Effect of phospholipase A on erythrocyte and thrombocyte aggregation]

A study was made of the effect of plasmin and trypsin on the phospholipase activation, and also of the action of phospholipase A (cobra venom) on the release reaction and the erythrocyte and thrombocyte aggregation. Trypsin and fibrinolysin proved to activate phospholipase, this being accompanied by the accumulation of nonesterified fatty acids in the blood serum. Phospholipase A caused a release of the thromboplastic factor from erythrocytes and thrombocytes and their aggregation. The later is inhibited by albumin and EDTA. It is suggested that the action of the proteolytic enzymes on the blood formed elements was realized through the phospholipase activation.     

Effect of CO2 on thrombocyte aggregation in the cat

The antiaggregation ability of CO2 during ADP- and collagen-induced platelet aggregation has been discovered in cats under hypercapnia. The effect persisted after Pco2 normalization. The inhibition of cyclooxygenase by indomethacin suppressed the antiaggregation activity of CO2 in vivo but not in vitro. While estimating the regulatory role of CO2 in the metabolic control of cerebral circulation, it is also of importance to take into account the antiaggregation ability of CO2.     

Effect of tetracaine on thrombocyte aggregation and mobilization of the intracellular calcium

Tetracaine (1 mM), a local anesthetics, lowers a degree of aggregation of human thrombocytes which is induced by thrombin (0.15 u/ml) and suppresses its appearance. Aggregation of thrombocytes induced by phorbol ester, TPA (10-8 M), an activator of protein kinase C, is inhibited completely by the mentioned doses of the anesthetics. In the presence of tetracaine the release of intracellular Ca is lower to some extent, but then it surpasses the control level. It is established that under the action of ionophore A23187 tetracaine exerts no effect on mobilization of intracellular Ca2+.     

Inhibition of thrombocyte aggregation by antioxidants

The effects of antioxidants (3-hydroxypyridines, 5-hydroxypyrimidines, hindered phenols) on platelet aggregation were studied. All the compounds under study possessed low anti-aggregation activity against indometacin-sensitive aggregation (activation with arachidonic acid, 50 M). Half-maximal inhibition of aggregation was achieved at a concentration similar to that of the compounds used (10(-3) M in cases of indomethacin-insensitive aggregation, platelet activation by thrombine 1.5 mu/ml and Ca2+-ionophore A23187 1.5 g/ml). 4-methyl-2.6-ditretbutyl phenol (BHT) in the concentration range of 10(-5)-4 X 10(-5) M inhibited and in the concentration range of 4 X 10(-5)-10(-4) M activated indomethacin-sensitive aggregation. The latter effect was not observed in the absence of Ca2+ ions in the incubation medium. It is concluded that the effects of the antioxidants studied on platelet aggregation were due to their non-specific action on platelet membranes.     

Standardization of ADP-induced thrombocyte aggregation]

It is the purpose of this study to standardize platelet aggregation according to the method of Born. It was found that aggregation is influenced by the time of storage, the pH and temperature of plasma. However, there is no significant correlation between platelet number versus aggregation in healthy subjects. To get reproducible results, the plasma samples should be investigated within 2 hours after venipuncture. During storage temperature of all samples should be constant.     

Effect of thrombomodulin on specific thrombin functions: fibrinogen coagulation and thrombocyte aggregation

The effect of thrombomodulin (TM), prepared from rabbit lungs, on fibrinogen clotting and platelets aggregation by alpha-thrombin has been investigated. It has been established that TM caused a dose-dependent decrease in fibrinogen-clotting activity of thrombin (Ki = 14.7 +/- 1.24 nM). TM was shown to reduce thrombin-induced platelet aggregation but not to alter ADP-induced one. It was found that the kinetic parameters for hydrolysis of synthetic substrates by alpha-thrombin were not altered by TM.     

Mechanisms of thrombocyte aggregation in experimental hypoparathyroidism

Inhibitors of thromboxane synthetase (imidazole), cyclooxygenase (indomethacin), phospholipase A2 (Mepacrine) were used in the experiments on rabbits with experimental hypoparathyroidism to study the role of aggregation factors in the changes of ADP- and collagen-induced platelet aggregation. The enhancement of arachidonic acid metabolism and the release of platelet aggregation factor are discussed.     

