Abstract 141: Anti-thrombin Perfluorocarbon Nanoparticles Decrease Clot Burden in a Murine Model of Venous Thrombosis

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Chandu Vemuri ◽  
Batool Arif ◽  
Susannah A Grathwohl ◽  
John S Allen ◽  
Peter K Henke ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Murine Model ◽  
Safety Margin ◽  
Vena Cava ◽  
Clot Lysis ◽  
Control Group ◽  
Treatment Regimens ◽  
Significant Difference ◽  
Initial Work ◽  
Clot Burden

Objective: Venous thromboembolism (VTE) afflicts nearly an million Americans with significant mortality and long-term morbidity. Current medical treatment regimens pose significant bleeding risks and recurrence risks. The purpose of this work is to determine if anti-thrombin perfluorocarbon nanoparticles (NP-PPACK) can attenuate clot progression after vascular injury in a murine model of venous thrombosis. Methods: Male, C57 black-6 mice underwent inferior vena cava (IVC) ligation through an institutionally approved protocol. Following ligation, groups of ten mice were randomized to receive intravenous, weight-based (1 ml/kg) tail vein injections of saline, plain nanoparticles, NP-PPACK or heparin (80 units/kg). After 6 hours the animals were sacrificed, IVC with clot excised and weight and length recorded. Clot integrity (N=4) analysis was then performed by incubating clots with 750 units of streptokinase for 90 minutes at 37 degrees Celsius, removing liquid clot and recording the percent change in clot weight. Results: There was a significant difference in clot burden between NP-PPACK and the control group (0.59 mg/mm ± 0.063 vs. 1.26mg/mm ± 0.85, p=.0001). Immunofluorescent histology performed on a subgroup of animals verified nanoparticle tracking to venous thrombus. Additionally, using exogenous clot lysis as a surrogate for clot integrity, NP-PPACK treated animals exhibited a trend towards enhanced lysis over saline treatments (change in clot weight over 90 minutes: 57.8 ±14.4 vs. 21.5 ± 7.49, NP PPACK vs saline p=.067). Conclusions: This initial work demonstrates that NP-PPACK significantly decreases clot burden by local targeting and reduces clot strength in this model of VTE. We have shown previously that the system is locally active for hours against thrombosis yet produces no sustained systemic anticoagulant effect beyond 60 minutes, indicative of its significant safety margin for clinical application.

Abstract 32: Ly6C Lo Monocyte/Macrophages Are Essential for Thrombus Resolution in a Murine Model of Venous Thrombosis

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Andrew S Kimball ◽  
Cathy Luke ◽  
Qing Cai ◽  
Andrea Obi ◽  
Farouc Jaffer ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Murine Model ◽  
Inferior Vena ◽  
Tissue Injury ◽  
Vena Cava ◽  
Venous Reflux ◽  
Western Immunoblotting ◽  
Vein Wall ◽  
Wall Injury

Venous thrombosis (VT) results in vein wall injury by promoting inflammation and fibrosis leading to venous reflux, swelling, pain, and potentially, recurrent thrombosis. While prior work has shown that infiltrating leukocytes are important for VT resolution, as of yet, the precise roles of different leukocyte subsets are not well understood. Monocyte/macrophages (Mo/MΦs) are essential for the repair and resolution of tissue injury in other models, and come in inflammatory (Ly6C Hi ) or pro-resolution (Ly6C Lo ) subtypes. We hypothesized that infiltrating Mo/MΦs would be critical to VT resolution. In order to study this in vivo , we utilized a conditional macrophage depletion technique, using CD11b-DTR mice, to examine the effects of Mo/MΦs in a murine model of stasis VT by inferior vena cava ligation. Administration of 10ng/g diphtheria toxoid (DTx) every 48 hours by intra-peritoneal injection in CD11b-DTR mice resulted in an 89% and 55% decrease in circulating monocytes at 24hrs and 48hrs, respectively. When compared to saline controls, DTx injection had no effects on thrombogenic response or IVC thrombus cell populations in C57BL/6 control mice. At 8 days’ post-ligation, DTx treated CD11b-DTR mice had preferentially decreased vein wall-thrombus Ly6C Lo Mo/MΦs as compared with controls. DTx treated mice had significantly larger thrombi (1.7-fold) and less TGF-β, FSP-1, and plasminogen by western immunoblotting (all P-values ≤ 0.01). Consistent with a reduction in Ly6C Lo Mo/MΦs was a significant decrease in cellular TGF-β by intra-cellular flow cytometry. These findings suggest that Ly6C Lo Mo/MΦs are essential for normal VT resolution and may promote thrombus resolution via a plasminogen-mediated mechanism.

