Evaluation of two experimental venous thrombosis models in the rat

Peternel, Luka; Drevenšek, Gorazd; Černe, Manica; Štalc, Anton; Stegnar, Mojca; Budihna, Marjan

doi:10.1016/j.thromres.2004.10.007

Cited by 15 publications

(11 citation statements)

References 13 publications

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“…As a relevant discrepancy to most venous thromboses in human, blood flow does not establish. Peternel et al used the stasis occlusion model in rats and found it well-suited for evaluating antithrombotic therapies (14).…”

Section: Inferior Vena Cava Stasis Occlusion Modelmentioning

confidence: 99%

Extracellular DNA—A Danger Signal Triggering Immunothrombosis

et al. 2020

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Clotting and inflammation are effective danger response patterns positively selected by evolution to limit fatal bleeding and pathogen invasion upon traumatic injuries. As a trade-off, thrombotic, and thromboembolic events complicate severe forms of infectious and non-infectious states of acute and chronic inflammation, i.e., immunothrombosis. Factors linked to thrombosis and inflammation include mediators released by platelet granules, complement, and lipid mediators and certain integrins. Extracellular deoxyribonucleic acid (DNA) was a previously unrecognized cellular component in the blood, which elicits profound proinflammatory and prothrombotic effects. Pathogens trigger the release of extracellular DNA together with other pathogen-associated molecular patterns. Dying cells in the inflamed or infected tissue release extracellular DNA together with other danger associated molecular pattern (DAMPs). Neutrophils release DNA by forming neutrophil extracellular traps (NETs) during infection, trauma or other forms of vascular injury. Fluorescence tissue imaging localized extracellular DNA to sites of injury and to intravascular thrombi. Functional studies using deoxyribonuclease (DNase)-deficient mouse strains or recombinant DNase show that extracellular DNA contributes to the process of immunothrombosis. Here, we review rodent models of immunothrombosis and the evolving evidence for extracellular DNA as a driver of immunothrombosis and discuss challenges and prospects for extracellular DNA as a potential therapeutic target.

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Section: Inferior Vena Cava Stasis Occlusion Modelmentioning

confidence: 99%

Extracellular DNA—A Danger Signal Triggering Immunothrombosis

et al. 2020

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“…In the chosen model, the venous thrombus induced by partial stasis combined with a vessel injury allows some blood flow around the formed thrombosis, and the tested drug and blood components can circulate around the thrombus because the blood flow is only partially stenosis, and this property makes the model more comparable with the clinical situation. According to Luka' study (Peternel et al, 2005), there are high associations between thrombus wet, dry or partially dry weights, so we used the thrombus wet weight as the pharmacological index to simplify the experiment procedures.…”

Section: Discussionmentioning

confidence: 99%

“…Venous thrombosis was induced by a combination of partial stasis and topical vessel injury induced by FeCl 3 , as described by Peternel et al (2005). The abdomen was opened by making an incision along the liner Alba towards the sternum, and the surface was cleared by blunt dissection between the renal and iliolumbar veins.…”

Section: Effect Of Vpa On Venous Thrombosismentioning

confidence: 99%

Total steroidal alkaloids from Veratrum patulum L. Inhibit platelet aggregation, thrombi formation and decrease bleeding time in rats

Song

Wang

Zhao

2012

Journal of Ethnopharmacology

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“…Thrombus formation was induced by a combination of complete stasis and vessel injury by ferric chloride according to the modification of the method described by Peternel et al (2005). Rats were anesthetized i.p.…”

Section: Methodsmentioning

confidence: 99%

Ir-CPI, a coagulation contact phase inhibitor from the tick Ixodes ricinus, inhibits thrombus formation without impairing hemostasis

Decrem

Rath

Blasioli

et al. 2009

Journal of Experimental Medicine

109

100

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Blood coagulation starts immediately after damage to the vascular endothelium. This system is essential for minimizing blood loss from an injured blood vessel but also contributes to vascular thrombosis. Although it has long been thought that the intrinsic coagulation pathway is not important for clotting in vivo, recent data obtained with genetically altered mice indicate that contact phase proteins seem to be essential for thrombus formation. We show that recombinant Ixodes ricinus contact phase inhibitor (Ir-CPI), a Kunitz-type protein expressed by the salivary glands of the tick Ixodes ricinus, specifically interacts with activated human contact phase factors (FXIIa, FXIa, and kallikrein) and prolongs the activated partial thromboplastin time (aPTT) in vitro. The effects of Ir-CPI were also examined in vivo using both venous and arterial thrombosis models. Intravenous administration of Ir-CPI in rats and mice caused a dose-dependent reduction in venous thrombus formation and revealed a defect in the formation of arterial occlusive thrombi. Moreover, mice injected with Ir-CPI are protected against collagen- and epinephrine-induced thromboembolism. Remarkably, the effective antithrombotic dose of Ir-CPI did not promote bleeding or impair blood coagulation parameters. To conclude, our results show that a contact phase inhibitor is an effective and safe antithrombotic agent in vivo.

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Evaluation of two experimental venous thrombosis models in the rat

Cited by 15 publications

References 13 publications

Extracellular DNA—A Danger Signal Triggering Immunothrombosis

Extracellular DNA—A Danger Signal Triggering Immunothrombosis

Total steroidal alkaloids from Veratrum patulum L. Inhibit platelet aggregation, thrombi formation and decrease bleeding time in rats

Ir-CPI, a coagulation contact phase inhibitor from the tick Ixodes ricinus, inhibits thrombus formation without impairing hemostasis

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