Kramer H J, Gospodinov D, Krück F
Nephron. 1976;16(5):344-58. doi: 10.1159/000180621.
Red blood cells from 7 out of 13 patients with chronic uremia were found to have increased intracellular concentrations of sodium associated with a reversible inhibition of ouabain-sensitive Na efflux when incubated in control plasma. Although mean Na-K-ATPase activity of RBC hemolysates was only moderately decreased (21.8 +/- 1.5 vs. 26.5 +/- 1.8 nmol Pi/mg protein/h), enzyme kinetics revealed a significant increase in KmATP values for this enzyme in uremic RBCs (1.01 +/- 0.1 vs. 0.58 +/- 0.03; p less than 0.001) which was closely correlated to serum creatinine concentration (r = 0.9034). While aerobic glycolysis was unaltered, an increase in glucose-6-phosphate dehydrogenase activity was observed, i.e. the enzyme initiating the pentose-phosphate cycle. In addition, intracellular ATP concentrations of uremic RBCs were significantly higher than ATP concentrations of control RBCs (2.13 +/- 0.22 vs. 1.32 +/- 0.06 mmol/l RBC; p less than 0.01). These data suggest that high intracellular concentrations of Na and ATP in uremic RBCs partially result from a competitive reversible inhibition of the transport ATPase by uremic toxins.
在对照血浆中孵育时，13例慢性尿毒症患者中有7例的红细胞细胞内钠浓度升高，伴有哇巴因敏感的钠外流可逆性抑制。尽管红细胞溶血产物的平均钠钾ATP酶活性仅适度降低（21.8±1.5对26.5±1.8 nmol Pi/mg蛋白/小时），但酶动力学显示尿毒症红细胞中该酶的KmATP值显著升高（1.01±0.1对0.58±0.03；p<0.001），这与血清肌酐浓度密切相关（r = 0.9034）。虽然有氧糖酵解未改变，但观察到葡萄糖-6-磷酸脱氢酶活性增加，即启动磷酸戊糖途径的酶。此外，尿毒症红细胞的细胞内ATP浓度显著高于对照红细胞的ATP浓度（2.13±0.22对1.32±0.06 mmol/l红细胞；p<0.01）。这些数据表明，尿毒症红细胞中高细胞内浓度的钠和ATP部分是由尿毒症毒素对转运ATP酶的竞争性可逆抑制导致的。
