Exceptional CO₂ tolerance in white sturgeon (Acipenser transmontanus) is associated with protection of maximum cardiac performance during hypercapnia in situ.

White sturgeon rank among the most CO₂-tolerant fish species examined to date. We investigated whether this exceptional CO₂ tolerance extended to the heart, an organ generally viewed as acidosis intolerant. Maximum cardiac output (Q(max)) and maximum cardiac power output (PO(max)) were assessed using a working, perfused, in situ heart preparation. Exposure to a Pco₂ of 3 kPa for 20 min had no significant effect on maximum cardiac performance, while exposure to 6-kPa Pco₂ reduced heart rate, Q(max), PO(max), and rate of ventricular force generation (F(O)) by 23%, 28%, 26%, and 18%, respectively; however, full recovery was observed in all these parameters upon return to control conditions. These modest impairments during exposure to 6-kPa Pco₂ were associated with partially compensated intracellular ventricular acidosis. Maximum adrenergic stimulation (500 nmol L⁻¹ adrenaline) during 6-kPa Pco₂ protected maximum cardiac performance via increased inotropy (force of contraction) without affecting heart rate. Exposure to higher CO₂ levels associated with morbidity in vivo (i.e., 8-kPa Pco₂) induced arrhythmia and a reduction in stroke volume during power assessment. Clearly, white sturgeon hearts are able to increase cardiac performance during severe hypercapnia that is lethal to other fishes. Future work focusing on atypical aspects of sturgeon cardiac function, including the lack of chronotropic response to adrenergic stimulation during hypercapnia, is warranted.