作者: K. E. Matthys , H. Bult
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摘要: Atherosclerosis is a chronic inflammatory process in the intima of conduit arteries, which disturbs endothelium-dependent regulation vascular tone by labile liposoluble radical nitric oxide (NO) formed constitutive endothelial synthase (eNOS). This defect predisposes to coronary vasospasm and cardiac ischaemia, with anginal pain as typical clinical manifestation. It now appreciated that dysfunction an early event atherogenesis it may also involve microcirculation, atherosclerotic lesions do not develop. On other hand, environment plaques result expression inducible NO (iNOS) isozyme. Whether production causal to, or of, lesion formation still highly debated. Most evidence supports hypothesis release protects against e.g. preventing smooth muscle cell proliferation leukocyte adhesion. Nitric generated isozyme be beneficial replacing failing but excessive damage wall cells, especially combination reactive oxygen intermediates.