In situ cardiac function in Atlantic cod (Gadus morhua): effects of acute and chronic hypoxia

Recent in vivo experiments on Atlantic cod (Gadus morhua) acclimated to chronic hypoxia (6-12 weeks at 10 degrees C; Pw(O(2)) approximately 8-9 kPa) revealed a considerable decrease in the pumping capacity of the heart. To examine whether this diminished cardiac performance was due to the direct effects of chronic moderate hypoxia on the myocardium (as opposed to alterations in neural and/or hormonal control), we measured the resting and maximum in situ function of hearts from normoxia- and hypoxia-acclimated cod: (1) when initially perfused with oxygenated saline; (2) at the end of a 15 min exposure to severe hypoxia (P(O(2)) approximately 0.6 kPa); and (3) 30 min after the hearts had been reperfused with oxygenated saline. Acclimation to hypoxia did not influence resting (basal) in situ cardiac performance during oxygenated or hypoxic conditions. However, it caused a decrease in maximum cardiac output (Q(max)) under oxygenated conditions (from 49.5 to 40.3 ml min(-1) kg(-1); by 19%), that was due to diminished values for maximum stroke volume (V(S)) and scope for V(S). Severe hypoxia reduced in both groups to approximately 20 ml min(-1) kg(-1), yet, the hearts of hypoxia-acclimated fish were better able to sustain this level of Q under hypoxia, and the recovery of Q(max) (as compared with initial values under oxygenated conditions) was significantly improved (94% vs 83%). These data show that acclimation to hypoxia has a direct effect on cod myocardial function and/or physiology, and suggest that the cod heart shows some adaptations to prolonged hypoxia.