Abstract
Whether inflammatory responses are always initiated in the vessel wall, followed by secondary blood cell activation, or are initiated by activated circulating cells that trigger secondary changes in arterial structure remains unproved. In a rabbit angioplasty injury model we studied changes in aortic atherosclerotic plaque after autologous re-infusion of blood cells pre-activated in vitro with thrombin. Fluorescence spectroscopic analysis (FSA) was used to measure membrane fluidity of circulating platelets, as well as quantitative changes in collagen and elastin at the arterial inner surface. The results were correlated with atherosclerotic plaque structural characteristics. Injection of activated circulating blood cells caused a significant increase in fluorescence emission intensity (FEI) from the abdominal aorta at 450 and 500 nm 3 days later. In blood samples treated with thrombin, membrane fluidity was significantly increased compared to controls (p<0.0001). In conclusion, our results indicate that activated circulating blood cells can trigger arterial responses, acting not only as a secondary response to arterial inflammation, but also as a primary activation mechanism.