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本文报告30只家兔食饵性高脂血症时所发生的早期病理解剖变化:(一)主动脉、肺动脉及冠状动脉的早期粥样硬化,这是由血浆脂质浸入动脉内膜而引起的病变;(二)脾、骨髓中出现泡沫细胞,这是单核细胞、巨噬细胞吞噬血浆脂质所致;(三)肝、肾组织中亦出现泡沫细胞,这些变化可能系糖原潴留于肝细胞及肾小管上皮细胞所致。我们在观察家兔食饵性高脂血症的病理解剖变化时,除见动脉粥样硬化外,还在脾、骨髓及肾脏等处见到多少不等的泡沫细胞灶。关于前一病变的形态观察及其发生机理,国内外已有不少报导;但后一病变在国内文献中尚未见详细介绍。由于上述各种变化均于造型后的第6周至第12周内(本实验总共历时12周)即已见到,故统称之为早期病变。现将这些病变叙述如后。
In this paper, we report the early pathological changes that occur in prey hyperlipidemia in 30 rabbits: (1) early atherosclerosis of the aorta, pulmonary artery, and coronary arteries caused by plasma lipid penetration into the intima of the artery Lesions; (B) the spleen, bone marrow cells appear in foam cells, which is monocytes, macrophages phagocytose plasma lipid; (C) the liver and kidney cells also appear foam cells, these changes may be glycogen retention in Liver cells and tubular epithelial cells caused. We observed rabbit alimentary hyperlipidemia pathological anatomy changes, in addition to see atherosclerosis, but also in the spleen, bone marrow and kidney, etc. to see how many ranging from the foam cell foci. About the morphological observation of the previous lesion and its mechanism, there are many reports at home and abroad; but the latter lesion has not been described in detail in the domestic literature. As the above mentioned changes were all seen in the 6th week to the 12th week after the modeling (for a total of 12 weeks in this experiment), it is collectively referred to as the early stage lesion. These lesions are described below.