[Pathogenetic characteristics of hemostatic disorders in chronic renal failure]. / Patogeneticheskie osobennosti gemostaticheskikh narushenii pri khronicheskoi pochechnoi nedostatochnosti.

As many as 45 patients with terminal chronic renal failure (CRF) admitted to the hospital were examined for hemocoagulation and blood plasma content of medium-sized molecules (MSM). Animal (rabbit) experiments were made in vitro and in vivo to study the effect produced on hemocoagulation of MSM isolated from CFR patients' blood by acidic deproteinization, ultrafiltration and gel chromatography. Integrally, the MSM fraction was shown to exert marked anticoagulant and antiaggregation effects, to increase vascular permeability, promoting the development of hemorrhagic diathesis in CRF patients. Hemodialysis (HD) is an effective method for treating hemorrhagic diathesis of the given genesis. At the same time under the conditions of the presence of the cellular template (red blood cell hemolysis, platelet destruction as a result of HD) MSM may give rise to the development of thrombotic complications after HD completion and heparin neutralization. Therefore accumulation of MSM may play an important part in the onset of hemocoagulation disorders in patients with CRF.

[Effects of middle-weight molecules on the mechanism of hemostasis]. / Vliianie molekul srednei massy na mekhanizmy gemostaza.

Middle-weight molecules exert a marked anticoagulant effect, inhibit fibrinolysis and promote disaggregation of spontaneously aggregated blood platelets, decrease the degree of ADP-induced aggregation of blood platelets, and raise vascular permeability thus influencing the hemostatic potential of the blood. The types of the activity established are mainly detectable in the dialysed fraction of middle-weight molecules. After purification by means of dialysis the middle-weight molecule fraction promotes the formation of an active prothrombin-transforming complex without Ca++ in the presence of the matrix (tissue thromboplastin). On storage of the conserved donor's blood and plasma there occurs an accumulation of middle-weight molecule substances. This process is of moderate character, being two times more pronounced in the blood than in the plasma.

[Effect of nucleotide aggregants and anti-aggregants on the coagulation potential of blood plasma]. / O vliianii nukleotidnykh agregantov i antiagregantov na koaguliatsionnyi potentsial plazmy krovi.

The authors studied the influence of adenine and pyridine nucleotides on platelet aggregation and on the time of calcium-induced coagulation of citrate plasma, rich or poor in platelets, with deficiency of membrane fragments and its compensation with exogenous small-dispersed tissue thromboplastin. Calcium ions stimulated the conversion of small-dispersed inactive thromboplastin into a larger and more active substance. The antiaggregation agents AMP and NAD+ inhibited inclusion of phospholipid membrane fragments into the process of recalcified plasma coagulation, i.e. expressed an anticoagulant effect, while the aggregation agents (ADP, NADH) intensified their procoagulant action.

[Clinico-laboratory and pathomorphologic study of intravascular blood coagulation syndrome in experimental amniotic embolism]. / Kliniko-laboratornye i patomorfologicheskie issledovaniia DVS- sindroma pri émbolii okoloplodnymi vodami v éksperimente.

The time-course of hemocoagulative and morphological changes affected by intravenous administration of amniotic fluids was examined in experiments on Chinchilla rabbits weighing 2.0-2.5 kg. Laboratory studies revealed profound phasic changes in hemocoagulation (hyper- and hypocoagulation) which were typical of the DIC syndrome. At the same time, pronounced hemocirculatory abnormalities were pathomorphologically detected chiefly in the lung; there were also highly moderate phenomena of platelet aggregation and thrombus formation. These findings suggest that the contribution made by the demands of coagulative factors is not so significant in the pathogenesis of microcirculatory abnormalities in amniotic embolism as it is generally accepted today. The paper provides evidence for expediency of performing special investigations to elucidate the real role which the DIC syndrome plays in the pathogenesis of microcirculatory abnormalities in other diseases.