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人们发现高血压能促进和加重动脉粥样硬化已有50年的历史,然而对其机制的阐述却一直是众说纷坛。正常状态下,进入动脉壁的脂蛋白量与通过动脉壁的输出量是保持动态平衡的。从理论上讲,高血压造成脂蛋白进入动脉壁的量增多或输出量减少都可能增加脂蛋白在动脉壁内的潴留,从而促进动脉粥样硬化。但是目前关于高血压引起脂蛋白从动脉壁输出减少而促进粥样硬化的机制是不明确的,且这方面的报告极少。本文目的试图从结构改变入手,通过确定高血压时动脉壁(包括肺动脉)自身结缔组织变化及其与脂质分布的关系,从而为探讨高血压促进动脉粥样硬化的机制提供新的依据。
It has been 50 years since hypertension was found to promote and aggravate atherosclerosis. However, the explanation of its mechanism has always been a fallacy. Under normal conditions, the amount of lipoproteins entering the arterial wall and the amount of output passing through the arterial wall are maintained homeostasis. Theoretically, the increase in the amount of lipoproteins that enter the arterial wall caused by hypertension or the decrease in output may increase the retention of lipoproteins in the arterial wall, thereby promoting atherosclerosis. However, at present, the mechanism of hypertension promoting the reduction of lipoprotein output from arterial wall to promote atherosclerosis is unclear, and there are few reports on this. The purpose of this paper is to start with structural changes and to determine the relationship between the changes in connective tissue and its distribution with the lipid in the arterial wall (including the pulmonary artery) during hypertension, so as to provide a new basis for exploring the mechanism of hypertension in promoting atherosclerosis.