scholarly journals Right ventricular failure and pulmonary hypertension at recurrent thromboembolism of small branches of the pulmonary artery in cancer patients

2015 ◽  
Vol 96 (4) ◽  
pp. 492-497
Author(s):  
I A Kamalov ◽  
M G Tukhbatullin
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Venous Thrombosis ◽  
Malignant Tumors ◽  
Vena Cava ◽  
Right Heart Failure ◽  
Main Group ◽  
Control Group ◽  
Right Heart

Aim. Develop new approaches to the diagnosis of right heart failure and pulmonary hypertension in recurrent thromboembolism of small branches of the pulmonary artery in patients with malignant tumors. Methods. 83 patients with malignant tumors of various localizations were examined and followed-up. The main group included 49 patients with malignant tumors of various localizations and related venous thrombosis. The control group included 34 patients who did not have venous thrombosis. Patients in both groups underwent ultrasonography of inferior vena cava system veins and echocardiography at intervals of 3-4 days during the diagnosis and treatment of malignant tumors. Right ventricle ejection fraction and systolic pressure in the pulmonary artery were calculated at echocardiography. Results. No signs of inferior vena cava system veins thromboses, right heart failure, pulmonary hypertension were identified in patients of the control group while setting up the diagnosis and treatment of malignancies. In 38 out of 49 patients of the main group, right ventricular failure and pulmonary hypertension of varying severity were detected. The condition of 46 patients of the main group gradually improved after treating with anticoagulants. Conclusion. Recanalization of venous thrombosis is accompanied by frequent rejection of micro thrombi and embolization of small branches of pulmonary artery, causing right heart failure and pulmonary hypertension, which can be promptly detected by repeated echocardiography.

scholarly journals the NADPH Oxidase Catalytic Subunit Nox2 Displays Differential Roles in Arterial Vs. Venous Thrombosis

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 4907-4907
Author(s):  
Vijay Sonkar ◽  
Melissa J Jensen ◽  
Steven R. Lentz ◽  
Sanjana Dayal
Keyword(s):  
Nadph Oxidase ◽  
Venous Thrombosis ◽  
Platelet Activation ◽  
Vena Cava ◽  
Catalytic Subunit ◽  
Advisory Committees ◽  
Small Vessels ◽  
Fibrinogen Binding ◽  
Significant Difference

Abstract NADPH oxidase is a major superoxide generating enzyme in vascular tissues. Deficiency of the Nox2 (gp91phox) catalytic subunit of NADPH oxidase is a genetic cause of X-linked chronic granulomatous disease. These patients are prone to infection due to loss of oxidant production by neutrophils, and recent evidence suggests they also have a defect in platelet adhesion to collagen. However, the role of Nox2 in thrombosis is controversial, with one study demonstrating no effect of murine Nox2 deficiency on platelet activation and another study implicating Nox2 in platelet aggregation as well as thrombosis in small vessels. Given that Nox2 may be important for both platelet activation as well as release of neutrophil extracellular traps (NETs, a mediator of venous thrombosis), we hypothesized that genetic deficiency in murine Nox2 leads to decreased susceptibility to experimental thrombosis in both arterial and venous systems. We studied male Nox2 deficient (Cybb-/y) mice and wild type (Cybb +/y) littermates at 10-14 weeks of age. There were no differences in platelet count (921.9±33.6 x103/µl vs. 978±85.2 x103/µl), hematocrit (36.5±0.6% vs. 38.7±0.8% ) or white blood cell count (5.5±0.3 x103/µl vs. 6.1±0.6 x103/µl) between Cybb+/y and Cybb-/y mice. We next, examined platelet activation in response to thrombin (0.05 and 0.2 U/ml) or collagen (80 and 320 ng/ml) using flow cytometry. We observed similar levels of integrin α2bβ3 activation, fibrinogen binding, and intra-platelet levels of H2O2 in platelets from Cybb+/y and Cybb-/y mice after activation with either agonist, which suggests no alteration in platelet inside-out signaling due to loss of Nox2. No significant difference in susceptibility to carotid artery thrombosis in a photochemical injury model was observed between Cybb+/y and Cybb-/- mice (time to stable occlusion 21.97±4.7 vs 27.6±4.2, P>0.4). In contrast, Cybb-/y mice demonstrated significant decreases in the weight and length of venous thrombi in the inferior vena cava after 48 hours of stenosis (P<0.05). Our findings suggest that Nox2 is not a major mediator of platelet activation or arterial thrombosis but contributes to the development of venous thrombi. Future studies are warranted to examine the role of NETs and the prothrombotic effects of Nox2 in association with other cardiovascular risk factors. Disclosures Lentz: Novo Nordisk: Consultancy, Research Funding; Celgene: Equity Ownership; Opko: Membership on an entity's Board of Directors or advisory committees.

