Repositori URV

Identificador: TDX:436

Handle: https://hdl.handle.net/20.500.11797/TDX436

Autores:
Tous Màrquez, Mònica

Resumen:
Atherosclerosis, the main cause of coronary artery disease (CAD), is an inflammatory disease. It is commonly accepted that chronic inflammation, as observed in periodontal disease,lupus erythematosus, rheumatoid arthritis, or chronic bronchitis, contributes to higher mortality and morbidity from cardiovascular disease. However, experiments are needed to ascertain the long-term effects of chronic inflammation and the effect of anti-inflammatory agents onthe development and progression of atherosclerosis. It has been suggested that the use of antiinflamatory drugs could offer new opportunities for the prevention and treatment of CAD.Previous studies indicate the efficacy of aspirin and other antiplatelet drugs in reducing the risk of a serious vascular event, such as nonfatal myocardial infarction, nonfatal stroke or death from vascular diseases. These effects have been demonstrated using low-dose aspirin resulting in the permanent inactivation of a key platelet enzyme, cyclooxygenase 1 (COX-1) that mainly catalyzes the conversion of arachidonic acid into tromboxane A2 (TXA2), resulting in lower levels of TXA2, thus inhibits platelet aggregation. Higher levels of aspirin are needed to inhibit COX-2 than to inhibit COX-1. Vascular prostacyclin (PGI2) is derived predominantly from COX-2 and is less susceptible to inhibition by low doses of aspirin. Previous studies have shown that short-term administration of high doses of aspirin reduces the atherosclerotic lesion size in apolipoprotein E-deficient mice. However, to date it has not been studied the effect of long-term administration of high doses of aspirin in the apolipoprotein E-deficient mice.The results presented in this thesis show that long-term administration of high doses of aspirin does not attenuate the progressi