Randall D J, Heisler N, Drees F
Am J Physiol. 1976 Mar;230(3):590-4. doi: 10.1152/ajplegacy.1976.230.3.590.
Dogfish were exposed to sudden changes of Pco2 in inspired seawater. During hypercapnia breathing frequency remained constant, but gill ventilation was transiently increased to about 140% of control levels in the 1st h. O2 uptake was significantly increased also, but returned to the initial level before nomalization of gill ventilation. In contrast to the transient rise in gill ventilation and O2 uptake, arterial Po2 was increased for the whole period of hypercapnia. Hypercapnia results in a marked fall in pHa which returned to the initial value in 4-5 h even though hypercapnia is maintained. This rise in pHa with little change in PaCO2 was associated with an increase in plasma bicarbonate concentration. The increase of plasma bicarbonate was in part due to compensatory bicarbonate uptake from the seawater across the gills and in part was effected by transfer between intracellular tissue compartments and extracellular spaces. The compensatory bicarbonate exchange mechanism in the gills seems to have a delay both after onset and termination of hypercapnia.
将星鲨暴露于吸入海水中Pco2的突然变化中。在高碳酸血症期间，呼吸频率保持恒定，但鳃通气量在第1小时内短暂增加至对照水平的约140%。氧气摄取也显著增加，但在鳃通气恢复正常之前恢复到初始水平。与鳃通气量和氧气摄取的短暂增加相反，在整个高碳酸血症期间动脉血氧分压升高。高碳酸血症导致动脉血pH值显著下降，即使高碳酸血症持续存在，在4-5小时内也会恢复到初始值。动脉血pH值的这种升高而动脉血二氧化碳分压变化不大与血浆碳酸氢盐浓度增加有关。血浆碳酸氢盐的增加部分是由于通过鳃从海水中代偿性摄取碳酸氢盐，部分是通过细胞内组织隔室与细胞外空间之间的转移实现的。鳃中的代偿性碳酸氢盐交换机制在高碳酸血症开始和终止后似乎都有延迟。
