scholarly journals ALTERATIONS IN THE BLOOD COAGULATION SYSTEM INDUCED BY BACTERIAL ENDOTOXIN

1958 ◽  
Vol 107 (3) ◽  
pp. 353-367 ◽  
Author(s):  
Donald G. McKay ◽  
Sandor S. Shapiro
Keyword(s):  
Blood Coagulation ◽  
Marked Decrease ◽  
Fibrinogen Level ◽  
Normal Values ◽  
Bacterial Endotoxin ◽  
Coagulation System ◽  
Bacterial Endotoxins ◽  
Shwartzman Reaction ◽  
The One

The intravenous injection of bacterial endotoxins alter the coagulation system of rabbits' blood in vivo. Twenty-four hours after the first injection the fibrinogen level rises to twice normal values. The second injection at this time causes a 30 to 40 per cent decrease in fibrinogen content in 4 hours. Twenty hours later it again rises to twice normal values. A marked decrease in whole blood coagulation times in silicone occurs 4 hours after both injections but rises to normal values 24 hours following each injection. The circulating platelets drop from average levels of 300,000/c.mm. to 150,000/c.mm. after the first injection. The platelets remain at this low level and decrease to less than 100,000 after the second injection. During this time no fibrinolytic or fibrinogenolytic activity can be detected. Also, there is no significant change in the one stage prothrombin times or antithrombin titres. The marked decrease in circulating fibrinogen at the time when intracapillary thrombi are formed suggests that the "hyaline" thrombi of the generalized Shwartzman reaction are composed, in part, of fibrin. There appears to be a relationship between the level of circulating fibrinogen at the time of injection of bacterial endotoxin and the extent of the thrombosis. The higher the preinjection fibrinogen level, the more extensive is the thrombosis. There is also a relationship between the amount of fibrinogen loss and the extent of thrombosis after the injection. The more extensive the thrombosis the greater is the postinjection decrease in circulating fibrinogen. A comparison between the response of the hemostatic mechanism to tissue thromboplastin and bacterial endotoxin indicates that the latter acts in a unique manner and not by way of a simple "thromboplastic" activity. From the hematological standpoint, "preparation" for the generalized Shwartzman reaction is accompanied by an increased circulating fibrinogen, leukocytosis, and thrombocytopenia.

scholarly journals ANTIGEN-ANTIBODY REACTION IN THE PATHOGENESIS OF BILATERAL RENAL CORTICAL NECROSIS

1963 ◽  
Vol 117 (3) ◽  
pp. 365-376 ◽  
Author(s):  
Leung Lee
Keyword(s):  
Immune Complexes ◽  
Coagulation System ◽  
Cortical Necrosis ◽  
Renal Cortical Necrosis ◽  
Bacterial Endotoxins ◽  
Shwartzman Reaction ◽  
Soluble Immune Complexes ◽  
Antigen Antibody ◽  
Glomerular Capillaries

In the presence of reticuloendothelial blockade, the intravenous injection of a protein antigen into specifically immunized rabbits or the infusion of soluble immune complexes into normal animals has been shown to result in the production of bilateral renal cortical necrosis. The similarity in the pathogenesis of this lesion and that seen in the classical generalized Shwartzman reaction produced by bacterial endotoxins is indicated by (a) the failure of both lesions to develop in animals pretreated with large doses of heparin, (b) by the finding of "heparin-precipitable fibrinogen" in the circulation, and (c) by the presence of massive fibrin deposits within the glomerular capillaries. These findings indicate that antigen-antibody reactions in vivo are capable of activating the blood coagulation system and that the mode of action of bacterial endotoxins may have an immunological basis.

scholarly journals ALTERATIONS IN THE BLOOD COAGULATION SYSTEM INDUCED BY BACTERIAL ENDOTOXINS

