Induction of disseminated intravascular coagulation by endotoxin and saline loading in rats II. Fibrin deposition and removal

1975 ◽  
Vol 7 (1) ◽  
pp. 47-58 ◽  
Author(s):  
Wolfram Theiss ◽  
Peter Hilgard ◽  
Heinrich Heyes
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Fibrin Deposition ◽  
Intravascular Coagulation ◽  
Saline Loading

Fibrin Deposition and Removal in Disseminated Intravascular Coagulation Induced by Endotoxin and Saline Loading: Radioautographic Findings in Rats

1978 ◽  
Vol 40 (02) ◽  
pp. 499-511 ◽  
Author(s):  
H Heyes ◽  
W Mohr ◽  
W Theiss
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Degradation Products ◽  
Radioactive Material ◽  
Fibrin Deposition ◽  
Intravascular Coagulation ◽  
Saline Loading ◽  
Shwartzman Reaction ◽  
Kidney Liver ◽  
Kinetics Of ◽  
Glomerular Capillaries

SummaryIn rats a single injection of endotoxin followed by an infusion of normal saline induced the generalized Shwartzman reaction. The presence of disseminated intravascular coagulation (DIC) was demonstrated by measuring plasma fibrinogen, platelet counts, schistocytes, plasma haemoglobin, fibrin(ogen) degradation products, and fibrin thrombi in the glomerular capillaries. 125I-fibrinogen was given after triggering DIC in order to examine the fibrinogen turnover in plasma and the kinetics of fibrin deposition and removal in kidney, liver, and spleen. 125I-fibrinogen turnover was found to be highly accelerated. Early deposition and removal were observed in the kidneys, while a later peak with a more delayed fall of radioactivity was noted in liver and spleen. On histological examination fibrin could be seen only in the glomerular capillaries and only in the early phase of DIC. In radioautographs radioactive material was localized in the glomerular capillaries, the Kupffer’ cells of the liver, and in the perifollicular macrophages of the spleen. Comparing the results obtained by scintillation counting to those obtained by light microscopy it can be assumed that radioactivity in kidneys is correlated to fibrin deposition in glomerular capillaries and to an accumulation of fibrin(ogen) degradation products in liver and spleen.

Therapeutical Effects of Heparin and Aprotinin on Experimental Disseminated Intravascular Coagulation in the Rat

1975 ◽  
Author(s):  
H. Heyes ◽  
B. Slijepcevic ◽  
D. Glück
Keyword(s):  
Single Dose ◽  
Disseminated Intravascular Coagulation ◽  
Bolus Injection ◽  
Fibrinogen Level ◽  
Isotonic Saline ◽  
Plasma Fibrinogen Level ◽  
Fibrin Deposition ◽  
Intravascular Coagulation ◽  
Fibrin Thrombi ◽  
Fibrin Monomers

A disseminated intravascular coagulation (DIC) was induced in rats by injection of 1 mg endotoxin and subsequent infusion of isotonic saline (500 ml/kg/5 hours) over a period of 5 hours. Animals were treated beginning at the time of initial glomerular fibrin deposition with heparin (1000 IU/kg) or aprotinin (40000 KIU/kg) or heparin-aprotinin in combination (each drug as given as in single dose). The first half-dasc was given as an bolus injection 2 hours after the endotoxin injection, the second dose immediately was added to the saline infusion. The extent of DIC was controlled by several blocdparameters, histological examination of the kidneys, and by the application of 125–I-fibrinogen (given after starting DIC) and 131-I-fibrinogen (injected after beginning the therapy). By the use of two isotopes it was possible to observe the behaviour of the fibrinogen in two different phases.Heparin had clearly favorable effects stabilizing the situation of hemostasis, although the fibrinogen turnover was not normalised completely, probably due to fibrin monomers which even polymerize in presence of heparin. The beneficious effect of heparin was diminished by the addition of aprotinin which given alone had deleterious effects inhibiting the spontaneous removal of fibrin thrombi. The fibrinogen turnover was clearly enhanced supporting the concept that the plasma fibrinogen level cannot be protected by blocking the fibrinolysis which is very rarely generalized.

scholarly journals Ultramicronized Palmitoylethanolamide in the Management of Sepsis-Induced Coagulopathy and Disseminated Intravascular Coagulation

2021 ◽  
Vol 22 (21) ◽  
pp. 11388
Author(s):  
Ramona D’Amico ◽  
Francesco Monaco ◽  
Rosalba Siracusa ◽  
Marika Cordaro ◽  
Roberta Fusco ◽  
...  
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Serine Proteases ◽  
Lung Damage ◽  
Bleeding Tendency ◽  
Fibrin Deposition ◽  
Severe Condition ◽  
Intravascular Coagulation ◽  
Lung Dysfunction ◽  
Ultramicronized Palmitoylethanolamide ◽  
Inflammatory Action

