This model provides a total stasis environment and results in the most severe vein wall reaction to thrombosis of the models discussed.8 (link),17 (link),20 (link),23 Studies in rats suggest that after IVC ligation a combination of stasis-induced vein wall injury and enhanced tissue factor expression in endothelial cells and leukocytes produce thrombosis.42 (link) In this model, mice are anesthetized and a midline laparotomy is performed. The small bowel is exteriorized and placed on a moistened gauze pad to the animal’s left. The infrarenal IVC is identified and all side branches are ligated with nonreactive 7-0 Prolene suture. Posterior venous branches are cauterized.23 A 7-0 Prolene suture is tied down on the IVC, caudal to the left renal vein. This model has been widely used by our group for the study of venous thrombosis.8 (link),17 (link),20 (link),21 (link) It provides reproducible thrombus weights beginning at 3 hours and extending to 21 days, for most mouse strains. It has proven valuable in the study of interactions between the vein wall and thrombus during the progression from acute to chronic inflammation and remodeling of the vein wall. Disadvantages include the lack of blood flow. A technical pitfall unique to this procedure is the potential to induce initial hypotension. However, compensation by vertebral veins is observed and the survival rate for this model is around 95%, based on our laboratory’s observations. In addition, the IVC cannot reopen because of the ligature. This model cannot reproduce the clinical scenario where a thrombus is nonocclusive, but it can mimic complete occlusion (Figure 2 and Table). As a guideline, data from our laboratories in C57BL/6 mice shows, approximate thrombus weights (IVC+thrombus at harvest), of 33 mg at day 2, 29 mg at day 6, and 18 mg at day 14.