1958 ◽  
Vol 107 (3) ◽  
pp. 369-376 ◽  
Author(s):  
Donald G. McKay ◽  
Sandor S. Shapiro ◽  
Jacob N. Shanberge
Keyword(s):  
Red Blood Cells ◽  
Blood Coagulation ◽  
Whole Blood ◽  
Blood Cells ◽  
Coagulation System ◽  
Coagulation Time ◽  
Hemophilic Patient ◽  
Bacterial Endotoxins

Bacterial endotoxins in vitro are capable of shortening the coagulation time of normal whole blood, native platelet-rich and platelet-poor plasma, and the blood of a hemophilic patient in silicone but not in glass. The point in the coagulation system at which the endotoxins act has not been found but the search has been narrowed by the demonstration that these materials act independently of leukocytes and red blood cells, and do not act as preformed thromboplastin or thrombin. The shortening of the coagulation time in vivo 4 hours after endotoxin injection is probably through a different mechanism than in vitro.

scholarly journals Contradictory functions of sulfatide in the blood coagulation system as coagulant and anticoagulant.

1998 ◽  
Vol 45 (2) ◽  
pp. 493-499 ◽  
Author(s):  
M Kyogashima ◽  
J Onaya ◽  
A Hara ◽  
T Taketomi
Keyword(s):  
Blood Coagulation ◽  
Thrombus Formation ◽  
Coagulation Factor ◽  
Coagulation System ◽  
Factor Xii ◽  
Blood Coagulation System ◽  
Coagulant Activity ◽  
J 13

Sulfatide (galactosylceramide I3 -sulfate) has been reported to activate blood coagulation factor XII (Hageman factor), which suggests that it exhibits coagulant activity (Fujikama et al., 1980 Biochemistry 19, 1322-1330) However, sulfatide administered into animals as a bolus shot without subsequent thrombus formation, prolonged conventional clotting times and bleeding time (Hara et al., 1996 Glycoconjugate J. 13, 187-194). These findings suggest that it may exhibit anticoagulant rather than coagulant activity. Following this suggestion we found in vitro that binding of sulfatide to fibrinogen resulted in disturbance of fibrin formation. To examine a possible pharmacological effect of sulfatide on blood coagulation in vivo we continuously infused sulfatide into rats through plastic cannulae and found formation of giant thrombi around the tips of the cannulae. These data suggest that sulfatide may exhibit contradictory functions in the blood coagulation system.

scholarly journals HOST-PARASITE FACTORS IN GROUP A STREPTOCOCCAL INFECTIONS

1960 ◽  
Vol 111 (2) ◽  
pp. 255-284 ◽  
Author(s):  
Dennis W. Watson
Keyword(s):  
Scarlet Fever ◽  
Intravenous Injections ◽  
Streptolysin O ◽  
Bacterial Endotoxins ◽  
Group A ◽  
Shwartzman Reaction ◽  
Host Parasite ◽  
Parasite Factors ◽  
Pyrogenic Activity

The factors present in streptococcal lesion extracts (SLE) which enhanced the lethal and tissue-damaging properties of Gram-negative bacterial endotoxins and streptolysin O were identified with the scarlet fever group of toxins. Toxic manifestations attributed to this group of toxins included lethality, cardiotoxic and other tissue damage, enhancement of toxicity, and pyrogenicity. Of these, the measurement of febrile response in American Dutch rabbits was the most useful parameter of toxicity. In rabbits, repeated daily intravenous injections of 0.125 Lf of a purified erythrogenic toxin immunizes specifically against the pyrogenic activity; this technique was used to type the toxins and to distinguish them from exogenous and endogenous pyrogens; non-specific pyrogens, such as streptococcal endotoxin, were not found in SLE. All types of the Lancefield Group A streptococci tested produced one or or more immunologically distinct toxins in vivo in contrast to Groups B and C which did not produce them; toxins A and B, previously distinguished by neutralization of rash-inducing activity in the skin, were produced in vivo. The A toxin was the most common, as indicated by its presence in extracts prepared with Types 28, 12, 17, and 10 (NY-5); B toxin was found in 10 (NY-5) and 19. A new toxin, designated C, was obtained from a Type 18. In American Dutch rabbits, purified toxin at a concentration of 15 Lf (900,000 STD) neither gave a Dick test nor prepared the skin for the local Shwartzman reaction; by this route, however, in contrast to classical endotoxins, they enhance the lethal and tissue-damaging properties of sublethal doses of these and other toxins. These properties of the immunologic distinct exotoxins as demonstrated in American Dutch rabbits suggest by analogy their importance in the pathogenesis of streptococcal disease in man. Evidence that might implicate them in sequelae, in addition to scarlet fever, is discussed.

