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促红细胞生成素改变了慢性贫血-尿毒症大鼠中哇巴因的心脏作用。

Erythropoietin modified the cardiac action of ouabain in chronically anaemic-uraemic rats.

作者信息

Wald M, Gutnisky A, Borda E, Sterin-Borda L

机构信息

Cefybo-Conicet, Buenos Aires, Argentina.

出版信息

Nephron. 1995;71(2):190-6. doi: 10.1159/000188711.

Abstract

The results of the studies reported here demonstrate the cardiac non-haematopoietic effect of erythropoietin, providing a new physiological function of the hormone. We demonstrate that myocardium from rat with chronic renal failure (CRF) showed an abnormal response to ouabain associated with an inhibition of cardiac Na+/K+/ATPase activity and with a decrease in the high affinity 3H-ouabain binding sites. The extent to which both actions were improved with the recombinant human erythropoietin (rHuEpo) treatment suggests that the lack of the hormone is responsible for this phenomenon. The fact is that neither contractile nor enzymatic action of rHuEpo was accompanied with the improvement of the functional renal and haematologic parameters, indicating a primary effect on myocardial contractile function of rHuEpo, independent of the anaemic and uraemic state of the animal. The reason why erythropoietin is able to modulate directly the cardiac Na+/K+ pump makes it possible to conclude that the lack of erythropoietin in CRF may be at least in part responsible for the inhibition of cardiac enzymes, altering the contractile behaviour of the heart.

摘要

此处报告的研究结果证明了促红细胞生成素的心脏非造血作用,揭示了该激素的一项新的生理功能。我们发现,慢性肾衰竭(CRF)大鼠的心肌对哇巴因表现出异常反应,这与心脏钠钾ATP酶活性受到抑制以及高亲和力3H-哇巴因结合位点减少有关。重组人促红细胞生成素(rHuEpo)治疗使这两种作用均得到改善,这表明缺乏该激素是导致此现象的原因。事实上,rHuEpo的收缩作用和酶促作用均未伴随着功能性肾脏和血液学参数的改善,这表明rHuEpo对心肌收缩功能具有原发性作用,与动物的贫血和尿毒症状态无关。促红细胞生成素能够直接调节心脏钠钾泵的原因,使我们可以得出结论,CRF中促红细胞生成素的缺乏可能至少部分导致了心脏酶的抑制,从而改变了心脏的收缩行为。

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