Abstract
In humans, aging is associated with endothelial dysfunction and an increased risk of venous thromboembolism. Although intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) at a ratio of 6:1 by old rats improved the endothelial dysfunction in arteries, the impact on veins remains unclear. Eight-month-old male Wistar rats were either untreated or orally administered corn oil, EPA:DHA 1:1, or EPA:DHA 6:1 (500 mg/kg/d) for seven days. Vascular reactivity was studied by myography. In middle-aged femoral artery rings, acetylcholine caused a partial relaxation at low concentrations and a contractile response at high concentrations, whereas in the old femoral vein only a partial relaxation was observed. The EPA:DHA 6:1 treatment blunted the contractile response to acetylcholine in the middle-aged femoral artery and both EPA:DHA 6:1 and 1:1 increased the relaxation to acetylcholine in the old femoral vein. No such effects were observed with corn oil. Both the non-selective cyclooxygenase inhibitor indomethacin and the COX-1 inhibitor SC-560 increased the relaxation to acetylcholine in the middle-aged femoral artery whereas the COX-2 inhibitor NS-398 increased that in the middle-aged femoral vein. In conclusion, our results indicate that aging is associated with an endothelial dysfunction in the femoral artery and vein, which can be improved by EPA:DHA 6:1 treatment—most likely via a cyclooxygenase-dependent mechanism.
Highlights
Venous thromboembolism (VTE), which includes deep vein thrombosis and pulmonary embolism, is a major cause of cardiovascular mortality [1,2]
A similar contractile response to ACh at concentrations greater than 3 μM was observed in the corn oil group and the eicosapentaenoic acid (EPA):docosahexaenoic acid (DHA) 1:1 group, whereas the contractile response was significantly smaller in the EPA:DHA 6:1 group (Figure 1)
The present findings indicate that in middle-aged rats, endothelial dysfunction was observed in both the femoral artery and vein
Summary
Venous thromboembolism (VTE), which includes deep vein thrombosis and pulmonary embolism, is a major cause of cardiovascular mortality [1,2]. The identification of other risk factors for venous thrombosis remains a major issue in the prevention of VTE and its recurrence, and they are key determinants for the treatment intensity and duration [3]. Up to 50% of VTEs remain unprovoked and lead to long-term anticoagulation therapy which exposes patients to an increased hemorrhagic risk [5,6,7,8]. Almost one-third of patients are exposed to VTE recurrence within 10 years in spite of the long-term anticoagulation therapy [9]. As VTE and bleeding risk increase with age, new therapeutic approaches for the prevention of VTE are needed [11]
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