Heisler N, Forcht G, Ultsch G R, Anderson J F
Respir Physiol. 1982 Aug;49(2):141-58. doi: 10.1016/0034-5687(82)90070-6.
The partial pressure of CO2 (PCO2) in certain areas of the aquatic habitat of the salamanders Siren lacertina and Amphiuma means frequently rises to values of up to 60 mm Hg. This ambient hypercapnia occurs due to hindrance of gas exchange between water and air caused by dense water-surface vegetation. In order to investigate the acid-base regulation in response to the respiratory acidosis, which wound be expected to result from the high CO2 conductance of the amphibian skin, specimens of both species were subjected to water PCO2 of 47 mm Hg while having free access to normocapnic air in a closed water recirculation system. Arterial PCO2 rose considerably from 12 to 35 mm Hg in Siren and from 17 to 36 mm Hg in Amphiuma. The resultant fall in plasma pH remained uncompensated, whereas intracellular pH of white muscle and heart muscle of Siren were little affected owing to elevated intracellular bicarbonate concentrations. The bicarbonate accumulated in the intracellular compartments was in part produced by intracellular and extracellular nonbicarbonate buffering, and in part gained from the environment in exchange for Cl- ions. Elevated water bicarbonate concentration or bicarbonate infusion into Siren had no effect on the acid-base regulation. These data suggest that the availability of bicarbonate is not a limiting factor for extracellular compensation of increased PCO2, but that the threshold of the bicarbonate-regulating structures is simply not readjusted in hypercapnia. This type of regulation may have evolved as a result of the specific environmental conditions of these animals and may be considered as an energetically efficient way of maintaining a constant milieu for the pH-sensitive intracellular structures.
在蝾螈（鳗螈和鳗螈属）水生栖息地的某些区域，二氧化碳分压（PCO₂）常常会升至高达60毫米汞柱的值。这种环境高碳酸血症是由于密集的水面植被阻碍了水与空气之间的气体交换所致。为了研究对呼吸性酸中毒的酸碱调节，鉴于两栖动物皮肤的高二氧化碳传导性预计会导致呼吸性酸中毒，在封闭的水循环系统中，让这两个物种的标本接触47毫米汞柱的水体PCO₂，同时它们可以自由接触正常碳酸血症的空气。动脉PCO₂在鳗螈中从12毫米汞柱大幅升至35毫米汞柱，在鳗螈属中从17毫米汞柱升至36毫米汞柱。血浆pH值的下降没有得到代偿，而鳗螈白色肌肉和心肌的细胞内pH值受影响较小，这是由于细胞内碳酸氢盐浓度升高。细胞内隔室中积累的碳酸氢盐部分是由细胞内和细胞外的非碳酸氢盐缓冲产生的，部分是通过与Cl⁻离子交换从环境中获得的。升高水体碳酸氢盐浓度或向鳗螈注入碳酸氢盐对酸碱调节没有影响。这些数据表明，碳酸氢盐的可用性不是细胞外代偿增加的PCO₂的限制因素，而是碳酸氢盐调节结构的阈值在高碳酸血症中根本没有重新调整。这种调节类型可能是由于这些动物的特定环境条件而进化而来的，并且可以被视为一种在能量上高效的方式，用于为对pH敏感的细胞内结构维持恒定的环境。