THE EFFECTS OF VASOPRESSIN ON FIBRINOLYSIS AND FACTOR VIII ARE NOT MEDIATED THROUGH V2 RECEPTORS

1987 ◽  
Author(s):  
P J Grant ◽  
K K Hampton ◽  
P G Wiles ◽  
C R M Prentice
Keyword(s):  
Factor Viii ◽  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Treated Group ◽  
Clot Lysis ◽  
Control Group ◽  
Synthetic Analogue ◽  
Control Subjects ◽  
Significant Difference ◽  
Long Acting

Vasopressin (aVP) mediates its effects on smooth muscle through V1 receptors and on the kidney via pharmacologically distinct V2 receptors. Infusions of aVP and its long acting synthetic analogue DDAVP both produce increases in factor VIII and fibrinolytic activity in man. V1 receptors are known not to mediate this effect, however it has been suggested that the FVIII response might be mediated by V2 receptors as patients with nephrogenic diabetes insipidus are reported to have no FVIII response to DDAVP. It remains unclear whether this is a true phenomenon or reflects tachyphylaxis to the high vasopressin levels found in nephrogenic diabetes insipidus. The aim of this study was to investigate whether the pharmacological V2 receptor blocker lithium alters the effect of aVP infusions on FVIII and fibrinolysis in man. 4 control subjects and 6 patients taking long term lithium therapy (mean serum lithium 1.09 mmbl/l) were infused with 2.0 units aVP over 1 hour. Samples were collected for assay of aVP, euglobulin clot lysis time (ECLT) and FVIII coagulant activity (FVIIIC) before and at the end of infusion. In the control subjects median aVP rose from 0.5 to 83 pg/ml at the end of infusion. FVIIIC rose frcm 100 to 333% and plasminogen activator activity (PAA: 106 /ECLT) from 198 to 437 units. In the lithium treated group median aVP rose frcm 0.5 to 68 pg/ml at the end of infusion. FVIIIC rose from 100 to 263% and PAA from 102 to 453 units. There was a significant correlation between the plasma aVP and FVIIIC (r = 0.89 p < 0.005) and PAA (r = 0.92 p < 0.001) in the control group and the lithium treated group (FVIIIC r = 0.81 p < 0.002; PAA r = 0.69 p < 0.02). There was no significant difference between the rise in either FVIIIC or PAA in the lithium treated group compared with controls. These results do not support the hypothesis that the action of aVP on FVIII or fibrinolysis is mediated by V2 receptors. The effects of aVP on haemostasis may either be mediated directly through a third class of receptor or indirectly by the release of an intermediate hormone.

In Vivo Monitoring of Venous Thrombosis In Mice Using Ultrasonography

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4214-4214
Author(s):  
Meghedi Aghourian ◽  
Catherine Lemarie ◽  
Mark Blostein
Keyword(s):  
Venous Thrombosis ◽  
Murine Model ◽  
Conflicts Of Interest ◽  
Genetically Modify ◽  
Vena Cava ◽  
Venous Stasis ◽  
Clinical Aspects ◽  
Reliable Technique ◽  
Over Time

