文摘

Experiments were performed in vivo to elucidate the underlying mechanism(s) of apparent diffusion limitations for CO₂ excretion in rainbow trout (Oncorhynchus mykiss). Ligation of two gill arches and the associated expected reduction in gill surface area of 30 % caused pronounced respiratory acidosis as indicated by elevated arterial blood P_CO2 (Pa_CO2) and reduced arterial blood pH. Under conditions of normoxia, arterial blood P_O2 (Pa_O2) was not significantly (statistically) reduced. However, during hypoxia (water P_O2=70–80 mmHg), the apparent trend for reduced Pa_O2 values became statistically significant in fish with 15 % surface area reduction. To determine whether the elevated Pa_CO2 in fish with reduced surface area (30 % ) reflected true diffusion limitations or chemical equilibrium limitations imposed by the relatively slow rate of red blood cell Cl⁻/HCO₃⁻ exchange, fish were injected with carbonic anhydrase (CA) to permit catalysis of HCO₃⁻ dehydration within the plasma. Injection of CA caused a lowering of Pa_CO2 by 0.87±0.32 mmHg within 120 min and thus essentially eliminated the increase in Pa_CO2 (1.04±0.33 mmHg) that was caused by the reduction in surface area. These results clearly demonstrate that the elevation in Pa_CO2 evoked by gill surface area reduction is a consequence of chemical equilibrium limitations rather than true diffusion limitations, per se.