Potential function of cholesterol in blood coagulation: Amplification of phospholipid thromboplastic activity

Lipids ◽  
1971 ◽  
Vol 6 (2) ◽  
pp. 139-141 ◽  
Author(s):  
Oyvind Sorbye ◽  
Fred C. Phillips ◽  
W. O. Lundberg
Keyword(s):  
Blood Coagulation ◽  
Potential Function ◽  
Thromboplastic Activity

scholarly journals The Preparation of Plasma Thromboplastin Antecedent (PTA) and its Assay with Purified Clotting Components

Blood ◽  
1960 ◽  
Vol 15 (3) ◽  
pp. 404-412
Author(s):  
HAROLD GALLICK ◽  
L. A. HYNDMAN ◽  
K. B. MCCALL
Keyword(s):  
Human Plasma ◽  
Blood Coagulation ◽  
Barium Sulfate ◽  
Test System ◽  
Clotting Factors ◽  
Discrete Component ◽  
Deficient Patient ◽  
Thromboplastic Activity

Abstract By replacing the three crude reagents commonly used in thromboplastin generation tests—washed platelets, barium sulfate- or alumina-adsorbed plasma, and serum—with purified clotting factors, many variables and uncertainties were eliminated. It was demonstrated that plasma thromboplastin antecedent (PTA) was required for the generation of thromboplastic activity. A method was developed for the preparation of purified PTA from fraction IV-1 of human plasma. Its identity was established by its ability to correct, in vitro, the defect in the plasma of a PTA-deficient patient. Thus, further evidence in support of the belief that PTA is a discrete component, essential for blood coagulation, was obtained. More specifically, it was found to be essential in the generation of thromboplastic activity in plasma. A test system for thromboplastin generation was described which was used to assay PTA in vitro and which did not require the use of PTA-deficient plasma or serum. Omission of any one of the components of this system resulted in a marked loss of thromboplastic activity; restoration of activity was proportional to the amount of the component that was added. Thus, with this system of purified components, it was possible to assay any one of them without the use of, or requirement for, plasma or serum specimens from patients with specific coagulation deficiencies.

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

2019 ◽  
Vol 5 (3) ◽  
pp. 34-39
Author(s):  
G. Jafarova
Keyword(s):  
Blood Coagulation ◽  
Blood Clotting ◽  
Prenatal Hypoxia ◽  
Thrombin Time ◽  
Adult Rats ◽  
Long Term Effect ◽  
Thromboplastic Activity ◽  
Blood Coagulability ◽  
The Relationship

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.

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

2013 ◽  
Vol 94 (5) ◽  
pp. 755-760 ◽  
Author(s):  
V N Timerbaev ◽  
S V Kiselev
Keyword(s):  
Blood Coagulation ◽  
Molecular Mechanisms ◽  
Vascular Wall ◽  
Cellular Membranes ◽  
Initiation Mechanism ◽  
Modern Biology ◽  
Signal Systems ◽  
Contact Complex ◽  
Thromboplastic Activity ◽  
Tissue Thromboplastin

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.

Overview of Blood Coagulation

2001 ◽  
Vol 5 (1) ◽  
pp. 70-73
Author(s):  
David Green
Keyword(s):  
Blood Coagulation

Effect of experimental thyrotoxicosis onto blood coagulation – A proteomics study

2015 ◽  
Vol 122 (03) ◽  
Author(s):  
B Engelmann ◽  
J Bischof ◽  
AL Dirk ◽  
N Friedrich ◽  
E Hammer ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Experimental Thyrotoxicosis ◽  
Proteomics Study

Current perspectives in antithrombotic therapy

2001 ◽  
Vol 21 (03) ◽  
pp. 82-96 ◽  
Author(s):  
D. Hoppensteadt ◽  
O. Iqbal ◽  
R. L. Bick ◽  
J. Fareed
Keyword(s):  
Blood Coagulation ◽  
Antithrombotic Therapy ◽  
Thrombotic Event ◽  
The United States ◽  
Vascular Thrombosis ◽  
Common Cause ◽  
Coagulation Protein ◽  
Coronary Events ◽  
Platelet Defects

SummaryThrombotic disorders are the most common cause of death in the United States. About two million individuals die each year from an arterial or venous thrombosis or related disorders. About 80% to 90% of all cases of thrombosis can now be defined with respect to cause. Of these, over 50% occur in patients who harbor a congenital or acquired blood coagulation protein or platelet defect which caused the thrombotic event. It is obviously of major importance to define those individuals harboring such a defect as this allows: 1) appropriate antithrombotic therapy to decrease risks of recurrence; 2) determination of the length of time the patient must remain on therapy for secondary prevention; and 3) allow for testing of family members of those harboring a blood coagulation protein or platelet defect which is hereditary (about 50% of all coagulation and platelet defects mentioned above). Aside from mortality, significant additional morbidity occurs from both arterial or venous thrombotic events, including, but not limited to paralysis (non-fatal thrombotic stroke), cardiac disability (repeated coronary events), loss of vision (retinal vascular thrombosis), fetal waste syndrome (placental vascular thrombosis), stasis ulcers and other manifestations of post-phlebitic syndrome, etc.

Self-Damping Mechanism in Blood Coagulation

1974 ◽  
Vol 32 (01) ◽  
pp. 057-064 ◽  
Author(s):  
Y Nemerson ◽  
S.A Silverberg ◽  
J Jesty
Keyword(s):  
Tissue Factor ◽  
Blood Coagulation ◽  
Calcium Ions ◽  
Control Mechanism ◽  
Factor Vii ◽  
Damping Factor ◽  
Factor V ◽  
Factor X ◽  
Extrinsic Pathway ◽  
Two Systems

SummaryTwo reactions of the extrinsic pathway of coagulation, the activations of Factor X and prothrombin, have been studied in purified systems and shown to be self-damping. Factor X was activated by the tissue factor - Factor VII complex, and prothrombin by two systems: the coagulant protein of Taipan venom, and the physiological complex of activated Factor X, Factor V, lipid, and calcium ions. In each case the yield of enzyme, activated Factor X or thrombin, is a function of the concentration of activator. These and other observations are considered as a basis for a control mechanism in coagulation.

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