Abstract Abstract 4214 Deep venous thrombosis is an important cause of morbidity and mortality in clinical medicine. There has been extensive research dedicated to the clinical aspects of venous thrombosis, especially with regards to its diagnosis and treatment. However, animal models studying this phenomenon are scarce and, in most cases, very crude, relying on sacrificing animals to excise the formed thrombi. Developing an in vivo murine model of venous thrombosis, detecting and monitoring thrombi non-invasively as is done in humans can be a powerful tool given our ability to genetically modify the murine genome. Therefore, we developed such a murine model using the Vevo770®, a microimaging ultrasound system previously developed to study the arterial circulation of mice. Two different thrombosis models were employed to generate clots in the inferior vena cava (IVC) of wild type C57Bl6 mice: 1) ligation of the IVC to generate venous stasis and 2) application of Ferric Chloride (FeCl3) to the outer layer of the IVC to injure the endothelium. Using both of these techniques, adequate thromboses were generated in the IVCs of mice as determined pathologically. Other mice were allowed to recover after surgery, and the development of venous thrombosis was assessed by ultrasonography using the Vevo 770®. In order to assess the precision of clot measurements using this novel technique, we then sacrificed the mice and excised the clots. In both models, the measurement of the clot pathologically correlates favorably (R2= 0, 9116 for the ligation model, and R2 = 0,905 for the FeCl3 model) with measurements done by ultrasonography (n=20 for the ligation model, and n=5 for the FeCl3 injury model). In the ligation model, a thrombus develops less than an hour after ligation of the IVC, and the size of the clot increases over time. For example, five hours after the ligation of the IVC, a clot develops and has a cross sectional area of 4,5 mm2. The clot size increases significantly (p=0.001) over time to 6.2 mm2 at 24 hours post ligation (n=20). Treatment of these mice with an anticoagulant (dalteparin at a dose of 200 u/kg) prior to the procedure prevented the development of IVC thrombosis as determined by ultrasonagraphy. These data suggest that the Vevo770® can be used as a reliable technique for the non-invasive assessment of venous thrombosis in mice. Developing a murine model for thrombosis using more accurate, and clinically more relevant techniques such as ultrasonography, is a step towards better understanding the pathophysiology of venous thromboembolism. Figure 1. Clot length correlation using histology and ultrasonography, 24 hrs post ligation of the IVC in 20 mice. R2= 0,9116. Figure 1. Clot length correlation using histology and ultrasonography, 24 hrs post ligation of the IVC in 20 mice. R2= 0,9116. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Comparison of Enoxaparin and Rivaroxaban in the Prophylaxis of Deep Venous Thrombosis in Arthroplasty

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Necati Çiçek ◽  
İsmail Ağir ◽  
Hacı Bayram Tosun ◽  
Abuzer Uludağ ◽  
Abdulkadir Sari
Keyword(s):  
Pulmonary Embolism ◽  
Postoperative Complications ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Ease Of Use ◽  
Group Iii ◽  
Treatment Regimens ◽  
Group I ◽  
Significant Difference ◽  
Subcutaneous Enoxaparin

Background. Pulmonary embolism is a serious early complication of arthroplasty procedures that can develop after deep venous thrombosis. The present study aimed to compare rivaroxaban and enoxaparin in terms of preventing DV and PE, and also in this study, we compared the complications due to these drugs in patients undergoing elective arthroplasty. Materials and Methods. 214 patients were divided into three groups based on their treatment regimens. In group I, enoxaparin was used, in group II, rivaroxaban was used, and in group III, enoxaparin was used throughout hospitalization, and after hospital discharge, rivaroxaban was used. These three groups were compared according to the occurrence of deep venous thrombosis, pulmonary embolism, and major and minor complications. Results. Major postoperative complications occurred in 5, 15, and 6 patients in group I, II, and III, respectively. Minor postoperative complications occurred in 10, 24, and 11 patients in group I, II, and III, respectively. No significant difference was found among the three groups. Deep venous thrombosis or pulmonary embolism was not observed in any patient. Conclusion. Rivaroxaban was found to be as effective as enoxaparin in the prevention of deep venous thrombosis and other complications after arthroplasty. Moreover, oral rivaroxaban provided greater ease of use compared to subcutaneous enoxaparin. Based on these findings, we consider that rivaroxaban could be an effective alternative to enoxaparin.

