作者: N. Lahat , S. Shapiro
DOI: 10.1016/B978-044450669-6/50007-4
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摘要: Publisher Summary Atherosclerosis is a complex and multifactorial process. The atherosclerotic lesions, which occur principally in large medium sized elastic muscular arteries, can lead to ischemia of the heart, brain or extremities, resulting infarction. Primary manifestations atherosclerosis, so-called "fatty streaks", appear already arteries developing fetus [2], are composed lipids accumulating inflammatory cells - monocyte derived macrophages T lymphocytes. While clearly abrupt clinical detrimental end process, it also be implicated induction disease. prevailing theory explaining mechanisms leading formation plaques "response injury". According this theory, initial damage may caused by variety insults including elevated oxidized low density lipoproteins, hypertension, infectious microorganisms, diabetes, genetic alternations, ischemia/reperfusion episodes with without significance. Alternative theories suggest that arterial hypoxia, whether from ischemic non-ischemic processes, involving not pathologies, primary mechanism at least very early occurrence Reperfusion tissues reoxygenation hypoxic critical for salvage repair cell injury. Paradoxically they also, temporarily, aggravate damage.