Influence of antenatal hypoxia on coagulation properties of the blood in sexual mature rats

The paper presents the results of studies on the effects of hypoxia in the antenatal period on a number of blood coagulability indicators in adult rats. It was revealed that the long-term effect of prenatal hypoxia contributes to the acceleration of certain parameters of blood clotting. The established hypercoagulable shift in the system. It was shown that at the same time the blood coagulation time and recalcification accelerated; thromboplastic activity, prothrombin and thrombin time increased, and at the same time plasma high tolerance to heparin was noted. These studies suggest that prenatal hypoxia alters the overall state of blood coagulation, where it forms a qualitatively new stereotype of the relationship between hemocoagulation and fibrinolysis factors.

The development of the blood clotting initiation conceptions: from A.A. Schmidt to D.M Zubairov

The objective of the review is to cover the formation of modern understanding of molecular mechanisms of blood coagulation initiation. It was provided mainly by the research of Professor D.M. Zubairov and his colleagues. Since 1963, he has established that blood coagulation initiation is not connected to the phenomenon of vascular wall moistening and contact complex factors activation. Research of the thromboplastic activity distribution in tissue cells, blood and in the serum phospholipid microparticles allowed to conclude that blood coagulation is initiated by long-term expression of tissue factor and rapid massive alterations in cellular membranes. This was confirmed by the detection of the turned phospholipids mesophases in tissue thromboplastin preparations and heterogeneity of vitamin К-depending factors binding. Based on the results of the research, a functional conception of blood coagulation initiation by phase alteration of bilayer structure of cellular membranes to a mesomorphic structure was developed. It is caused by different agonists through receptor dependant Са 2+-mobilizing cell signal systems or by massive migration of calcium ions into the cell at its damage. An initial bioimitating non-enzymatic proteolysis vitamin of К-dependant factors and their massive enzymatic activating in the ensembles of enzymatic complexes takes place on heterophase phospholipids surface. Clotting is limited by blood and tissue macrophages, removing cells and phospholipids particles with heterophase surface from cell circulation, and also by anticoagulant factors action. Based on this conception, the researches revealed the pathogenetic of role thrombogenic micro vesicles originating form the cellular membranes transformation in the development of disseminated intravascular coagulation syndrome, myocardial infarction, leucosis, autoimmune and infectious diseases. Finding out the basic concepts of blood coagulation initiation mechanism puts D.M. Zubairov in one row with scientists, pawning the bases of modern biology and medicine.

THE ROLE OF VARIOUS HAEMOSTASIS PARAMETERS IN MONITORING FIBRINOLYSIS WITH PRO-UROKINASE/STREPTOKINASE IN TREATMENT OF MYOCARDIAL INFARCTION

The new drug pro-urokinase, a proenzyme of urokinase (scu-PA), seems to have advantages in comparison with other fibrinolytic agents. Properties like higher fibrin specifity, non-systemic activity and lower antigenity may lead to a lower rate of complications. In a pilot study 10 patients with acute myocardial infarction have been treated under angiographical control with pro-urokinase (3-9 millions IU) by i.v. application. In case of no perfusion a further administration of streptokinase was carried on. The blood samples were obtained at therapy begin and after 5, 10, 30, 60 and 120 minutes. The therapy monitoring was performed by determination of established haemostasis parameters, like fibrinogen, fibrin(ogen)-split products (FSP), a2-antiplasmin. Plasminogen and batroxobin-time. Furthermore, the diagnostic relevance of new laboratory tests for fibrinolysis, D-Dimer and thrombin-anti thrombin Ill-complex (TAT) has been investigated considering some typical follow-ups. D-Dimer were determined by latex agglutination test and TAT by enzyme immunoassay.Generally the application of pro-urokinase in contrast to streptokinase results in minimal changes of the classic fibrinolysis parameters like fibrinogen, FSP, batroxobin-time etc. demonstrating no systemic lysis. The appearance of plasmic degradation products of cross-linked fibrin (D-Dimer) is a specific indi-cater of the release of thrombotic material. Other non-specific degradation products (fibrinogenolysis) were detected by the measurement of FSP. In some cases in which perfusion ocurred an increase of TAT followed by a rapid decrease was observed. This indicates a higher thromboplastic activity which may originate from the infarcted area producing TAT complex formation.