Abstract 36: Alpha 2-antiplasmin Prevents the Resolution of Deep Vein Thrombosis

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Satish Singh ◽  
Aiilyan K Houng ◽  
Samantha Howard ◽  
B Tyler Emerson ◽  
Guy L Reed
Keyword(s):  
Venous Thrombosis ◽  
Vena Cava ◽  
Relative Effect ◽  
Vein Thrombosis ◽  
Significant Difference ◽  
Tissue Plasminogen ◽  
Deep Vein ◽  
Metalloproteinase 9 ◽  
One Way Anova

Introduction: Deep venous thrombosis is a major cause of death and disability. Despite anticoagulation treatment, venous thrombi persist for months, causing chronic venous obstruction, inflammatory remodeling and post-thrombotic syndrome. The mechanisms responsible for impaired clearance of venous thrombi are poorly understood. Alpha 2-antiplasmin (a2AP) is the primary physiological inhibitor of plasmin and a key regulator of the fibrinolytic pathway. The role of a2AP in the resolution of venous thrombosis has not been determined. Hypothesis: We tested the hypothesis that a2AP prevents the resolution of experimental deep venous thrombi. Methods and Results: Thrombus resolution and content were examined in a2AP +/+ and a2AP -/- mice using a well-established, fibrinolytic-resistant, stasis model induced by ligation of the inferior vena cava (IVC). Thrombus weight and composition were determined after 7 days. Data was analyzed by one-way ANOVA with Neumann-Keul’s correction. Thrombus weight was reduced in a2AP -/- mice by >90% when compared to a2AP +/+ mice (p<0.001); there was no significant difference between a2AP -/- mice and shams. Histochemical and immunofluorescence staining showed significant reductions in IVC fibrin content, neutrophil recruitment and matrix metalloproteinase-9 expression in a2AP -/- mice (p<0.001) vs. a2AP +/+ mice. The relative effect of plasminogen activation and a2AP on resolution of preformed venous thrombi was examined in wild-type a2AP +/+ mice treated 24 h after IVC ligation with tissue plasminogen activator (TPA) (1.2 or 5 mg/kg) or a monoclonal antibody inactivating a2AP (10 mg/Kg). By comparison to 7 day old venous thrombi in untreated mice, treatment with TPA at 1.2 mg/kg or 5 mg/kg did not decrease thrombus size after 7 days. In contrast, a2AP inactivation significantly reduced thrombus weight vs. untreated and TPA-treated mice (p<0.01 to p<0.001). Conclusions: In experimental venous thrombosis, a2AP was required for the persistence of venous thrombi 7 days after formation. Venous thrombi resisted TPA, but were sensitive to resolution after a2AP inactivation. This suggests that a2AP may be responsible for the persistence of clinical venous thrombosis in humans.

Study of a new benzimidazole derivative having in its structure a sterically hindered phenolic substituent on models of arterial and venous thrombosis

2020 ◽  
Author(s):  
А.А. Спасов ◽  
А.Ф. Кучерявенко ◽  
К.А. Гайдукова ◽  
В.С. Сиротенко ◽  
О.Н. Жуковская
Keyword(s):  
Venous Thrombosis ◽  
Arterial Thrombosis ◽  
Benzimidazole Derivative ◽  
Vena Cava ◽  
Male Rats ◽  
Control Group ◽  
Vena Cava Inferior ◽  
Antithrombotic Activity ◽  
Thrombosis Model ◽  
Venous Thromboses

