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心肌钠泵对慢性钾缺乏的适应性

Adaptation of the cardiac muscle sodium pump to chronic potassium deficiency.

作者信息

Ward J P, Cameron I R

出版信息

Cardiovasc Res. 1984 May;18(5):257-63. doi: 10.1093/cvr/18.5.257.

Abstract

During chronic dietary K+ depletion in rabbits there is a significant reduction of intracellular K+ concentration [( K+]i) in skeletal muscle, but not in the heart. After 1 week of subsequent K+ repletion both plasma [K+] and skeletal muscle [K+]i had returned to control levels. Cardiac muscle on the other hand showed a significant increase in [K+]i above control. It has been suggested that the heart is protected during K+ depletion by some modification to the sarcolemmal Na+ pump. The Na+ pump density was estimated in membrane preparations from normal and K+ depleted rabbits by the specific binding of 3H-ouabain. 3H-ouabain binding in cardiac muscle preparations was increased significantly after 2 weeks of K+ depletion, and remained so for a further 2 weeks of depletion. There was no significant change in 3H-ouabain binding to skeletal muscle preparations after 4 weeks of K+ depletion. After 1 week of subsequent K+ repletion 3H-ouabain binding was still increased in cardiac muscle preparations, corresponding to the overshoot in cardiac muscle [K+]i. These results support the hypothesis that cardiac muscle is protected against K+ loss during chronic K+ depletion by an adaptive increase in Na+ pump density.

摘要

在兔慢性饮食性钾缺乏期间,骨骼肌细胞内钾浓度[K⁺]i显著降低,但心脏中则不然。在随后补钾1周后,血浆[K⁺]和骨骼肌[K⁺]i均恢复到对照水平。另一方面,心肌的[K⁺]i显著高于对照水平。有人提出,在钾缺乏期间,心脏通过对肌膜钠泵的某种修饰而得到保护。通过³H-哇巴因的特异性结合来估计正常和钾缺乏兔的膜制剂中的钠泵密度。在钾缺乏2周后,心肌制剂中的³H-哇巴因结合显著增加,并且在进一步缺乏2周后仍保持增加。在钾缺乏4周后,³H-哇巴因与骨骼肌制剂的结合没有显著变化。在随后补钾1周后,心肌制剂中的³H-哇巴因结合仍然增加,这与心肌[K⁺]i的过冲相对应。这些结果支持这样的假说,即慢性钾缺乏期间,心肌通过钠泵密度的适应性增加来防止钾流失。

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