Role of interleukin-2 and mononuclear cells in platelet-tumor interactions.

Interleukin-2 (IL-2) has been reported to induce mononuclear cell-dependent platelet perturbations and to reduce the incidence of metastases in rodent models. In this study, MC-1 leukemic cell-induced platelet aggregation was associated with a significant increase in thromboxane B2 (TXB2) secretion, quantified by RIA, but a decrease in leukotriene B4 (LTB-4) secretion compared to incubations of tumor cells alone. Whereas MC-1 cells also activated platelets as observed by a significant increase in scanning electron-microscopic spheroidal forms distributed throughout the platelet pool, increasing concentrations of IL-2-activated peripheral blood mononuclear cells (PBMC), but not IL-2 or PBMC alone, reversed this effect with a reduction in activated spheroidal forms. The addition of IL-2-activated PBMC to MC-1 platelet incubations inhibited platelet-tumor cell adhesion and suppressed MC-1-induced aggregation. In order to investigate the mechanism resulting in inhibition of MC-1-induced platelet aggregation, short-term PRP-MC-1 preparations were incubated with IL-2-activated PBMC and assayed for TXB2 and LTB-4 by RIA. LTB-4 levels were significantly elevated in these preparations while levels of TXB2 were significantly reduced compared with control platelet-rich plasma (PRP)-MC-1 incubations. Our results showed that inhibition of MC-1-induced platelet activation, aggregation and tumor-platelet adhesion by the addition of IL-2-activated PBMC was consequent to a cellular effect of IL-2 on PBMC. These findings may be important in understanding the observed antimetastatic effect of IL-2.

[The role of thrombocytes in blood coagulation disorders in infectious pathology]. / Rol' trombotsitov v koaguliatsionnykh narusheniiakh pri infektsionnoi patologii.

Platelets play the leading role in circulatory disorders seen in patients with infectious diseases. Endotoxinemia leads to platelet activation which shows up by the transformation of platelet forms from disk-shaped to spheroidal and by changes in aggregation and secretion. The degree of those changes correlates with the disease gravity. Experimental endotoxinemia (in vivo and in vitro experiments) demonstrated the same changes in the morphofunctional properties of platelets together with a possibility of correcting circulatory disorders by blockers of prostaglandin biosynthesis, such as indomethacin++, trental and emoxipine.

[The action of interferon and reaferon on the functional activity of human thrombocytes]. / Deistvie interferona i reaferona na funktsional'nuiu aktivnost' trombotsitov cheloveka.

The functional activity of thrombocytes (aggregation, endo- and exocytosis) and erythrocytes (aggregation) in healthy persons given a course of interferon or reaferon treatment has been studied. The results obtained in this study indicate that these preparations produce a modulating effect on the functions of thrombocytes and erythrocytes of donors having shown abnormal functional activity of these blood cells prior to the course of treatment.

[The thrombocyte-activation factor and endotoxin-induced thrombocyte activation]. / Faktor aktivatsii trombotsitov i éndotoksinindutsirovannaia aktivatsii trombotsitov.

The effect of PAF in aggregation of platelets induced by endotoxin was studied in experiments in vitro. It is indicated that in high concentration (1.10(-7)-1.10(-6) M) PAF did not affect the degree of aggregation of platelets induced by lipopolysaccharides (LPS) S. typhimurium and N. meningitidis. Successive addition to PRP LPS and PAF or joint addition of PAF and LPS did not change the degree of aggregation of each inductor or their sum. A lower concentration of PAF (1.10(-11)-1.10(-9) M) and endotoxin caused a more expressive aggregation of platelets than their successive addition. Stimulating activity of PAF on endotoxin-induced aggregation, perhaps, is caused by involvement of metabolism of arachidonic acid during blood platelets activation.

[Effect of hyperbaric oxygenation on the disease course and blood coagulation function in patients with acute viral hepatitis]. / Vliianie giperbaricheskoi oksigenatsii na techenie zabolevaniia i sostoianie gemokoaguliatsii u bol'nykh ostrym virusnym gepatitom.

The paper is concerned with an analysis of clinico-biochemical indices and 14 parameters of the plasmatic and platelet links of hemostasis in 29 patients with acute virus hepatitis of a varying degree of severity treated by hyperbaric oxygenation and in 40 controls. HBO made a modulating effect on most indices of hemocoagulation and fibrinolysis bringing them nearer to a certain standard which was optimum for a certain stage and degree of AVH. Probable mechanisms of the HBO effect on various indices of homeostasis in AVH and clinico-pathogenetic importance of the state of hemocoagulation against a background of HBO-therapy were discussed.

[Role of arachidonic acid in platelet aggregation induced by S. typhimurium endotoxin]. / K voprosu o roli arakhidonovoi kisloty v agretatsii trombotsitov, vyzvannoi éndotoksinom S. typhimurium.

The platelet aggregation reaction was used to assess the influence of arachidonic acid (AA), endotoxin (E) S. typhimurium and ADP on platelet aggregation properties. All the three substances induced platelet aggregation. A higher degree of aggregation was attained by the application of E combined with AA and ADP as compared with the effects produced by E and ADP alone. Prolonged incubation of platelet-rich plasma (PRP) samples with E led to an essential decrease of the aggregation degree on ADP addition. Incubation of PRP samples with E and ADP did not evoke any analogous decrease in the platelet aggregation degree. The data obtained indicate that AA stimulates platelet aggregation induced by E and ADP.