Введение: Тромбоциты являются ключевыми медиаторами патогенеза артериальных тромбозов и атеросклероза. Поэтому изучение антиагрегантных средств на предмет антитромботической активности на различных моделях артериальных и венозных тромбозов является актуальным. Цель исследования: изучение антитромботической активности соединения РУ-1144 (производного бензимидазола) в сравнении с ацетилсалициловой кислотой (АСК) и клопидогрелом на моделях артериального и венозного тромбозов. Материалы и методы: Артериальный тромбоз моделировали на сонной артерии крыс-самцов аппликацией постоянного электрического тока. Воздействие на сосуд выполняли до момента полной окклюзии, регистрируемой на мониторе доплерографа. Венозной тромбоз моделировали на крысах-самцах полной перевязкой нижней полой вены на 24 ч; через сутки проводили изъятие тромба из сосуда и его взвешивание. В экспериментальных группах животным внутрижелудочно вводили соединение РУ-1144 и препараты сравнения — АСК и клопидогрел, в контрольной группе животным внутрижелудочно вводили дистиллированную воду. Для подтверждения отсутствия влияния хирургических манипуляций на организм животного в исследование модели венозного тромбоза была включена группа ложнооперированных крыс. Результаты: На модели артериального тромбоза установлена более высокая антитромботическая активность соединения РУ-1144 по сравнению с АСК и клопидогрелом в 2,5 и 7,4 раза соответственно. В модели венозного тромбоза соединение РУ-1144 уменьшало среднюю массу венозных тромбов в 5,3 раза по сравнению с группой контроля и превосходило по антитромботической активности АСК и клопидогрел в 3,5 и 1,9 раза. Заключение: Соединение РУ-1144 способно предотвращать патологические процессы, связанные с тромбообразованием, не только в сонной артерии, но и в нижней полой вене. Background: Platelets are key mediators of the pathogenesis of arterial thrombosis and atherosclerosis. So, that is actual to study antithrombotic activity of antiplatelet agents in various models of arterial and venous thromboses. Objectives: to study the antithrombotic activity of RU-1144 compound (benzimidazole derivative) as compared with acetylsalicylic acid (ASA) and clopidogrel on models of arterial and venous thromboses. Materials/Methods: Arterial thrombosis was modeled on the carotid artery of male rats by application of direct electric current. Exposure was performed until full vessel occlusion recorded by Dopplerograf. Venous thrombosis was modeled on male rats by complete ligation of vena cava inferior for 24 hours; a day later the thrombus was removed from the vessel and weighed. In the experimental groups the animals were injected intragastrically with the compound RU-1144 and the comparison drugs — ASA and clopidogrel; in the control group the animals were administered distilled water intragastrically. To confirm the absence of the effect of surgical manipulations on the animal’s organism, a group of false-operated rats was included in the study of venous thrombosis model. Results: In arterial thrombosis model RU-1144 compound had a higher antithrombotic activity as compared with ASA and clopidogrel by 2.5 and 7.4 times, respectively. In venous thrombosis model RU-1144 compound reduced the average weight of venous clots by 5.3 times as compared with the control group and exceeded antithrombotic activity of ASA and clopidogrel by 3.5 and 1.9 times. Conclusions: RU-1144 compound capable to prevent the pathological processes associated with thrombus formation in carotid artery as well as in vena cava inferior.

In Vivo Monitoring of Venous Thrombosis in Mice.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 5061-5061
Author(s):  
Meghedi Aghourian ◽  
Mark Blostein
Keyword(s):  
Venous Thromboembolism ◽  
Venous Thrombosis ◽  
Murine Model ◽  
Conflicts Of Interest ◽  
Vena Cava ◽  
Reliable Technique ◽  
Non Invasive ◽  
Post Surgery ◽  
Ultrasound Technology

Abstract Abstract 5061 Venous thromboembolism afflicts 117 people per 100,000 each year and is an important cause of morbidity and mortality. There has been extensive research dedicated to the clinical aspect of venous thrombosis, especially with regards to its diagnosis and treatment. However, animal models studying this phenomenon are scarce and, in most cases, very crude. Developing a murine model of venous thrombosis using techniques similar to the ones used to detect thrombosis in humans can be a constructive step in studying this phenomenon in more detail. The model developed in our lab uses ultrasound imaging to visualize venous clots in the Inferior Vena Cava (IVC) of mice, allowing for precise measurements of the formed clot. Ligation of the IVC is one of the well established models for studying thrombosis in mice. We ligated the IVC of wild type C57B6 mice, and allowed them to recover. We then followed clot formation at several time points after the operation using micro-ultrasonography, the Vevo 770®, a novel imaging ultrasound technology designed to monitor murine vasculature. To assess the precision of the clot measurements, we then sacrificed the mice, and dissected out the thrombi in order to precisely measure and weigh them. A thrombosis develops only after 5 hours of ligation post surgery when a clot is visualized in the IVC. The clot increases slightly over the next 24 hours. The measurements of the clot after dissection correlates favourably with the measurements done by ultrasonagraphy using the Vevo770®. These data suggest that the Vevo770® can be used as a reliable technique for non-invasive assessment of venous thromboembolism in mice. Developing a murine model for thrombosis using more accurate, and clinically more relevant techniques such as ultrasonography, is a step towards better understanding and treatment of venous thromboembolism. Disclosures No relevant conflicts of interest to declare.

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