Disseminated intravascular coagulation (DIC) is a severe condition characterized by the systemic formation of microthrombi complicated with bleeding tendency and organ dysfunction. In the last years, it represents one of the most frequent consequences of coronavirus disease 2019 (COVID-19). The pathogenesis of DIC is complex, with cross-talk between the coagulant and inflammatory pathways. The objective of this study is to investigate the anti-inflammatory action of ultramicronized palmitoylethanolamide (um-PEA) in a lipopolysaccharide (LPS)-induced DIC model in rats. Experimental DIC was induced by continual infusion of LPS (30 mg/kg) for 4 h through the tail vein. Um-PEA (30 mg/kg) was given orally 30 min before and 1 h after the start of intravenous infusion of LPS. Results showed that um-PEA reduced alteration of coagulation markers, as well as proinflammatory cytokine release in plasma and lung samples, induced by LPS infusion. Furthermore, um-PEA also has the effect of preventing the formation of fibrin deposition and lung damage. Moreover, um-PEA was able to reduce the number of mast cells (MCs) and the release of its serine proteases, which are also necessary for SARS-CoV-2 infection. These results suggest that um-PEA could be considered as a potential therapeutic approach in the management of DIC and in clinical implications associated to coagulopathy and lung dysfunction, such as COVID-19.

Fibrin Deposition in the Kidney and Renal Blood Flow during Intravascular Coagulation in the Rat: Influence of the Renin–Angiotensin System

1982 ◽  
Vol 62 (1) ◽  
pp. 35-41 ◽  
Author(s):  
E. Ståhl ◽  
B. E. Karlberg ◽  
L. Rammer
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Fibrin Deposition ◽  
Angiotensin System ◽  
Intravascular Coagulation ◽  
Blood Flows ◽  
Aortic Blood ◽  
Saline Loading

1. Intravascular coagulation in the kidneys of rats was induced by intravenous infusion of thrombin and by inhibition of fibrinolysis with tranexamic acid under α-chloralose anaesthesia. The amount of fibrin in the kidneys was measured with radioactively labelled fibrinogen. Chronic saline loading and inhibition of angiotensin II (ANG II) with saralasin reduced the fibrin deposition in the kidneys. Infusion of ANG II had the opposite effect. 2. Renal and aortic blood flows were measured by injection of radioactively labelled microspheres. After thrombin infusion the renal and aortic blood flows were reduced to about one-third of the pre-infusion values. Chronic saline loading diminished these changes, but saralasin had no effect. 3. Plasma renin activity (PRA), measured by radioimmunoassay, decreased by about 50% after thrombin infusion. 4. The reduction in PRA and the lack of effect of saralasin indicate that the renin—angiotensin system is not the mediator of the observed decrease in the renal blood flow. As saralasin reduced the amount of fibrin the mechanism regulating fibrin deposition appears to be independent of the mechanism that reduces the renal blood flow.

Beneficial effects of urokinase on lipopolysaccharide-induced disseminated intravascular coagulation in rats

2005 ◽  
Vol 93 (04) ◽  
pp. 724-728 ◽  
Author(s):  
Risa Asamura ◽  
Yasuo Ontachi ◽  
Tomoe Hayashi ◽  
Mika Omote ◽  
Masahisa Arahata ◽  
...  
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Plasma Levels ◽  
Plasminogen Activator Inhibitor ◽  
Fibrin Deposition ◽  
Intravascular Coagulation ◽  
Beneficial Effects ◽  
Dose Dependent Fashion ◽  
Dose Dependent ◽  
Activator Inhibitor

SummaryIn a rat model of lipopolysaccharide (LPS)-induced disseminated intravascular coagulation (DIC), we used urokinase (UK) in an attempt to clarify the role of fibrinolysis and to investigate changes in plasma endothelin levels. Two kinds of experiment were performed. The first one: experimental DIC was induced by sustained infusion of 30 mg/kg LPS for 4 h via the tail vein, and two doses of UK (2.0 or 10.0 IU/g/4.5 h) were administered to rats 30 min before infusion of LPS, after which UK infusion was continued for a further 4 h. The second one: experimental DIC was induced by sustained infusion of 1 mg/kg/10 min LPS for 10 min, and two doses of UK (2.0 or 10.0 IU/g/4 h) were administered to rats at 30 min after LPS infusion. The parameters described below were determined at 4 h in the first experiment, at 4 h and 8 h in the second one. The similar results were observed in both kinds of experiment. There were no significant differences in plasma thrombin-antithrombin complex, fibrinogen or platelet number among the three DIC groups, in both kinds of experiment. Plasma levels of D-dimer were significantly increased in the LPS + higher dose of UK group when compared with the LPS group. The increased plasma plasminogen activator inhibitor (PAI) activity seen in the LPS group was significantly suppressed in the groups receiving UK (especially higher dose of UK). In addition, the increased plasma levels of creatinine and alanine aminotransferase seen in the LPS group were significantly suppressed in the groups receiving UK (especially higher dose of UK). Plasma levels of endothelin, known to be a potent vasoconstrictive agent, were markedly elevated by LPS infusion, and were significantly suppressed in the groups receiving UK of both kinds of experiment, in a dose-dependent fashion compared with LPS group. Glomerular fibrin deposition was significantly suppressed in the groups receiving UK when compared with the LPS group. No manifestations of bleeding were observed in any of the groups. Enhanced fibrinolysis and depressed endothelin induced by UK thus appear to play an important role in preventing the development of organ failure in the LPS-induced DIC model.

