[The functional status of circulating lymphoid and phagocytic cells in patients with tropical malaria, living in the endemic areas of Guinea]. / Funktsional'noe sostoianie tsirkuliruiushchikh limfoidnykh i fagotsitiruiushchikh kletok u bol'nykh tropicheskoi malariei--zhitelei éndemichnykh raionov Gvinei.

The paper presents the results of a study of immunological parameters in the indigenous adult population of an endemic area of Guinea in tropical malaria of varying severity and the time course of changes in these parameters in different phases of the disease during delagil treatment. Examination of 101 patients has established that tropical malaria in re-infected patients is not accompanied by severe immunosuppression though there is a clear tendency towards lymphocytic immunodeficiency in patients with higher parasitemia and a severe course of the disease. The greatest manifestations of immunosuppression coincide with the high oxygen metabolism of phagocytes, which confirms their important role in the pathogenesis of immune disorders and common syndrome in malaria.

[Effect of heparin on the activation of the anticoagulation system by alpha-thrombin]. / Vliianie geparina na aktivatsiiu protivosvertyvaiushchei sistemy al'fa-trombinom.

Heparin-regulated alpha-thrombin ability to activate the response of the anticoagulation system has been studied by the perfusion of sinocarotid area of rabbits with DIP-alpha-thrombin-heparin complex. In a series of experiments the area was perfused with 1.8 micron DIP-alpha-thrombin and significant changes in anticoagulation parameters have been registered in systemic circulation. During perfusion of sinocarotid area by DIP-alpha-thrombin-heparin complex (2 microns) no activation of anticoagulation system was noted. DIP-alpha-thrombin-heparin perfusates contained no endogenic heparin, unlike DIP-alpha-thrombin perfusates. This confirms the absence of anticoagulation system response to DIP-alpha-thrombin. Control perfusion by heparin alone in equimolar concentrations revealed no changes in anticoagulation system. It is assumed that heparin, blocking cation subcentre of the recognition centre for high molecular compounds in the enzyme molecule, prevents the response of anticoagulation system, disturbing the enzyme ability to bind to specific receptors of the vascular walls.

[Prevention of intravascular blood coagulation in rats by DIP-alpha-thrombin administration]. / Preduprezhdenie vnutrisosudstogo svertyvaniia krovi u krys vvedeniem DIF-alpha-trombina.

The possibility of prevention of intravascular blood coagulation in rats by DIP-alpha-thrombin devoid of proteolytic activity and capable of stimulating the reaction of anticoagulation system was studied. The injection of lethal thromboplastin dose was shown to produce a sharp increase in soluble fibrin blood content, total disappearance of fibrinolytic activity and intravascular blood coagulation. The animals died of thrombosis in 90% of cases. It was established that the injection of lethal thromboplastin dose 5 min after DIP-alpha-thrombin injection caused a 13% lethality from thrombosis. No reliable changes in fibrinolytic activity and soluble fibrin content were observed. A significant increase in thrombin and recalcification time was recorded. It is suggested that DIP-alpha-thrombin prevents intravascular blood coagulation induced by lethal thromboplastin dose due to mobilization of the reserve capacities of neuro-humoral anticoagulation system.

[Heparin-induced impairment of thrombin interaction with fibrinogen and receptors of the anti-coagulation system]. / Narushenie geparinom vzaimodeistviia trombina s fibrinogenom i retseptorami protivosvertyvaiushchei sistemy.

Administration of heparin (2 un) into rats with depression of the anticoagulation system before treatment of the animals with alpha-thrombin (8 NIH un) inhibited the enzyme interaction with blood fibrinogen, which was manifested as a distinct decrease in content of soluble fibrin in blood as compared with its concentration evaluated after the treatment with thrombin. Heparin inhibited the reaction of thrombin with specific receptors in vascular walls. The effector response of the anticoagulation system, which is specific for interaction of free alpha-thrombin with the cell wall receptors, was not observed if thrombin was administered intravenously together with heparin. The patterns of the anticoagulation system were not altered after administration of the equimolar complex of DIP (diisopropyl phosphoryl)-alpha-thrombin and heparin, although free DIP-alpha-thrombin activated distinctly the anticoagulation system. The data obtained suggest that heparin, which inhibits partially the recognition site in thrombin molecule, impaired also the enzyme ability to bind to the specific receptors of vascular walls and therefore it impaired the distinct response of the anticoagulation system.

[Heparin secretion by mast cells as an index of the status of the anticoagulant system]. / Sekretsiia geparina tuchnymi kletkami kak pokazatel' sostoianiia protivosvertyvaiushchei sistemy.

The status of the mast cell population was studied and compared after administration of trypsin or alpha-thrombin in similar molar concentrations. Morphometry disclosed a substantial shift of the mast cell population towards light, heparin-free cells within one minute after alpha-thrombin administration. The index of mast cell saturation with heparin dropped below 1. The maximal heparin secretion was observed at the 5th minute of experiment. The morphometric criteria of the mast cell population returned to basal level in 120 minutes. These data along with a significant increase in the level of complex heparin compounds and plasma thrombin time indicate heparin release as a result of the effector action of the anticoagulation system. No changes were observed in the activity of complex heparin compounds and in thrombin time after intravenous injection of trypsin. It is suggested that high heparin secretion by mast cells may serve as criterion of the active status of the anticoagulation system.