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尿毒症血浆对正常女性红细胞中速尿敏感的钠外流的刺激作用。

Stimulation by uraemic plasma of frusemide-sensitive sodium efflux in erythrocytes from normal women.

作者信息

Corry D B, Tuck M L, Lee D B

机构信息

Department of Medicine, Olive View Medical Center, Sylmar, California 91342-1495.

出版信息

Clin Sci (Lond). 1989 May;76(5):559-63. doi: 10.1042/cs0760559.

Abstract
  1. Reduced Na+,K+ pump activity has been reported in uraemic erythrocytes, and this has been attributed to the presence of a circulating ouabain-like inhibitor. Since we have previously reported marked suppression of Na+,K+ co-transport activity in erythrocytes from dialysis patients, we have now examined the effect of incubation with uraemic plasma on Na+ efflux through the Na+,K+ pump and the co-transport pathway in normal erythrocytes from both men and women. 2. The results show that Na+ efflux via the Na+,K+ pump is not different between men and women (3.14 +/- 0.14 vs 3.68 +/- 0.18 mmol h-1 litre-1 of cells) and is not inhibited by incubation with uraemic plasma. 3. In contrast, co-transport-mediated Na+ efflux is lower in erythrocytes from normal women when compared with normal men (0.17 +/- 0.02 vs 0.25 +/- 0.05 mmol h-1 litre-1 of cells, P less than 0.001). 4. Moreover, incubation with uraemic plasma causes stimulation of Na+ efflux through the co-transport pathway in erythrocytes of healthy women (0.17 +/- 0.02 vs 0.27 +/- 0.03 mmol h-1 litre-1 of cells, P less than 0.005), but not in erythrocytes of healthy men (0.27 +/- 0.03 vs 0.25 +/- 0.05 mmol h-1 litre-1 of cells). 5. Our data do not support the presence of either a Na+,K+ pump or a co-transport inhibitor in plasma from dialysed uraemic patients. Thus, the suppressed co-transport activity demonstrated in uraemic erythrocytes cannot be attributed to a circulating inhibitor, and may reflect an acquired membrane or transport defect.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 据报道,尿毒症患者红细胞中的钠钾泵活性降低,这归因于循环中存在哇巴因样抑制剂。由于我们之前报道过透析患者红细胞中钠钾协同转运活性受到显著抑制,因此我们现在研究了尿毒症血浆孵育对男性和女性正常红细胞通过钠钾泵和协同转运途径的钠外流的影响。2. 结果表明,通过钠钾泵的钠外流在男性和女性之间没有差异(3.14±0.14对3.68±0.18 mmol·h⁻¹·升⁻¹细胞),并且不受尿毒症血浆孵育的抑制。3. 相比之下,正常女性红细胞中由协同转运介导的钠外流低于正常男性(0.17±0.02对0.25±0.05 mmol·h⁻¹·升⁻¹细胞,P<0.001)。4. 此外,尿毒症血浆孵育会刺激健康女性红细胞通过协同转运途径的钠外流(0.17±0.02对0.27±0.03 mmol·h⁻¹·升⁻¹细胞,P<0.005),但不会刺激健康男性红细胞(0.27±0.03对0.25±0.05 mmol·h⁻¹·升⁻¹细胞)。5. 我们的数据不支持透析后的尿毒症患者血浆中存在钠钾泵或协同转运抑制剂。因此,尿毒症红细胞中显示的协同转运活性受到抑制不能归因于循环抑制剂,可能反映了一种后天获得的膜或转运缺陷。(摘要截短为250字)

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