Bettice J A, Wang B C, Brown E B
Respir Physiol. 1976 Oct;28(1):89-98. doi: 10.1016/0034-5687(76)90087-6.
Changes in the total CO2 content of tissues were determined in order to characterize variations in intracellular acid-base parameters during the onset of hypercapnia. Within two minutes after an increasement in the CO2 tension of the inspired air of rats, there were large increases in the intracellular bicarbonate concentrations of both cardiac and skeletal muscles. Greater changes occurred in the heart, and its intracellular pH remained near normal during the first hour of hypercapnia; whereas there was an intracellular acidosis in skeletal muscle. This greater capacity of the heart to buffer excess CO2 has been linked to an increased movement of bicarbonate ions into and/or hydrogen ions out of cardiac cells during hypercapnia (Lai et al., 1973c). Yet, the buffer capacity of the heart was not compromised by metabolic acidosis during which there was a greatly reduced extracellular bicarbonate ion concentration and a greatly increased extracellular hydrogen ion concentration. The intracellular pH of the cardiac ventricle was stable following the imposition of a noncarbonic acid load on normocapnic rats.
为了描述高碳酸血症发作期间细胞内酸碱参数的变化，对组织中总二氧化碳含量的变化进行了测定。在大鼠吸入空气的二氧化碳张力增加后两分钟内，心肌和骨骼肌的细胞内碳酸氢盐浓度大幅增加。心脏的变化更大，在高碳酸血症的第一个小时内其细胞内pH值保持接近正常；而骨骼肌则出现细胞内酸中毒。心脏缓冲过量二氧化碳的能力更强，这与高碳酸血症期间碳酸氢根离子进入心肌细胞和/或氢离子从心肌细胞中流出增加有关（Lai等人，1973c）。然而，心脏的缓冲能力并未因代谢性酸中毒而受损，在此期间细胞外碳酸氢根离子浓度大幅降低，细胞外氢离子浓度大幅增加。在给正常碳酸血症大鼠施加非碳酸酸性负荷后，心室的细胞内pH值保持稳定。
