in vivo was found in experimental animals. Elevated levels of some coagulation factors were found in samples of human hyperlipoproteinemic plasma. Experimental hypertension induced significant rise of serum cholesterol and some coagulation factors also. If thrombosis is important in the genesis of atheroclerosis, these findings could indicate that elevation of plasma lipids may play a role, via the coagulation pathway, in the production of human vascular disease. These findings encouraged us to test the group of patients with rised blood pressure and to correlate their lipid and coagulation status. Statistically significant difference between hyperlipemia and normolipemic hypertonics was seen in level of factors V and VII reduced fibrinolytic activity, decreased antithrombin III, and in higher rate of hypercoagulabilic thromboelastograms.