摘要
用过劳及饮食失节法塑造大鼠脾气虚模型、结果表明，随着造模时间的延长，脾气虚大鼠肝细胞线粒体的肿胀、基质变浅、空泡变淡、嵴断裂及排列紊乱等逐渐加重，同时空肠细胞线粒体也有类似变化。提示脾气虚大鼠肝细胞线粒体的变化是一个由轻到重的渐进过程，其病变程度与空肠细胞线粒体的病变程度密切相关；随着营养物质吸收障碍的逐渐加重，肝细胞线粒体的病变程度也渐趋严重，肝脏合成血浆蛋白的能力逐渐下降，是脾气虚证低蛋白血症逐渐加重的形态学基础和发病机制。
The spleen-qi-deficiency rat models were induced by overstrain and improper dieting. The swelling, matrixes shallowing, vacuolar degeneration, breakage and derangement ofhepatic cell mitochondria (HCM ) were aggravated over time. The mitochondria of jejunum(MOJ ) showed similar change as HCM. The results showed that pathologic changes of HCM inspleen dericiency rats was closely associated with the change of MOJ. With the aggravation ofdysfunction of absorption of nutritive substances, the ability of liver cells to synthesize plasmaproteins was gradually impaired and the pathologic changes of HCM also worsen. These are thepathologic mechanism of hypoalbuminemia of patients with spleen-qi deficiency.
基金
安徽省自然科学基金!95-医-17
关键词
脾气虚
肝细胞线粒体
超微结构
空肠细胞线粒体
ultrastructure
deficiency of spleen-qi
hepatic cell mitochondria
mitochondria of jejunum
