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[代谢性碱中毒。基于新实验数据的代偿机制]

[Metabolic alkalosis. Compensation mechanisms in the light of new experimental data].

作者信息

Randazzo A, Cremonesi G, Martinotti R, Cremonini L, Parziale M, Santambrogio S

出版信息

Minerva Med. 1975 Oct 17;66(69):3623-36.

PMID:241948
Abstract

Changes in arterial blood and erythrocyte acid-base and electrolyte balance in the course of acute alkalinisation caused by bicarbonate loading showed that extracellular alkalosis has no significant effect on the concentration of intraerythrocyte bicarbonate concentration, though a marked increase in pH and electrolyte balance within the red cell is apparent. Erythrocyte alkalinisation may thus be seen as essentially due to the escape of H+ ions, while the entry of Na+ ions is the main device by which the law of electroneutrality is respected. The literature suggests that lactic acid offers a source of H+ ions for destruction of bicarbonate, whereas the diffusion of the ion lactate within the cell is compensated by the release of Cl-. In addition, the data now reported indicate that the red cell is a sufficiently valid model for the study of phenomena occurring within the intracellular compartment when a state of extracellular alkalinisation in created.

摘要

碳酸氢盐负荷引起急性碱化过程中动脉血及红细胞酸碱和电解质平衡的变化表明,细胞外碱中毒对红细胞内碳酸氢盐浓度无显著影响,尽管红细胞内pH值和电解质平衡有明显升高。因此,红细胞碱化本质上可能被视为由于H⁺离子的逸出,而Na⁺离子的进入是维持电中性定律的主要机制。文献表明,乳酸为破坏碳酸氢盐提供了H⁺离子来源,而细胞内乳酸离子的扩散通过Cl⁻的释放得到补偿。此外,现在报告的数据表明,当产生细胞外碱化状态时,红细胞是研究细胞内区室中发生现象的一个足够有效的模型。

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