scholarly journals Activation of the Coagulation System by Endotoxin in Frog (Rana Esculenta L.)

1977 ◽  
Author(s):  
G. Csåko ◽  
E. Gazdy ◽  
H. Csernyånszky ◽  
S. Toth ◽  
T. Szilågyi
Keyword(s):  
Fibrinogen Level ◽  
Lethal Effect ◽  
Rana Esculenta ◽  
Coagulation System ◽  
High Dose ◽  
Consumption Coagulopathy ◽  
Initial Value ◽  
Thrombocyte Count ◽  
E Coli ◽  
Shwartzman Reaction

The frogs, unlike mammals, are extremely resistant to the lethal effect of gram-negative endotoxins. Even injecting enormous doses we were unable to determine the DL50 value at their usual ambient temperature. The finding by Levin and Bang that endotoxin activates the coagulation in the invertebrate Limulus suggested, however, a similar effect in frogs as well. Frogs were, therefore, injected with a high dose of E. coli Olll endotoxin (Boivin). Four hours later the fibrinogen level was 30 %, the thrombocyte count 50 %, and the neutrophil count 70% lower than the initial value. By 24 hours a further drop of fibrinogen level appeared, whereas the thrombocyte and neutrophil counts started to normalize. At that time, repeating the endotoxin injection (generalized Shwartzman reaction) a decrease of all 3 parameters studied was again observable in 4 hours. When frogs were treated i.p. with high endotoxin doses 72: 72 and 48; or 72, 48 and 24 hours before blood sampling, progressively prolonged prothrombin (Quick) and thrombin times were obtained, indicating a consumption coagulopathy. (Unfortunately, reptilase times are hardly measurable in frog plasma- Blut 30: 233, 1975) Also, abnormal clotting times were found when according to the previous schedule protamine HCl, known to exert multiple effects on the coagulation system, was given frogs (50 mg/100 g). The results show that endotoxin is able to trigger, like in mammals and Limulus, the clotting mechanism in frog.

scholarly journals STUDIES OF THE EFFECT OF BACTERIAL ENDOTOXINS ON RABBIT LEUCOCYTES

1953 ◽  
Vol 98 (4) ◽  
pp. 331-348 ◽  
Author(s):  
Morgan Berthrong ◽  
Leighton E. Cluff
Keyword(s):  
Intravenous Injection ◽  
Inhibitory Effect ◽  
Buffy Coat ◽  
Single Intravenous Injection ◽  
Bacterial Endotoxins ◽  
Leucocyte Migration ◽  
Shwartzman Reaction ◽  
Local Shwartzman Reaction

