Evidence that hypoxemia promotes catecholamine release during hypercapnic acidosis in rainbow trout (Salmo gairdneri).

The concentrations of plasma catecholamines, epinephrine and norepinephrine, were monitored in rainbow trout (Salmo gairdneri) after acute (30 min) exposure to various levels of external hypercapnia (water PCO2 (PwCO2) = 0-11.3 Torr) under normoxic (water PO2 (PwO2) = 153 +/- 1.1 Torr) or hyperoxic (PwO2 = 653 +/- 27.0 Torr) conditions. Whole blood pH decreased to a similar extent as a function of external carbon dioxide tensions in both the normoxic and hyperoxic hypercapnic groups. Arterial oxygen content, however, declined only during normoxic hypercapnia. Similarly, plasma catecholamines (primarily epinephrine) increased only during normoxic hypercapnia in proportion to the severity of the whole blood acidosis. Epinephrine levels were elevated 10-fold from 0.70 +/- 0.06 nM to 7.06 +/- 3.7 nM at the highest concentration of external CO2 (11.3 Torr) whereas norepinephrine increased 3-fold from 0.56 +/- 0.07 nM to 1.62 +/- 0.40 nM. The absence of catecholamine release into the circulation during hyperoxic hypercapnia was not due to inhibition of the 'catecholamine-releasing process' by abnormally elevated arterial oxygen tensions (PaO2 = approximately 400 Torr) because acutely anaemic and thus hypoxemic fish (haematocrit = 4.9 +/- 0.7%) displayed identical elevations of plasma catecholamines under both normoxic and hyperoxic conditions. The results of these experiments demonstrate that arterial hypoxemia, rather than blood acidosis per se, is the proximate stimulus causing catecholamine mobilization in rainbow trout during short-term environmental hypercapnia.