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人工低压舱内模拟高原低氧24h,并与2300m对照组比较,观察不同发育年龄大鼠SGOT活力,肝溶酶体总酸性磷酸酶、非沉淀酸性磷酸酶和芳基硫酸酯酶活力及肝重、肝细胞糖原、蛋白和总脂含量的变化。在海拔5000m高度,10天鼠各酶活力、570天鼠总酸性磷酸酶和芳基硫酸酯酶活力明显升高;35和75天鼠各酶活力未见显著变化;在海拔8000m高度,各年龄组鼠上述各酶活力均显著升高。随着海拔高度的升高,各组大鼠肝重呈不同程度的下降,肝细胞糖原含量非常明显地减少,35和75天鼠8000m组全肝蛋白含量下降明显,10、35、75天鼠肝细胞总脂累积。上述结果综合分析表明:低氧致使大鼠肝细胞损伤属一普遍性效应,新生期和老年期大鼠肝细胞耐低氧能力不及幼年期和成年期大鼠。
Artificial hypobaric chamber simulated altitude hypoxia 24h, and compared with 2300m control group, to observe SGOT vitality, hepatic lysosomal total acid phosphatase, non-precipitated acid phosphatase and aryl sulfatase activity and liver weight , Hepatocytes glycogen, protein and total lipid content changes. At 5000m above sea level, the activity of total acid phosphatase and arylsulfatase was significantly increased in 570 days mice at 10 days and no significant changes were observed at 35 and 75 days. At the altitude of 8000m, The above groups of mice activity were significantly increased. With the increase of altitude, the liver weight of rats in each group decreased to some extent, the content of glycogen in hepatocytes decreased significantly, and the content of hepatic protein in 8000m group decreased significantly on days 35 and 75, Total accumulation of rat hepatocytes. The above results of a comprehensive analysis showed that: Hypoxia caused rat liver cell damage is a universal effect, neonatal and senile rat hepatocytes hypoxia tolerance less than juvenile and adult rats.