Rozhkova T A, Aripovsky A V, Yarovaya E B, Kaminnaya V I, Kukharchuk V V, Titov V N
The Federal state budget scientific institution "The Russian cardiologic R&D production complex" of Minzdrav of Russia, 121552, Moscow, Russia.
The Federal budget Institution of Science "The state research center of applied microbiology and biotechnology" of Gossanepidnadzor of Russia, Obolensk, Russia.
Klin Lab Diagn. 2017;62(11):655-665. doi: 10.18821/0869-2084-2017-62-11-655-665.
The atherosclerosis and atheromotosis are supposed to be, according to phylogenetic theory of general pathology, two etiologically different aphysiological processes, unified by community of pathogenesis. The atherosclerosis is a derangement of biological function of trophology (feeding), biological reaction of exotrophy (external feeding) and biological function of adaptation, biological reaction of compensation in response to deficiency of ῳ-3 and ῳ-6 polyenoic fatty acids. In case of deficiency of polyenoic fatty acids in cells and during synthesis of eicosanoids of group I from unsaturated endogenous ῳ-6 С20: 3 digomo-γ-linoleic unsaturated fatty acid, atherosclerosis is developed, a complex metabolism disorder in vivo. The atheromotosis is a derangement of biological function of endoecology, biological reactions of inflammation and inherent immunity. This incomplete utilization in intima of arteries of non-ligand palmitic lipoproteins of very low → low density under effect not of polyfunctional resident macrophage but monocytes of hematogenic origin without expression of acid hydrolase of polyenoic ethers of cholesterol. In intima, in area of cumulation of endogenous phlogogens (initiator of inflammation) from the pool of intra-vascular medium, polyenoic unsaturated fatty acids are cumulated that were not absorbed by cells in structure of ligand low density palmitic lipoproteins using apoB-100- endocytosis. The pathogenic factor of atherosclerosis - derangement of biological function of trophology. biological function of exotrophy under alimentary deficiency of in vivo of ῳ-3 and ῳ-6 polyenoic fatty acids with physiological parameters of feeding. The pathogenic factor of atheromotosis - phylogenetically herbivorous (carnivorous) human misusing of animal (meat) food, palmitic unsaturated fatty acids, development by hepatocytes of a large number of palmitic triglycerides and lipoproteins of very low density of the same name. The late in phylogenesis insulin-dependent lipoproteins of very low density transfer palmitic lipoproteins of very low density to cells slowly. The cells absorb them also slowly. The cumulation of non-ligand palmitic lipoproteins of very low density → low density in blood competitively blocks physiological absorption of polyenoic unsaturated fatty acids by cells in structure of physiological palmitic lipoproteins of low density. The atherosclerosis occurs blood flow and atheromotosis in intima of arteries of elastic type.
根据普通病理学的系统发育理论，动脉粥样硬化和动脉粥样变性被认为是两个病因不同的病理生理过程，它们在发病机制上具有共性。动脉粥样硬化是营养（喂养）生物学功能的紊乱、外营养（外部喂养）的生物学反应以及适应的生物学功能、对ω-3和ω-6多烯脂肪酸缺乏的代偿生物学反应。当细胞中多烯脂肪酸缺乏以及由不饱和内源性ω-6 C20:3二高-γ-亚麻酸不饱和脂肪酸合成I类二十碳烷酸时，就会发生动脉粥样硬化，这是体内一种复杂的代谢紊乱。动脉粥样变性是内生态学生物学功能的紊乱、炎症和固有免疫的生物学反应。这是在血管内介质池中的内源性致炎物质（炎症引发剂）作用下，动脉内膜中极低密度→低密度的非配体棕榈酸脂蛋白未被多功能常驻巨噬细胞而是造血来源的单核细胞完全利用，且胆固醇多烯醚酸水解酶未表达。在内膜中，在血管内介质池中内源性致炎物质积聚的区域，多烯不饱和脂肪酸积聚，这些脂肪酸未通过载脂蛋白B-100内吞作用被低密度棕榈酸脂蛋白结构中的细胞吸收。动脉粥样硬化的致病因素是营养生物学功能的紊乱。在体内ω-3和ω-6多烯脂肪酸饮食缺乏且具有生理喂养参数的情况下外营养生物学功能的紊乱。动脉粥样变性的致病因素是系统发育上食草（食肉）的人类滥用动物（肉类）食物、棕榈酸不饱和脂肪酸，肝细胞大量生成同名的棕榈酸甘油三酯和极低密度脂蛋白。系统发育后期胰岛素依赖的极低密度脂蛋白将极低密度棕榈酸脂蛋白缓慢转运至细胞。细胞对它们的吸收也很缓慢。血液中极低密度→低密度的非配体棕榈酸脂蛋白的积聚竞争性地阻断了细胞对低密度生理棕榈酸脂蛋白结构中多烯不饱和脂肪酸的生理吸收。动脉粥样硬化发生于弹性型动脉内膜的血流和动脉粥样变性。
