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正常和肥厚大鼠心肌的细胞内pH调节

Intracellular pH regulation of normal and hypertrophic rat myocardium.

作者信息

Gonzalez N C, Wemken H G, Heisler N

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1979 Oct;47(4):651-6. doi: 10.1152/jappl.1979.47.4.651.

Abstract

The myocardial cell pH (pHi) observed during breathing of 0, 7.5, or 10% CO2 in air for 3 h was studied in rats with myocardial hypertrophy due to aortic stenosis and in sham-operated rats. The change in pHi during hypercapnia was significantly smaller in the rats with myocardial hypertrophy, with the apparent nonbicarbonate buffer value (delta [HCO3-]i/delta pHi) being almost three times that of the sham-operated rats. In vitro CO2 equilibrium of myocardial tissue homogenates showed no difference in nonbicarbonate buffer value between homogenates obtained from normal rats and from rats with myocardial hypertrophy. Therefore, it appears that the increased ability of the myocardial cell to regulate its pH during hypertrophy is not due to an increase in the cellular level of nonbicarbonate buffers, but seems to be related to a larger bicarbonate uptake by the myocardial cell during hypercapnia.

摘要

在因主动脉狭窄导致心肌肥大的大鼠和假手术大鼠中,研究了在空气中呼吸含0%、7.5%或10%二氧化碳3小时期间观察到的心肌细胞pH值(细胞内pH值)。高碳酸血症期间,心肌肥大大鼠的细胞内pH值变化明显较小,表观非碳酸氢盐缓冲值(δ[HCO₃⁻]i/δpH值)几乎是假手术大鼠的三倍。心肌组织匀浆的体外二氧化碳平衡显示,正常大鼠和心肌肥大大鼠的匀浆在非碳酸氢盐缓冲值方面没有差异。因此,似乎心肌肥大期间心肌细胞调节其pH值的能力增强并非由于细胞内非碳酸氢盐缓冲物质水平增加,而是似乎与高碳酸血症期间心肌细胞对碳酸氢盐的摄取增加有关。

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