Abstract

During exposure to elevated water CO2 levels (hypercapnia), blood pH and tissue intracellular pH (pHi) in fish are initially reduced due to the rapid development of a respiratory acidosis. Blood pH recovery is associated with acid–base relevant ion transfer at the gills (i.e., Na+/H+ or Cl−/HCO3−), and generally occurs over 24–48 h during which time pHi recovery closely follows pH recovery of the blood. In the armoured catfish, Liposarcus pardalis, hypercapnia induces a large respiratory acidosis, but intracellular pH (pHi) of tissues such as the liver, heart and muscle is tightly regulated despite large reductions in plasma pH. Using an in situ perfused heart preparation, maximum cardiac performance (power output, cardiac output and stroke volume) was maintained at levels of up to 5% CO2 in L. pardalis. Maintenance of heart function under these conditions was associated with preferential pHi regulation. Following exhaustive exercise and 2 h of anoxia, there was little evidence for lactate incorporation into the skull or bony plates, but liver, heart and brain pHi were preferentially regulated despite a large uncompensated plasma acidosis, indicating that the type of acidosis does not alter the pattern of acid–base regulation in this species. This pattern of preferential pHi regulation differs markedly from that of most fish investigated to date; however, it has also been observed in two other facultative air-breathing fishes, Synbranchus marmoratus and Amia calva, and may be associated with the evolution of air-breathing.

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