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低碳酸血症对代谢性酸中毒时细胞内pH的影响。

Effect of hypocapnia on intracellular pH during metabolic acidosis.

作者信息

Bettice J A

出版信息

Respir Physiol. 1979 Dec;38(3):257-66. doi: 10.1016/0034-5687(79)90053-7.

Abstract

Separate and combined effects of acute metabolic acidosis and hypocapnia were determined in skeletal and cardiac muscles of intact rats. Normocapnic metabolic acidosis, imposed by intraperitoneal injection of hydrochloric acid (6 mEq/kg), did not change skeletal muscle intracellular acid--base parameters. Hypocapnia, induced by mechanical hyperventilation, resulted in intracellular alkalosis within skeletal muscle during both respiratory alkalosis and compensated metabolic acidosis; changes of skeletal muscle intracellular bicarbonate concentration per unit change in carbon dioxide tension were identical during these two experimental procedures. These data suggest that processes other than physicochemical buffering neutralize protons taken into skeletal muscle cells during acute metabolic acidosis. The acid--base state of the heart was quite stable during these experimental manipulations; thus, it appears that cardiac muscle has an extraordinary buffering ability. Moreover, our data suggest that processes other than physicochemical buffering maintain cardiac intracellular pH normal during hypocapnia.

摘要

在完整大鼠的骨骼肌和心肌中测定了急性代谢性酸中毒和低碳酸血症的单独及联合作用。通过腹腔注射盐酸(6 mEq/kg)造成的正常碳酸血症性代谢性酸中毒并未改变骨骼肌细胞内酸碱参数。机械性过度通气诱导的低碳酸血症在呼吸性碱中毒和代偿性代谢性酸中毒期间均导致骨骼肌细胞内碱中毒;在这两个实验过程中,骨骼肌细胞内碳酸氢盐浓度随二氧化碳张力单位变化的改变是相同的。这些数据表明,在急性代谢性酸中毒期间,除了物理化学缓冲作用外,还有其他过程可中和进入骨骼肌细胞的质子。在这些实验操作过程中,心脏的酸碱状态相当稳定;因此,心肌似乎具有非凡的缓冲能力。此外,我们的数据表明,在低碳酸血症期间,除了物理化学缓冲作用外,还有其他过程可维持心肌细胞内pH正常。

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