Toews D P, Heisler N
J Exp Biol. 1982 Apr;97:79-86. doi: 10.1242/jeb.97.1.79.
Toads (Bufo marinus) were exposed to environmental hypercapnia of 5% CO2 in air, and extracellular and intracellular acid-base parameters were determined 1 and 24 h after the onset of hypercapnia. The initial drop in pH was compensated by the elevation of extracellular and intracellular bicarbonate. Relating the pH compensation to the pH drop that is expected to occur by increased PCO2 at constant bicarbonate concentration, the pH compensation in the extracellular space was 30% and reached the following values for intracellular body compartments: 65% in skeletal muscle, 77% in heart muscle and 44% in skin. The additional bicarbonate was partly produced by blood and intracellular non-bicarbonate buffers; the major portion of the remainder was related to the excretion of ammonia into the environmental water. The hypercapnia-induced changes of pH were considerably smaller in all tissue cells than in the extracellular space. Thus Bufo marinus exhibits the relative preference of intracellular over extracellular acid-base regulation that has been observed in other vertebrates.
将海蟾蜍（Bufo marinus）暴露于空气中5%二氧化碳的环境高碳酸血症中，并在高碳酸血症开始后1小时和24小时测定细胞外和细胞内的酸碱参数。pH值的初始下降通过细胞外和细胞内碳酸氢盐的升高得到补偿。将pH补偿与在恒定碳酸氢盐浓度下由于PCO2升高预期发生的pH下降相关联，细胞外空间的pH补偿为30%，细胞内体腔达到以下值：骨骼肌为65%，心肌为77%，皮肤为44%。额外的碳酸氢盐部分由血液和细胞内非碳酸氢盐缓冲液产生；其余的大部分与氨排泄到环境水中有关。在所有组织细胞中，高碳酸血症引起的pH变化比细胞外空间中的变化小得多。因此，海蟾蜍表现出细胞内酸碱调节相对于细胞外酸碱调节的相对偏好，这在其他脊椎动物中也有观察到。
