Blood oxygenation and cardiorespiratory function in steelhead trout (Oncorhynchus mykiss) challenged with an acute temperature increase and zatebradine-induced bradycardia

To explore whether temperature-dependent increases in cardiac output (Q) are mediated solely through heart rate (fH) in fish to ensure adequate/efficient blood oxygenation, we injected steelhead trout with saline (control) or zatebradine hydrochloride (1.0 mg kg−1), and measured blood oxygen status, cardiorespiratory variables and cardiorespiratory synchrony during a critical thermal maximum (CTMax) test. The increasing temperature regimen itself (from 12 °C to CTMax) resulted in large decreases in arterial oxygen partial pressure (PaO2) and content (CaO2) (by ∼35% and 25%, respectively). Further, there was little evidence of cardiorespiratory synchrony at 12 °C, and the number of fish that showed synchrony at high temperatures only increased marginally (to 3 out of 7) despite the large decrease in PaO2. These results: (1) indicate that in some situations (e.g. when ventilation is exclusively/predominantly dependent on buccal–opercular pumping) the upper thermal tolerance of fish may be constrained by both cardiovascular and ventilatory performance; and (2) question the importance of cardiorespiratory synchrony (ventilation–perfusion matching) for gas exchange in salmonids, and fishes, in general.Zatebradine injection decreased heart rate (fH) at 12 °C by 11% and limited maximum fH to 78.6±5.9 vs. 116.5±5.7 beats min−1 in controls. However, it did not affect maximum cardiac output (due to a compensatory increase in SV), ventilation, cardiorespiratory synchrony or PaO2. In contrast, metabolic scope and CTMax were lower in the zatebradine vs. control group [184.5±17.4 vs. 135.7±21.5 mL kg−1 h−1 (p<0.05) and 23.7±0.2 vs. 22.6±0.4 °C (p<0.08), respectively]. This result was unrelated to maximum fH or scope for fH, and occurred despite higher values for blood oxygen content and haematocrit at>18 °C in the zatebradine-treated fish. These latter findings suggest that zatebradine has non-pacemaker effects that limit tissue oxygen utilization and its usefulness for in vivo studies.