Comparison of sea turtle thrombocyte aggregation to human platelet aggregation in whole blood

The endangered sea turtles are living "fossils" that afford us an opportunity to study the hemostatic process as it likely existed millions of years ago. There are essentially no data about turtle thrombocyte aggregation prior to our studies. Thrombocytes are nucleated cells that serve the same hemostatic functions as the anucleated mammalian platelet. Sea turtle thrombocytes aggregate in response to collagen and beta-thrombin. Ristocetin induces an agglutination/aggregation response indicating the presence of a von Willebrand-like receptor, GPIb, found in all mammalian platelets. Samples treated with alpha-thrombin plus gamma-thrombin followed by ristocetin results in a rapid, stronger response than ristocetin alone. These responses are inhibited by the RGDS peptide that blocks fibrinogen cross-linking of mammalian platelets via the fibrinogen receptor, GPIIb/IIIa. Three platelet-like proteins, GPIb, GPIIb/IIIa and P-selection are detected in sea turtle thrombocytes by fluorescence activated cell sorting. Turtle thrombocytes do not respond to ADP, epinephrine, serotonin, thromboxane A2 mimetic, U46619, trypsin, or alpha-thrombin and gamma-thrombin added alone. Comparison of hemostasis in sea turtles to other vertebrates could provide a framework for understanding the structure/function and evolution of these pathways and their individual components.     

Changes in erythrocyte and thrombocyte aggregation after ultraviolet irradiation

Lipid peroxidation which occurs in blood serum under ultraviolet irradiation was studied. The products of these reaction suppress ADP-induced aggregation of native platelets. The rouleaux-forming capacity increased after UV-irradiation of plasma and serum albumin. Under UV-irradiation the aggregates of albumin molecules are supposed to form the aggregates of albumin molecules which bind the erythrocytes in rouleaux.     

The effect of negatively charged liposomes on thrombocyte aggregation induced by ADP]

The incubation of platelet-rich plasma of rats with liposomes has changed cell functional activity. Lipid composition of liposomes modulated the ability of the platelets to respond to ADP. Vesicles, containing phosphatidylserine, phosphatidylinositol or stearylamine inhibited the aggregation by 70, 30 and 40%, respectively. The inhibition of aggregation by phosphatidylserine-containing liposomes was of linear and dose-dependent character. The maximal inhibition was reported at 10-min incubation of liposomes with platelets. The impairment of platelets aggregation can be explained by interactions of liposomes with plasma coagulation factors and blocking the receptors on the platelets membranes.     

Dependence of the thrombocyte aggregation reaction on plasma fibronectin and the tripeptide arginyl-glycyl-asparagilin

If was shown that the addition of fibronectin antibodies exerted the inhibition of platelet aggregation. The tripeptide RGD inhibited the platelet aggregation induced by the same agents (ADP, epinephrine, thrombin, collagen) both in blood plasma and in suspension of washed platelets.     

The effect of stabilizer composition on thrombocytes and thrombocyte function in stored whole blood. I. The thrombocyte count, thrombocyte aggregation and retraction during storage]

The behaviour of thrombocyte number and thrombocyte function aggregation and retraction in ACD, AcD-A and AcD-AG stabilized blood was examined in 18 apparently healthy test persons for a period of 9 days. On the one hand the addition of adenin or guanosin respectively increased the thrombocyte aggregation, on the other hand, however, a decrease of free, haemostatically efficient thrombocytes could be observed. Under the test conditions chosen retraction does not allow any statement to be made on the degree of the storage damage.     

Change in factor XIII activity in plasma during thrombocyte aggregation]

On addition to rat plasma, platelet-enriched, of active factor XIII (XIIIa), there occurred along with increase in the aggregation induced by ADP, a reduction in the activity of factor XIII in the plasma. Addition to the plasma of inactive factor XIII failed to influence either the degree of aggregation, or the change in the activity of factor XIII in the plasma in comparison with control samples. In platelet aggregation induced by thrombin, addition of factor XIII was accompanied by a marked fall of its activity in the plasma. In comparison with control, the extent of aggregation in this case decreased. The observed differences in the character of aggregation coursing in the presence of factor XIIIa when different aggregating agents (ADP and thrombin) were used were apparently due to the interaction of active factor XIII with thrombin added to the plasma in the capacity of an aggregating agent.