Intravenous injection into rabbits of bacterial endotoxins results in an inhibition of migration of leucocytes from the buffy coat of their blood in tissue culture or in "slide cell" preparations. This effect was demonstrable 5 minutes after the intravenous injection and persisted for from 6 to 12 hours after the injection. It is as marked in rabbits receiving only a single intravenous injection of endotoxin as in those previously prepared intradermally and developing a severe local Shwartzman reaction on intravenous injection. The preparation of the skin for the Shwartzman reaction does not in itself result in appreciable changes of leucocyte migration. The production of the effect depends upon some action in vivo, since leucocytes of uninjected rabbits migrate normally from the buffy coat in plasma substrates to which large concentrations of endotoxin are added in vitro. The inhibitory effect, as observed in these experiments, also depends upon the added influence of centrifugation. Leucocytes from a rabbit receiving endotoxin intravenously migrate normally from uncentrifuged lung or spleen fragments and migrate normally in blood on the warm stage prior to centrifugation. Identical centrifugation does not affect leucocytes from uninjected animals. The heparin inhibition of the local Shwartzman reaction does not alter this effect of endotoxins on leucocytes. Its possible role in the production of leucopenia and of the local Shwartzman reaction is briefly discussed.

A Re-Appraisal of the Role of Blood Coagulation and Platelets in the Generalized Shwartzman Phenomenon

1966 ◽  
Vol 15 (03/04) ◽  
pp. 519-538 ◽  
Author(s):  
J Levin ◽  
E Beck
Keyword(s):  
Blood Coagulation ◽  
The State ◽  
Coagulation System ◽  
Renal Lesions ◽  
Intravascular Coagulation ◽  
Renal Glomeruli ◽  
Coagulation Mechanism ◽  
Shwartzman Phenomenon ◽  
Do So

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.

A Comparison of the in Vitro and in Vivo Thrombogenic Activity of Factor IX Concentrates Using Stasis (Wessler) and Non-Stasis Rabbit Models

1980 ◽  
Vol 44 (02) ◽  
pp. 081-086 ◽  
Author(s):  
C V Prowse ◽  
A E Williams
Keyword(s):  
Platelet Rich Plasma ◽  
Thrombus Formation ◽  
Factor Ix ◽  
Coagulation System ◽  
In Vitro Tests ◽  
Clinical Use ◽  
Low Activity

SummaryThe thrombogenic effects of selected factor IX concentrates were evaluated in two rabbit models; the Wessler stasis model and a novel non-stasis model. Concentrates active in either the NAPTT or TGt50 in vitro tests of potential thrombogenicity, or both, caused thrombus formation in the Wessler technique and activation of the coagulation system in the non-stasis model. A concentrate with low activity in both in vitro tests did not have thrombogenic effects in vivo, at the chosen dose. Results in the non-stasis model suggested that the thrombogenic effects of factor IX concentrates may occur by at least two mechanisms. A concentrate prepared from platelet-rich plasma and a pyrogenic concentrate were also tested and found to have no thrombogenic effect in vivo.These studies justify the use of the NAPTT and TGt50 in vitro tests for the screening of factor IX concentrates prior to clinical use.

The Natural Course of Defibrination Syndrome Caused by Echis Colorata Venom in Man

1974 ◽  
Vol 31 (03) ◽  
pp. 420-428 ◽  
Author(s):  
M Fainaru ◽  
S Eisenberg ◽  
N Manny ◽  
C Hershko
Keyword(s):  
Factor Viii ◽  
Blood Coagulation ◽  
Major Bleeding ◽  
Renal Damage ◽  
Specific Treatment ◽  
Natural Course ◽  
Factor V ◽  
Thrombocyte Count

SummaryThe natural course of defibrination syndrome caused by Echis colorata venom (ECV) in five patients is reported. All patients developed afibrinogenemia within six hours after the bite. Concomitantly a depression in factor V was recorded. Factor VIII and thrombocyte count in blood were normal in most patients. In the light of the known effects of ECV on blood coagulation in vivo and in vitro it is concluded that the afibrinogenemia is due to intravascular clotting.Four patients had transient renal damage, manifested by oliguria, azotemia, albuminuria and cylindruria, ascribed to microthrombi in the renal glomeruli.After the bite, the natural course was benign, no major bleeding was observed, and all signs of coagulopathy reverted to normal within 7 days. Therefore we recommend no specific treatment for this condition. In the case of heavily bleeding patients, administration of antiserum against ECV and/or heparin should be considered.

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