Early changes in deep vein diameter and biochemical markers associated with thrombi formation after spinal cord injury in mice.

Spinal cord injury (SCI) is associated with the development of deep venous thrombosis (DVT) in the lower limbs and, hence, with rapidly increasing risks of cardiovascular and pulmonary complications soon after trauma. However, specific mechanisms underlying DVT formation following SCI are poorly understood. Here, we studied in mice, employing in vivo confocal microscopy, changes in deep vein size over 4 weeks after spinal cord transection (Tx). Changing levels of biochemical markers that may be associated with DVT formation were also examined. The results showed decreased concentrations of cholesterols, triglycerides, and low-density lipoprotein (LDL), but not of high-density lipoproteins (HDL) and platelets. Concentrations of creatinine, bilirubin, glucose, albumin, total protein and uric acid did not significantly change. In turn, the femoral and saphenous veins underwent a large increase (>1.5-fold) in diameter throughout the entire period studied. Overall, this study reveals that a profound change in deep vein size and, an unsuspected decrease in triglyceride and LDL levels, occur as early as at one week post-Tx in mice. This indicates, given the well-documented risk of DVT formation soon after SCI, that deep vein enlargement, but not lipoprotein level changes, may constitute an early event contributing to venous stasis and thrombi formation in paralyzed individuals.