Gilmour A, Fenwick J, Perry S
J Exp Biol. 1995;198(Pt 12):2557-67. doi: 10.1242/jeb.198.12.2557.
Gill O2 uptake, CO2 excretion, ventilation and blood respiratory/acidbase variables were evaluated in control and softwater-acclimated trout (Oncorhynchus mykiss) to test the hypothesis that gill chloride cell (CC) proliferation, elicited by 2 weeks of softwater exposure, impairs the diffusion of respiratory gases across the gill. The proliferation of CCs in softwater fish was verified using light microscopy, and its impact on respiratory gas transfer was assessed in vivo by continuous monitoring of arterial blood PO2 (PaO2), PCO2 (PaCO2) and pH (pHa) using an extracorporeal blood circulation under conditions of normoxia and graded hypoxia [water PO2 (PwO2) was lowered from 20.0 kPa to 5.3 kPa within 20 min]. During normoxia, ventilation frequency was significantly higher in the softwater trout (78±4 versus 57±4 breaths min-1; mean ± s.e.m.), while ventilation amplitude was similar in both groups (1.01.1 cm opercular displacement). PaCO2 and plasma HCO3- concentration were significantly lower in the softwater fish and the blood acidbase status was characterized by a mixed respiratory alkalosis and metabolic acidosis such that blood pH was not statistically different between the two groups. CO2 excretion (2.52.8 mmol kg-1 h-1) and O2 uptake rates (2.35.1 mmol kg-1 h-1), as measured during normoxia, were unaffected by acclimation to soft water. During hypoxia, ventilation frequency and amplitude increased in the control trout, whereas only ventilation amplitude increased in the softwater-acclimated fish. The rate of PaO2 reduction during hypoxia was significantly greater in the softwater fish (0.84±0.06 versus 0.65±0.06 kPa PaO2 kPa-1 PwO2) and, at the most severe level of hypoxia (PwO2=5.3 kPa), PaO2 was significantly lower in the softwater fish. The rate of PaCO2 reduction (caused by hyperventilation) was significantly lower in the softwater-acclimated fish (0.002±0.001 versus 0.005±0.001 kPa PaCO2 kPa-1 PwO2; mean ± s.e.m.; P<0.06) and, indeed, was not statistically different from zero. Blood pH did not change significantly during hypoxia in either group but, through much of the hypoxic period (715 kPa PwO2), pHa was statistically lower in the softwater-acclimated fish. These results demonstrate that exposure of trout to soft water for 2 weeks is associated with proliferation of lamellar CCs and impaired branchial gas transfer. Hyperventilation was identified as a compensatory physiological adjustment.
在对照和适应软水的虹鳟鱼（Oncorhynchus mykiss）中评估了鳃对氧气的摄取、二氧化碳的排泄、通气以及血液呼吸/酸碱变量，以检验以下假设：两周的软水暴露引发的鳃氯细胞（CC）增殖会损害呼吸气体在鳃中的扩散。使用光学显微镜验证了软水鱼中CC的增殖，并通过在常氧和分级低氧条件下（水的氧分压（PwO2）在20分钟内从20.0 kPa降至5.3 kPa）使用体外血液循环连续监测动脉血PO2（PaO2）、PCO2（PaCO2）和pH（pHa），在体内评估其对呼吸气体转移的影响。在常氧期间，软水虹鳟的通气频率显著更高（78±4次/分钟对57±4次/分钟；平均值±标准误），而两组的通气幅度相似（鳃盖位移1.0 - 1.1厘米）。软水鱼中的PaCO2和血浆HCO3 - 浓度显著更低，血液酸碱状态的特征是混合性呼吸性碱中毒和代谢性酸中毒，使得两组之间的血液pH没有统计学差异。在常氧期间测量的二氧化碳排泄率（2.5 - 2.8 mmol·kg-1·h-1）和氧气摄取率（2.3 - 5.1 mmol·kg-1·h-1）不受适应软水的影响。在低氧期间，对照虹鳟的通气频率和幅度增加，而适应软水的鱼仅通气幅度增加。软水鱼在低氧期间PaO2的降低速率显著更大（0.84±0.06对0.65±0.06 kPa·PaO2·kPa-1·PwO2），并且在最严重的低氧水平（PwO2 = 5.3 kPa）时，软水鱼中的PaO2显著更低。适应软水的鱼中PaCO2的降低速率（由过度通气引起）显著更低（0.002±0.001对0.005±0.001 kPa·PaCO2·kPa-1·PwO2；平均值±标准误；P<0.06），实际上与零没有统计学差异。两组在低氧期间血液pH均未显著变化，但在低氧期的大部分时间（7 - 15 kPa·PwO2），适应软水的鱼中的pHa在统计学上更低。这些结果表明，虹鳟暴露于软水两周与鳃小片CC的增殖和鳃气体转移受损有关。过度通气被确定为一种代偿性生理调节。
