Effects of hypercapnia on blood-gas and acid-base status in the white sturgeon, Acipenser transmontanus

The effect of environmental hypercapnia on respiratory and acid-base variables was studied in white sturgeon, Acipenser transmontanus. Blood PCO2, PO2, pH, hemoglobin concentration, and plasma lactate, glucose, catecholamines and cortisol were measured first under normocapnia (water PCO2 < 0.5 Torr, 1 Torr = 133.32 Pa), then under hypercapnia (25–35 Torr) and a final return to normocapnia at 19 ± 0.5 °C. Acute (≤ 2h) hypercapnia significantly increased arterial PCO2 (8-fold increase), ventilation frequency (2-fold increase), plasma HCO3− (2.3-fold) and decreased arterial pH (to 7.15 ± 0.02). After 24 h, norepinephrine, epinephrine and cortisol, were significantly increased, and arterial pH reached its nadir (7.10 ± 0.03). During the 72- and 96-h-periods, arterial PCO2 (24 ± 4.4 Torr) and ventilatory frequency (105 ± 5 breaths min−1) stabilized, HCO3− reached its apparent maximum (23.6 ± 0.0 mmol−1), glucose decreased by 32%, and pH increased significantly to 7.31 + 0.03. The return to normocapnia completely restored arterial PCO2 (2.5 ± 0.14 Torr), HCO3− (7.4 ± 0.59 mmol · l−1), ventilation frequency (71 ± 7 breaths · min−1), and pH (7.75 ± 0.04). Overall, hypercapnia produced a respiratory acidosis, hyperventilation, a transient norepinephrine “spike”, and increased plasma catecholamines, cortisol, and arterial PO2. The respiratory acidosis was only partially compensated (35% pH restoration) 96 h after the onset of hypercapnia and resulted in a significantly decreased blood-O2 affinity (Bohr effect), as determined by construction of in vitro blood O2 equilibrium curves at 15 °C and 20 °C. Prolonged exposure to hypercapnia may lead to acid-base disturbances and negatively affect growth of white sturgeon.