Apixaban for the Treatment of Chronic Disseminated Intravascular Coagulation: A Report of Two Cases

2018 ◽  
Vol 39 (03) ◽  
pp. 294-297
Author(s):  
Snjezana Janjetovic ◽  
Katharina Holstein ◽  
Christina Dicke ◽  
Carsten Bokemeyer ◽  
Florian Langer
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Fibrin Deposition ◽  
Elderly Male ◽  
Safety And Efficacy ◽  
Vascular Abnormalities ◽  
Intravascular Coagulation ◽  
Weber Syndrome ◽  
Characteristic Features

AbstractCharacteristic features of disseminated intravascular coagulation (DIC) are the opposing risks of bleeding (due to consumptive coagulopathy and hyperfibrinolysis) and organ failure (due to widespread microvascular thromboses). The purpose of anticoagulation in DIC is to attenuate excessive thrombin generation and fibrin deposition. While heparins have been shown to be beneficial in this context, the safety and efficacy of direct oral anticoagulants have not yet been sufficiently addressed. Here, we report two patients in whom chronic DIC was stabilized upon administration of apixaban: an elderly male with aortic dissection presenting with significant mucocutaneous bleeding and a younger female with Klippel–Trénaunay–Weber syndrome presenting with multiple superficial vein thromboses (SVTs). In addition to an improvement in DIC parameters, both patients benefited clinically with resolution of bleeding symptoms and prevention of further SVTs, respectively. Oral apixaban thus showed promising safety and efficacy in the management of DIC caused by vascular abnormalities; still further investigations are needed to support these findings.

Thrombin Elaboration in Endotoxin-Induced intravascular Fibrin Deposition

1976 ◽  
Vol 36 (03) ◽  
pp. 615-622 ◽  
Author(s):  
Boguslaw Lipinski ◽  
Victor Gurewich ◽  
Elisabeth Hyde
Keyword(s):  
Venous Thromboembolism ◽  
Disseminated Intravascular Coagulation ◽  
Thrombus Formation ◽  
Anticoagulant Activity ◽  
Blood Stream ◽  
Fibrin Deposition ◽  
Quantitative Technique ◽  
Intravascular Coagulation ◽  
Fibrin Monomer

SummaryIntravascular coagulation was induced by two appropriately spaced doses of endotoxin and by infusion of thromboplastin. The resulting fibrin deposition was measured by a previously described quantitative technique. Evidence of thrombin elaboration was obtained indirectly by measurement of fibrin monomer (FM) and by the detection and isolation of a thrombin-induced anticlotting activity. Venous segments were isolated at intervals and examined for thrombus formation following 40 minutes of stasis. Endotoxin triggered thrombin elaboration was not detectable in the circulation for at least one hour and was not accompanied by any thrombosis in isolated venous segments. No thrombin elaboration was found in leukopenic rabbits given endotoxin. In the thromboplastin infused animals, the quantity of fibrin deposited in the organs was comparable to that found after endotoxin. However, thrombin was found in the blood immediately and was associated with thrombosis in the isolatet venous segments. Less thrombin-induced anticoagulant activity was found after thromboplastin than after endotoxin. The findings suggest that endotoxin-induced intravascular coagulation is probably not caused by a mechanism of systemic hypercoagulability due to the release of thromboplastic material into the blood stream. A focal process of thrombin elaboration involving leukocytes is postulated. The study is believed relevant to patients with disseminated intravascular coagulation in whom venous thromboembolism is rarely found despite evidence of extensive microvascular fibrin deposition.

Subcutaneous Heparin In Prevention Of Disseminated Intravascular Coagulation In Patients With Serious Infections

1981 ◽  
Author(s):  
K Zawilska ◽  
M Kanamicki ◽  
P Psuja ◽  
J Sowier ◽  
S Kawczynski ◽  
...  
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Degradation Products ◽  
Heparin Therapy ◽  
Fibrin Deposition ◽  
Chromogenic Substrates ◽  
Gram Negative ◽  
Intravascular Coagulation ◽  
Subcutaneous Heparin ◽  
Serious Infections ◽  
At Iii

In a series of 21 patients with serious Gram-negative and Gram-positive infections, 5000u. heparin was admini- stred subcutaneously 12-hourly with the aim of reducing the incidence of disseminated intravascular coagulation.Before starting heparin therapy there were prolongation of partial thromboplastin time; moderately increased levels of fibrinogen degradation products (FDP); decreased antithranbin III (AT III) activity (measured with chromogenic substrates); and positive paracoagulaticn tests.On heparin therapy FDP decreased and platelet count and AT III increased; and there were no clinical or laboratory signs of DIC. In those who died there were no postmortem signs of intravascular fibrin deposition.19 of the 21 patients developed septic shock. These received standard therapy as well as subcutaneous heparin. 14 patients (66%) died. There were no complicaticns with heparin therapy.In serious infections prophylactic subcutaneous heparin is advisable as early as possible.

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