Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats

Asakura, Hitoshi; Suga, Yukio; Aoshima, Keiji; Ontachi, Yasuo; Mizutani, Tomoe; Kato, Minori; Saitô, Masanori; Morishita, Eriko; Yamazaki, Masahide; Takami, Akiyoshi; Miyamoto, Ken‐ichi; Nakao, Shinji

doi:10.1097/00003246-200201000-00023

Cited by 49 publications

(30 citation statements)

References 21 publications

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“…Thus, coagulation protease signaling may sustain a self-amplifying loop through direct and indirect TF induction that continues to drive the inflammatory escalation. Activation of the coagulation cascade by direct infusion of TF results in syndromes of disseminated intravascular coagulation without producing the escalating inflammation that leads to organ damage characteristic of endotoxin challenge (56). Together with the inefficiency of direct thrombin inhibitors (39), these data sup- Figure 2.…”

Section: Tf-dependent Pathways In Alimentioning

confidence: 99%

Tissue factor-dependent coagulation protease signaling in acute lung injury

Ruf

Riewald

2003

Critical Care Medicine

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The coagulation cascade signals via protease activated receptors in the tissue factor-initiation phase and downstream via the effector protease, thrombin. Bleomycin-induced acute lung injury is an example of thrombin signaling-dependent pathology. Frequently, thrombin signaling is a major contributor to inflammation in the extravascular space but intravascular thrombin signaling is a threshold-regulated event. At low concentrations, intravascular thrombin activates the protein C pathway by converting protein C (bound to endothelial cell protein C receptor) to activated protein C and this generates antiinflammatory signals along the activated protein C-endothelial cell protein C receptor-protease activated receptor 1 pathway on endothelial cells. Direct thrombin signaling only occurs when intravascular thrombin concentrations exceed a coagulant threshold. In systemic bacterial toxin-mediated inflammation, inhibition of thrombin is not sufficient to limit inflammation, whereas tissue factor inhibition interrupts a self-sustaining inflammatory escalation in acute lung injury. Therefore, in the vasculature, inflammatory signaling by the tissue factor initiation complex is favored over thrombin signaling.

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Section: Tf-dependent Pathways In Alimentioning

confidence: 99%

Tissue factor-dependent coagulation protease signaling in acute lung injury

Ruf

Riewald

2003

Critical Care Medicine

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“…Importantly such suppression of PAI-1 elevation was accompanied with higher concentration of FDP, suggesting that their fibrinolytic activities were improved. Since both animal models 14 and clinical studies 6,24 clearly showed that the enhancement of fibrinolysis is related to better outcome, elevated levels of FDP in the LPS ϩ nafamostat group in the present study suggest their beneficial prognosis.…”

Section: Discussionmentioning

confidence: 49%

“…18 In this paper, we examined whether nafamostat, a broad range protease inhibitor, may improve impaired fibrinolysis in an animal sepsis model. 14 We found that nafamostat attenuated the impairment of fibrinolysis in endotoxemia by suppressing the increase of plasma PAI-1 level.…”

Section: Discussionmentioning

confidence: 67%

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Nafamostat Attenuated the Impairment of Fibrinolysis in Animal Sepsis Model by Suppressing the Increase of Plasminogen Activator Inhibitor Type 1

Hryszko

Ihara

Mogami

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

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“…with the induced DIC model in rats) indicate that impaired fibrinolysis in conditions of ischaemia is a major pathogenetic factor for organ failure [25], which undoubtedly determines the survival of patients. On the other hand, the observation that our patients with increased levels of D-dimers and PAP were those who died early (group I) testifies to the secondary activation of fibrinolytic processes.…”

Section: Discussionmentioning

confidence: 99%

The character of haemostatic disorders and level of protein S-100 in acute ischaemic stroke can affect survival in the first week of follow-up

Jastrzębska

Chełstowski²,

Siennicka³

et al. 2011

Blood Coagulation & Fibrinolysis

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Disorders of haemostasis which result in ischaemic stroke usually appear as thromboembolism in peripheral veins and the pulmonary circulation, and to a lesser extent as coagulopathy. The S-100 protein, a marker of stroke, correlates positively with the neurological deficit National Institutes of Health Stroke Scale (NIHSS). We adopted the hypothesis that early death of patients with acute ischaemic stroke can be explained by changes in blood coagulation and fibrinolysis. The study included 84 patients hospitalized with acute ischaemic stroke. Three groups were created: I (death between 1 and 2 days), II (death between 5 and 7 days) and III (with no deaths in hospital). We measured levels of fibrinogen, antithrombin, D-dimers, plasmin-antiplasmin complexes, plasminogen and clotting times (prothrombin time and activated partial thromboplastin time), platelet number, euglobulin clot lysis time (ECLTindex) and S-100 protein, C-reactive protein and white blood cells (WBCs). Group I had lower concentrations of fibrinogen compared to groups II (3.13 vs. 4.18, P<0.01) and III (3.13 vs. 3.77, P<0.02) and higher levels of D-dimers (3643 vs. 2278, P<0.05), higher concentrations of plasmin-antiplasmin complexes (1410 vs. 882, P=0.03) and a lower ECLTindex (152 vs. 219, P<0.02) when compared with group III. Group I also had higher concentrations of protein S-100 (2.09 vs. 0.61, P<0.001), higher NIHSS (18.0 vs. 13.2, P=0.073) and number of WBC (14.1 vs. 11.1, P<0.02) than in group III. The observed abnormalities in haemostasis, either found systemically or locally as cerebral microvascular thrombosis, may be factors potentially associated with death of patients with the shortest survival time.

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Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats

Abstract: Because pathophysiology differed remarkably between the tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats, we recommend that they be assessed carefully as distinct entities to determine implications of their experimental and clinical use.

Cited by 49 publications

References 21 publications

Tissue factor-dependent coagulation protease signaling in acute lung injury

Tissue factor-dependent coagulation protease signaling in acute lung injury

Nafamostat Attenuated the Impairment of Fibrinolysis in Animal Sepsis Model by Suppressing the Increase of Plasminogen Activator Inhibitor Type 1

The character of haemostatic disorders and level of protein S-100 in acute ischaemic stroke can affect survival in the first week of follow-up

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