[A method for studying intravascular platelet aggregation in vitro]. / Sposob issledovaniia vnutrisosudistoi aggregatsii trombotsitov in vitro.

A simple available method for evaluating intravascular platelet aggregation is proposed. It consists in graphic recording of disaggregation of platelet-rich citrate plasma, which indicates the degree of intravascular aggregation. Intravascular aggregation is notably increased in coronary patients and negligible in normal subjects. The method may be used for the diagnosis of diseases with a high thrombogenic risk.

[A graphic method of determining plasminogen]. / Graficheskii metod opredeleniia plazminogena.

The author suggests a graphic method for plasminogen estimation. The euglobulin fraction lysis is recorded in the hemocoagulographer cuvette, this essentially improving the accuracy of studies.

[Clinical value of studying fibrinogen degradation products in patients with ischemic heart disease]. / Klinicheskoe znachenie issledovaniia produktov degradatsii fibrinogena u bo'lnykh ishemicheskoi bolez'niu serdtsa.

Study of fibrinogen degradation products in patients with angina pectoris and acute myocardial infarction proved to be of clinical importance. Their content in patients with acute myocardial infarction was increased more considerably than that in patients with angina pectoris. This parameter can be used for the differential diagnosis of angina pectoris and acute myocardial infarction.

[Immunologic diagnosis of intravascular blood clotting and intravascular thrombus formation among patients with ischemic heart disease]. / Immunologicheskaia diagnostika vnutrisosudistogo svertyvaniia krovi i vnutrisosudistogo tromboobrazovaniia u bol'nykh ishemicheskoi bolezn'iu serdtsa.

Rabbit plasmas immune to fibrinogen/fibrin and thrombin, with antibody titres of 1:1024, were obtained by rabbit immunization with fibrinogen and thrombin. Immunologic methods were shown to be capable of detecting thrombinemia and increased fibrinogen/fibrin levels, as well as reduced titres of anti-thrombin and anti-fibrinogen/fibrin antibodies, i. e. the presence of intravascular coagulation and thrombogenesis in the circulating blood. These changes are particularly pronounced in coronary patients during the first days of acute myocardial infarction and in those with thromboembolic complications of varying localization. Patients with unstable angina also show reduced titres of antithrombin and antifibrinogen/fibrin antibodies, as compared to clinically normal subjects; yet the reduction here is less marked than the one observed during the first days of acute myocardial infarction.

[Effect of lipoproteins of different classes on platelet aggregation]. / Vliianie lipoproteidov razlichnykh klassov na agregatsiiu trombotsitov.

The influence of high-, low- and very-low-density lipoproteins on platelet aggregation was examined in coronary patients and normal subjects. Preincubation with high-density lipoproteins was shown to drastically inhibit platelet aggregation capacity both in normal subjects and coronary patients. Preincubation with a mixture of low- and very-low-density lipoproteins had no significant effect on platelet aggregation. The suppression of platelet aggregation by high-density lipoproteins was the most obvious in washed platelets.

[Interrelationship of lipid metabolic disorders and hemostasis in arteriosclerosis]. / Vzaimosviaz' narushenii lipidnogo obmena i gemostaza pri ateroskleroze

Proceeding from the obtained data, the authors conclude that two factors are of paramount importance in the pathogenesis of atherosclerosis: 1) lipid infiltration, 2) fibrin and platelets deposits on the vascular wall. It seems hardly proper to oppose the lipid-infiltrationab of pathogenesis of atherosclerosis to the thrombogenic one, since they do not necessarily exclude one another. Moreover, they seem to present two aspects of a single process: on the one hand, lipids increase platelet adhesion and aggregation on the vascular wall; on the other hand, platelets during aggregation help the penetration of beta-lipoproteins into the arterial wall by increasing the permeability of the endothelium and by adsorbing cholesterol-rich beta-lipoproteins on their own surface. A vicious circle occurs that must underly one of the mechanisms of the atherosclerosis development.