OBJECTIVES: The aim of our study was to correlate flow dynamics and the release of inflammatory cytokines Interleukin 1, 2, 6, TNF (Tumour Necrosis Factor) alfa, both in vitro and in vivo. MATERIALS AND METHODS: Endothelial cells were exposed to laminar flow (6dyne/cm2) in an in vitro circulatory system and the release of Interleukin 1, 2, 6 and TNF alfa was quantified by ELISA. Interleukin 1, 2, 6 and TNF alfa release was also assessed in vein grafts implanted in the arterial circulation of Lewis rats. Arterial vein grafts were explanted at different time intervals from 3days to 12weeks after surgery. Vein grafts implanted in the arterial circulation for 4weeks, were re implanted in the venous circulation of syngenic Lewis rats, and the release of Interleukin 1, 2, 6 and TNF alfa, was assessed in an organ culture. Six vein grafts (4 occluded, 2 patent) implanted in humans as femorodistal bypass were examined for the presence of myointimal hyperplasia and perigraft inflammatory cells. RESULTS: In vitro, endothelial cells exposed to laminar flow released an increased amount of Interleukin 1, 2, 6 and TNF alfa in comparison to endothelial cells not exposed to flow. In experimental vein grafts implanted in the arterial circulation there was an increased release of inflammatory cytokines associated to inflammatory changes in the adventitia. Once the vein grafts were re implanted in the venous circulation, the release of these cytokines diminished, while the inflammatory changes in the adventitia regressed. CONCLUSIONS: Increased shear stress induces release of cytokines and inflammatory changes in the adventitia. These inflammatory changes can contribute to plaque progression and to un stable plaque. These findings support the use of anti-inflammatory therapy in patients prone to develop atherosclerosis and in those who had arterial reconstructive surgery.
OBJECTIVES: The aim of our study was to correlate flow dynamics and the release of inflammatory cytokines Interleukin 1, 2, 6, TNF (Tumour Necrosis Factor) alfa, both in vitro and in vivo. MATERIALS AND METHODS: Endothelial cells were exposed to laminar flow (6dyne/cm2) in an in vitro circulatory system and the release of Interleukin 1, 2, 6 and TNF alfa was quantified by ELISA. Interleukin 1, 2, 6 and TNF alfa release was also assessed in vein grafts implanted in the arterial circulation of Lewis rats. Arterial vein grafts were explanted at different time intervals from 3days to 12weeks after surgery. Vein grafts implanted in the arterial circulation for 4weeks, were re implanted in the venous circulation of syngenic Lewis rats, and the release of Interleukin 1, 2, 6 and TNF alfa, was assessed in an organ culture. Six vein grafts (4 occluded, 2 patent) implanted in humans as femorodistal bypass were examined for the presence of myointimal hyperplasia and perigraft inflammatory cells. RESULTS: In vitro, endothelial cells exposed to laminar flow released an increased amount of Interleukin 1, 2, 6 and TNF alfa in comparison to endothelial cells not exposed to flow. In experimental vein grafts implanted in the arterial circulation there was an increased release of inflammatory cytokines associated to inflammatory changes in the adventitia. Once the vein grafts were re implanted in the venous circulation, the release of these cytokines diminished, while the inflammatory changes in the adventitia regressed. CONCLUSIONS: Increased shear stress induces release of cytokines and inflammatory changes in the adventitia. These inflammatory changes can contribute to plaque progression and to un stable plaque. These findings support the use of anti-inflammatory therapy in patients prone to develop atherosclerosis and in those who had arterial reconstructive surgery.