scholarly journals The effects of FUT-175 (nafamostat mesilate) on blood coagulation and experimental disseminated intravascular coagulation (DIC)

1986 ◽  
Vol 40 ◽  
pp. 261
Author(s):  
Yoshiko Koshiyama ◽  
Akemi Motoyoshi ◽  
Madoka Ogihara ◽  
Yasuki Yokomoto ◽  
Kyoko Otani ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Disseminated Intravascular Coagulation ◽  
Nafamostat Mesilate ◽  
Intravascular Coagulation

scholarly journals The effects of FUT-175 (nafamostat mesilate) on blood coagulation and experimental disseminated intravascular coagulation(DIC).

1987 ◽  
Vol 90 (6) ◽  
pp. 313-320 ◽  
Author(s):  
Yoshiko KOSHIYAMA ◽  
Akemi KOBORI ◽  
Madoka OGIHARA ◽  
Yasuki YOKOMOTO ◽  
Kyoko OHTANI ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Disseminated Intravascular Coagulation ◽  
Nafamostat Mesilate ◽  
Intravascular Coagulation

scholarly journals Detection of disseminated intravascular coagulation with the help of the conception of constant intravascular microcoagulation

2010 ◽  
Vol 138 (suppl. 1) ◽  
pp. 53-58
Author(s):  
Igor Bokarev ◽  
Ludmila Popova
Keyword(s):  
Blood Coagulation ◽  
19Th Century ◽  
High Mortality ◽  
Disseminated Intravascular Coagulation ◽  
Intravascular Coagulation ◽  
Number Of Patients ◽  
Arteries And Veins ◽  
Exact Diagnosis

The possibility of intravascular blood coagulation existence in the microvascular vessels and capillaries without the presence of a large thrombus in the arteries and veins has been known from the middle of 19th century. It is impossible to know exactly about the prevalence of this pathology, because there is a jumble in terminology that does not help statistics to be exact. One of the reasons of so high mortality from disseminated intravascular coagulation (DIC) is due to the impossibility to always make exact diagnosis, and as ?. Levi thinks it is provoked in the absence of generally accepted idea of DIC syndrome. We investigated these markers and the intensity of intravascular blood coagulation in a number of patients. Our understanding of the problems of DIC was formulated on the grounds of a thirty-year study of the problem involving over 1,500 patients. Thereby, the conception of constant intravascular microcoagulation (CIMC) was developed with the following aims: to report the existing material and bring to researchers and doctors in practice information about the presence of the phenomenon of CIMC and to resolve debatable questions of definitions and practical usage of up-to-date information about DIC with the help of CIMC conception.

scholarly journals Diagnosis and treatment of disseminated intravascular coagulation syndrome

2012 ◽  
Vol 93 (2) ◽  
pp. 364-366
Author(s):  
S V Kemerov
Keyword(s):  
Blood Coagulation ◽  
Disseminated Intravascular Coagulation ◽  
Treatment Strategy ◽  
Diagnostic Algorithm ◽  
Diagnosis And Treatment ◽  
Intravascular Coagulation

Disseminated intravascular blood coagulation syndrome is a rather complex pathology, accompanied by multi-directional shifts in the overall haemostasis. This article presents the diagnostic algorithm and treatment strategy, depending on the stage of disseminated intravascular blood coagulation syndrome.

Recombinant Thrombomodulin and Activated Protein C in the Treatment of Disseminated Intravascular Coagulation

1999 ◽  
Vol 82 (08) ◽  
pp. 718-721 ◽  
Author(s):  
Ikuro Maruyama
Keyword(s):  
Endothelial Cells ◽  
Tissue Factor ◽  
Blood Coagulation ◽  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Activated Protein C ◽  
Coagulation Cascade ◽  
Regulation System ◽  
Luminal Surface ◽  
Intravascular Coagulation

IntroductionThe blood coagulation cascade is regulated by the luminal surface of the endothelial cell lining.1 Endothelial cells synthesize tissue factor pathway inhibitor (TFPI), which, in part, binds to the cell surface glycosaminoglycans and inhibits factors Xa, VIIa, and tissue factor.2 Endothelial cells also produce and exhibit thrombomodulin (TM) on their luminal surface.3 TM is a kind of thrombin receptor that forms a 1:1 complex with thrombin. In this complex, thrombin activates protein C (PC) more than 1,000-fold more than thrombin alone. TM then loses its procoagulant activities, which include fibrinogen clotting, activation of factors V and VIII, and platelet activation. Thus, TM converts thrombin from a procoagulant protease to an anticoagulant. Pathologic states, such as an endothelial injury or perturbation or continuous rapid coagulation cascade activation, overcomes the endothelial regulating activity, resulting in the development of intravascular coagulation and the induction of disseminated intravascular coagulation (DIC). Theoretically, then, supplementing soluble TM or activated PC (APC) to reconstitute the endothelial coagulation regulation system in the circulation and regulate pathologically-activated blood coagulation could be beneficial. In this chapter, application of soluble TM and APC in the treatment of DIC is reviewed.

scholarly journals Thrombotic Thrombocytopenic Purpura— Coagulation Parameters in Twelve Patients

Blood ◽  
1973 ◽  
Vol 42 (4) ◽  
pp. 499-507 ◽  
Author(s):  
Eric A. Jaffe ◽  
Ralph L. Nachman ◽  
Clarence Merskey
Keyword(s):  
Blood Coagulation ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Hemolytic Anemia ◽  
Disseminated Intravascular Coagulation ◽  
Temporal Relationship ◽  
Primary Factor ◽  
Thrombocytopenic Purpura ◽  
Intravascular Coagulation ◽  
Coagulation Abnormalities ◽  
Heparin Administration

Abstract Twelve patients with thrombotic thrombocytopenic purpura have been studied with emphasis on the changes in blood coagulation and the occurrence of disseminated intravascular coagulation (DIC). No coagulation abnormalities were found in six patients. Minimal abnormalities were present in three patients and major abnormalities compatible with DIC were present in three patients. There was little temporal relationship between the coagulation abnormalities and the clinical pathological course except for the extent of hemolysis. In addition, heparin administration in four patients had no effect on the course of the disease. Intravascular coagulation does not appear to be a primary factor in the pathogenesis of thrombotic thrombocytopenic purpura and the changes suggestive of DIC, when present, may well result from, rather than cause, the hemolytic anemia.

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