Abstract

Atlantic salmon Salmo salar with amoebic gill disease (AGD) were exposed to a graded hypoxia (135–40 mmHg water PO2) and blood samples analysed for respiratory gases and pH at 119, 79·5 and 40 mmHg water PO2. There were no differences in the rate of oxygen uptake between infected and control fish. However, arterial PO2, and pH were significantly lower in the infected fish whereas PCO2 was significantly higher in infected fish compared with controls prior to hypoxia and at 119 mmHg water PO2. At 79·5 and 40 mmHg water PO2 saturation, there were no significant differences in blood PO2 or pH although blood PCO2 was elevated in AGD affected fish at 50% hypoxia (79·5 mmHg water PO2). The elevated levels of PCO2 in fish affected by AGD resulted in a persistent respiratory acidosis even during hypoxic challenge. These data suggest that even though the fish were severely affected by AGD, the presence of AGD while impairing gas transfer under normoxic conditions, did not contribute to respiratory failure during hypoxia.

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