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以六十年代为界,可将有百多年历史的动脉粥样硬化发病机理研究分为二个阶段,即从“脂质渗入说”和“血栓源说”为代表的经典学说阶段和以“损伤反应假说”为代表的现代学说阶段。对斑块进行超微结构研究发现,在做为病灶最早表现的脂质条纹内就有荷脂的平滑肌细胞,在做为病灶典型代表的纤维斑块内的主要成份是平滑肌细胞(SMC),这些细胞除吞噬脂质外,还分泌大量结缔组织基质,病灶是否扩大进碱表现临床症状则取决于SMC是否继续增殖现代假说的核心则是要阐明中膜SMC怎样迁移至内膜,而且为什么继续增殖。美国华盛顿州立大学现任病理系主任Ross于1976年提出了“损伤反应假说”,并于1981年和1986年两次提出了修正。该假说基本思想
In the 1960s, the study on the pathogenesis of atherosclerosis with more than one hundred years of history can be divided into two stages, namely, the stage of classical theory represented by “lipid penetration theory” and “thrombosis theory” “Damage Response Hypothesis” as the representative of the modern doctrine stage. Ultrastructural studies of plaques revealed that liposomal smooth muscle cells were present in the lipid stripe that was the earliest manifestation of the lesion, and that the major component within the fibrous plaque, typical of lesions, was smooth muscle cells (SMCs) These cells, in addition to phagolipids, also secrete large amounts of connective tissue matrix. Whether the lesions expand into alkali to show clinical symptoms depends on whether SMC continues to proliferate The heart of the modern hypothesis is to elucidate how the mesangial SMC migrates to the intima, and why proliferation. Ross, director of the Department of Pathology at Washington State University in the United States, put forward the “damage response hypothesis” in 1976 and proposed amendments twice in 1981 and 1986. The basic idea of this hypothesis