Background. The pathophysiologic mechanism for tissue damage in chronic venous insufficiency (CVI) is venous hypertension (VH), the primary mediator behind leukocyte trapping in tissues, we developed a new rodent model of chronic hindlimb VH to allow testing of the microvascular dysfunction that occurs in clinical CVI. Materials and methods. Hindlimb VH was created in adult rats (~350 g, male, Wistar) by ligation of the inferior vena cava, bilateral common iliac veins, and bilateral common femoral veins. In a sham group, a loose tie was placed around the same vessels. One week later, pressure catheters were placed in the right common carotid artery, right internal jugular vein (forelimb), and right superficial epigastric vein (hindlimb). Measurements were taken 15 min later, to allow for stabilization. Bilateral forelimb and hindlimb skin specimens were harvested. The myeloperoxidase (MPO) assay, an indicator of tissue leukocyte trapping, was performed using a well-described, standard technique. Results. In the chronic rats (n = 8), the hindlimb pressures (12.6 ± 3.2 mm Hg) were significantly elevated (P < 0.05) when compared to forelimb pressures (1.75 ± 0.71) and to chronic sham rat (n = 6) hindlimb (3.3 ± 1.2) pressures. There was a significant (P < 0.05) elevation of MPO activity in hindlimbs of the chronic group (32.9 ± 13.9 units) when compared to forelimbs (17 ± 11.3) and sham hindlimbs (18 ± 10.2). Conclusions. In our chronic model, as in clinical studies and previous acute investigations, we have demonstrated, using an MPO assay, an increase in the amount of cutaneous leukocytes in the hindlimbs with chronic VII but not in experimental forelimbs or sham hindlimbs or forelimbs.
- Chronic venous hypertension
ASJC Scopus subject areas