ABSTRACT
It is widely recognized that a chronic inflammatory state ensues during hypercholesterolemia and atherosclerosis, which is characterized by enhanced oxidative stress, endothelial dysfunction, increased endothelial cell adhesion molecule (CAM) expression, and the activation and recruitment of circulating inflammatory blood cells (leukocytes and platelets). Cytokines such as tumor necrosis factor-a (TNF-a), interferon-g (IFN-g) and interleukin-12 (IL-12), released from both
infiltrating leukocytes and endothelial cells contribute to the development of the atherosclerotic lesion (1). While it is well established that large arteries assume an inflammatory phenotype following prolonged exposure to elevated cholesterol levels, it is becoming increasingly evident that acute exposure to hypercholesterolemia also induces a similar inflammatory phenotype in the microcirculation, long before the appearance of fatty streak lesions in larger arteries. In addition, it is becomingapparent thathypercholesterolemiaalso renders themicrovasculature more vulnerable to the deleterious effects of inflammatory stimuli such as ischemia-reperfusion (I=R) (2).
