Bright C M, Ellis D
Department of Physiology, University Medical School, Edinburgh, Scotland, UK.
J Mol Cell Cardiol. 1994 Apr;26(4):463-9. doi: 10.1006/jmcc.1994.1057.
The changes of intracellular pH (pHi) produced by hypoxia in sheep heart Purkinje fibres were studied using liquid ion exchanger-filled microelectrodes. A decrease of temperature from 35 degrees C to 22 degrees C caused an alkalinization of 0.3 pH units. Hypoxia (partial pressure of oxygen < 10 mm Hg) for 20 min induced an acidification of 0.26 +/- 0.18 units (n = 14) at 35 degrees C. The hypoxia-induced acidification at 22 degrees C was smaller than that at 35 degrees C by approximately 65%. Increasing the buffering capacity of the cells decreased the hypoxic acidification. This could be achieved either by use of high extracellular HEPES concentrations (40 mM) or by the use of bicarbonate buffers. Sodium cinnamate (5 mM) increased the hypoxic acidification and slowed the pHi recovery on reintroduction of oxygen, implying an importance role for lactate flux in pH regulation during hypoxia.
采用充有液体离子交换剂的微电极,研究了缺氧对绵羊心脏浦肯野纤维细胞内pH(pHi)的影响。温度从35℃降至22℃会导致碱化0.3个pH单位。在35℃下,缺氧(氧分压<10 mmHg)20分钟会诱导酸化0.26±0.18个单位(n = 14)。22℃时缺氧诱导的酸化比35℃时小约65%。增加细胞的缓冲能力可降低缺氧酸化。这可以通过使用高细胞外HEPES浓度(40 mM)或使用碳酸氢盐缓冲液来实现。肉桂酸钠(5 mM)会增加缺氧酸化,并减缓再给氧时pHi的恢复,这意味着乳酸通量在缺氧期间的pH调节中起重要作用。