Reticuloendothelial Function and Blood Coagulation in Rats

1969 ◽  
Vol 22 (03) ◽  
pp. 508-512
Author(s):  
L Pechet ◽  
Giselle S. Pechet ◽  
R. A MacDonald

SummaryIntravascular coagulation and its possible effect on carbon clearance was studied in rats following the injection of commercial india ink containing shellac; a shellac-free carbon preparation; gelatin; heat denatured albumin; colloidal iron; and heparin. No relationship was found between activation of coagulation and RES function as measured by clearance of intravenously injected carbon.

1966 ◽  
Vol 15 (03/04) ◽  
pp. 519-538 ◽  
Author(s):  
J Levin ◽  
E Beck

SummaryThe role of intravascular coagulation in the production of the generalized Shwartzman phenomenon has been evaluated. The administration of endotoxin to animals prepared with Thorotrast results in activation of the coagulation mechanism with the resultant deposition of fibrinoid material in the renal glomeruli. Anticoagulation prevents alterations in the state of the coagulation system and inhibits development of the renal lesions. Platelets are not primarily involved. Platelet antiserum produces similar lesions in animals prepared with Thorotrast, but appears to do so in a manner which does not significantly involve intravascular coagulation.The production of adrenal cortical hemorrhage, comparable to that seen in the Waterhouse-Friderichsen syndrome, following the administration of endotoxin to animals that had previously received ACTH does not require intravascular coagulation and may not be a manifestation of the generalized Shwartzman phenomenon.


2010 ◽  
Vol 138 (suppl. 1) ◽  
pp. 53-58
Author(s):  
Igor Bokarev ◽  
Ludmila Popova

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.


2012 ◽  
Vol 93 (2) ◽  
pp. 364-366
Author(s):  
S V Kemerov

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.


1999 ◽  
Vol 82 (08) ◽  
pp. 718-721 ◽  
Author(s):  
Ikuro Maruyama

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.


Blood ◽  
1973 ◽  
Vol 42 (4) ◽  
pp. 499-507 ◽  
Author(s):  
Eric A. Jaffe ◽  
Ralph L. Nachman ◽  
Clarence Merskey

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.


1975 ◽  
Author(s):  
S. Coccheri ◽  
C. Testa

In a group of patients with Traumatic Brain Laceration (TBL) studies on blood coagulation and platelet function were performed in blood samples obtained during angiography from the omolateral carotid artery and jugular vein. Intraoperatory microbiopsies were also performed during neurosurgical operations in patients with TBL at different stages of evolution. In the acute stages of TBL necrosis of the endothelium and extensive micro-thrombosis with platelet material occurs in the capillaries around the damaged area. In the blood obtained from the jugular vein a fall in platelet count, platelet materials and positive paracoagulation tests can be observed.These data suggest that a process of regional intravascular coagulation occurs after TBL around the damaged area. Resulting microthrombosis may be regarded as a significant factor in the pathogenesis of acute ischemic intracellular edema in neurotraumatology.


1987 ◽  
Vol 90 (6) ◽  
pp. 313-320 ◽  
Author(s):  
Yoshiko KOSHIYAMA ◽  
Akemi KOBORI ◽  
Madoka OGIHARA ◽  
Yasuki YOKOMOTO ◽  
Kyoko OHTANI ◽  
...  

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