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Recent in vivo experiments on Atlantic cod (Gadus morhua) acclimated to chronic hypoxia (6-12weeks at 10°C; Pwo2 -8-9kPa) 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 normoxiaand hypoxia-acclimated cod: (1) when initially perfused with oxygenated saline; (2) at the end of a 15min exposure to severe hypoxia (Po2 ∼0.6kPa); and (3) 30min 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 (Omax) under oxygenated conditions (from 49.5 to 40.3mlmin-1kg-1 by 19%), that was due to diminished values for maximum stroke volume (Vs) and scope for Vs. Severe hypoxia reduced in both groups to -20mlmin-1 kg-1, yet, the hearts of hypoxiaacclimated fish were better able to sustain this level of under hypoxia, and the recovery of Omax (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. [ABSTRACT FROM AUTHOR]

Oxygen consumption, as an indicator of routine metabolic rate (RoMR), and tissue-specific changes in protein synthesis, as measured by ³H-labelled phenylalanine incorporation rates, were determined in Astronotus ocellatus to investigate the cellular mechanisms behind hypoxia-induced metabolic depression and recovery. RoMR was significantly depressed, by approximately 50%, when dissolved oxygen levels reached 10% saturation (0.67±0.01 mg l-1 at 28±1°C). This depression in RoMR was accompanied by a 50-60% decrease in liver, heart and gill protein synthesis, but only a 30% decrease in brain protein synthesis. During recovery from hypoxia, an overshoot in RoMR to 270% of the normoxic rate was observed, indicating the accumulation of an oxygen debt during hypoxia. This conclusion was consistent with significant increase in plasma lactate levels during the hypoxic exposure, and the fact that lactate levels rapidly returned to pre-hypoxic levels. In contrast, a hyperactivation of protein synthesis did not occur, suggesting the overshoot in oxygen consumption during recovery is attributed to an increase in cellular processes other than protein synthesis. [ABSTRACT FROM AUTHOR]

Central vascular blood flows and ventilation were measured in conscious toads (Bufo marinus) at 15 and 25 degrees C. The animals were exposed to hypoxia (Fi(O)(sum)=0.10 and 0.05, where Fi(O)(sum) is the fractional oxygen concentration of inspired air) at both temperatures. In addition, the cardiorespiratory responses to hypercapnia (Fi(CO)(sum)=0.05) and atropine injection (5 mg kg(-)(1); 7.4 micromol kg(-)(1)) were studied at 25 degrees C. At 25 degrees C, systemic blood flow ( q_dot (sys)) exceeded pulmocutaneous blood flow ( q_dot (pc)), indicating a large net right-to-left shunt ( q_dot (pc)/ q_dot (sys) was 0.39). q_dot (pc)/ q_dot (sys) was reduced significantly to 0.22 at 15 degrees C. At both temperatures, q_dot (pc) increased significantly during hypoxia (from 26.2 to 50.8 ml min(-)(1 )kg(-)(1) at 25 degrees C and from 11. 2 to 18.9 ml min(-)(1 )kg(-)(1) at 15 degrees C), whereas q_dot (sys) changed little (from 77.2 to 66.2 ml min(-)(1 )kg(-)(1) at 25 degrees C and from 54.3 to 50.1 ml min(-)(1 )kg(-)(1) at 15 degrees C). As a result, the net right-to-left shunt was greatly reduced, while total cardiac output remained almost unaffected. The ventilatory response was more pronounced during hypercapnia but, since q_dot (pc) and q_dot (sys) were affected similarly, there was no change in the shunt pattern. In undisturbed toads at 25 degrees C, atropine injection increased q_dot (pc) and eliminated the net right-to-left shunt. This is consistent with the known vagal innervation of the pulmonary artery. The present study shows that the cardiac right-to-left shunt that prevails in undisturbed and resting toads is reduced with increased temperature and during hypoxia. These findings are consistent with the general view that the cardiac right-to-left shunt is regulated and reduced whenever oxygen delivery is compromised or metabolic rate is increased.