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体外实验观察大肠杆菌内毒素(ET)对人类红细胞胞浆游离钙浓度([Ca~(2+)]i)、膜钙泵(钙镁ATP酶)的作用。并在注射ET复制的家兔播散性血管内凝血(DIC)模型观察红细胞[Ca~(2+)]i,钙泵活性、钙调素活性、红细胞变形性、膜蛋白电泳和膜脂质流动性的变化,研究红细胞自身因素在DIC微血管溶血性贫血发病机制中的作用。实验结果提示内毒素引起家兔DIC出现的微血管溶血性贫血的发生机制可能是由于ET损伤膜结构,使膜对Ca~(2+)通透性升高和钙泵活性下降,从而红细胞[Ca~(2+)]i升高,激活一系列钙依赖蛋白酶和磷脂酶,进一步损伤膜,使红细胞处于“前溶解状态”,在血流冲击下容易破坏。
The effects of endotoxin of E. coli on cytosolic free calcium concentration in human erythrocytes ([Ca ~ (2 +)] i) and membrane calcium pump (calcium magnesium ATPase) were observed in vitro. The changes of erythrocyte [Ca ~ (2 +)] i, calcium pump activity, calmodulin activity, erythrocyte deformability, membrane protein electrophoresis and membrane lipid were observed in the disseminated intravascular coagulation (DIC) Liquidity changes in the study of erythrocyte factor DIC microvascular hemolytic anemia in the pathogenesis. The experimental results suggest that the mechanism of endotoxin-induced microvascular hemolytic anemia in DIC may be due to the damage of membrane structure by ET and the increase of Ca 2+ permeability and decrease of calcium pump activity, ~ (2 +)] i increased, activating a series of calcium-dependent proteases and phospholipases, further damage the membrane, so that the red blood cells in a “pre-dissolved state”, easy to damage under the impact of blood flow.