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本文评述慢性肾功能衰竭时的红、白细胞功能及代谢异常。红细胞:尿毒症时渗透压脆性及自身溶血现象均轻微或不增加。(Na~+K~+)-ATP 酶和酮基转移酶活性减低,而另数种酶活性则均增加。葡萄糖消耗量增加,乳酸产量亦增加。肾功能不全病人酸溶性有机磷(以2,3-二磷酸甘油酸盐 2,3-DPG 为主)增多,ATP、ADP、己糖磷酸酶、三磷鸟便嘌呤核甙(GTP)亦增高。除(Na~+K~+)-ATP 酶外,所有这些异常都反映了细胞代谢亢进状态。这一状态可由下述4个机制引起:血 pH 碱性、红细胞群体幼稚、血磷酸盐过商、血浆中有其他代谢刺激物。作者评述了种种实验资料,认为原因是多方面的,血磷酸盐过多和红细胞群体幼龄可能是原因之一,尿毒症血浆中
This article reviews the red and white blood cell function and metabolic abnormalities in chronic renal failure. Erythrocyte: uremic osmotic pressure fragility and hemolysis are minor or no increase. (Na ~ + K ~ +) - ATPase and ketotransferase activity decreased while the other enzyme activity increased. Increased glucose consumption, lactate production also increased. Acid-soluble organic phosphorus in patients with renal insufficiency (mainly 2,3-diphosphoglycerate 2,3-DPG) increased, ATP, ADP, hexose phosphatase, triphosphate birds purine nucleoside (GTP) also increased . Except for (Na ~ + K ~ +) - ATPase, all of these abnormalities reflect the state of cellular metabolism. This condition can be caused by the following four mechanisms: blood pH alkaline, erythrocyte population naïve, hyperphosphatemia, plasma other metabolic stimuli. The authors review a variety of experimental data that is due to many reasons, hyperphosphatemia and red blood cell population may be one of the reasons young, uremic plasma