论文部分内容阅读
本文对慢性常压缺氧和缺氧伴高二氧化碳大鼠红细胞膜带3蛋白相对含量、带3蛋白阴离子转运区域结构以及阴离子交换功能和动力学特征进行了研究。结果表明,慢性常压缺氧和缺氧伴高二氧化碳大鼠红细胞膜带3蛋白阴离子转运位点结构可能无异常,但阴离子交换功能降低。其产生机制可能是出于长期严重缺氧,氧分压降低使胞浆ATP含量减少,影响幼稚红细胞中带3蛋白的合成,致使网织红细胞阶段嵌入红细胞膜上的带3蛋白量减少,阴离子转运位点数目减少所致。因此,改善低氧状态,提高动脉血氧分压,将有助于恢复红细胞膜带3蛋白的正常功能。
In this paper, the relative content of erythrocyte membrane protein 3, the structure of anion transport region with 3 protein and the anion exchange function and kinetics of chronic hypobaric hypoxia and hypoxia with hypercapnia were studied. The results showed that there may be no abnormalities in the anion transport site of erythrocyte membrane protein 3 in chronic hypobaric hypoxia and hypoxia with high carbon dioxide, but the anion exchange function may be reduced. The mechanism may be due to long-term severe hypoxia, decreased partial pressure of oxygen to reduce the content of ATP in the cytoplasm, affect the synthesis of naive red blood cells with 3 protein, resulting in reticulocyte imbedding the red blood cell membrane with reduced protein 3, anion The number of transshipment sites is reduced. Therefore, to improve hypoxia and improve arterial oxygen tension, will help to restore the normal function of erythrocyte membrane protein 3.