THE EFFECTS OF HYPOXIA, HYPEROXIA OR HYPERCAPNIA ON THE ACID-BASE DISEQUILIBRIUM IN THE ARTERIAL BLOOD OF RAINBOW TROUT.

An extracorporeal circulation in combination with a stop­flow technique was used to characterize the acid­base disequilibrium in the arterial blood of rainbow trout Oncorhynchus mykiss during environmental hypoxia, hyperoxia or hypercapnia. Arterial blood was routed from the coeliac artery through an external circuit in which pH (pHa), partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2) were monitored continuously. The stop­flow condition was imposed by turning off the pump which drove the external loop. Water PO2 or PCO2 was adjusted to give the experimental conditions by bubbling N2, O2 or CO2 through a water equilibration column supplying the fish. During normoxia, the arterial blood exhibited a positive acid­base disequilibrium of approximately 0.04 pH units; that is, pH increased over the stop­flow period by 0.04 units. The extent of the imbalance was increased significantly by hypoxia (final PaO2=2.7­3.7 kPa; deltapH=0.05 units). In fish exposed to hyperoxia (final PaO2=47­67 kPa), the direction of the disequilibrium was reversed; pHa declined by 0.03 units. During hyperoxia, CO2 excretion was impaired by 63 % and the PCO2 of postbranchial blood was higher than that of prebranchial blood. It is therefore conceivable that a reversal of the normal, outwardly directed, diffusion gradient for CO2 accounted for the negative disequilibrium; CO2 uptake at the gills would drive plasma CO2/HCO3-/H+ reactions towards CO2 hydration and H+ formation. During hypercapnia, fish exhibited a twofold increase in the positive pH disequilibrium (deltapH=0.06 units). The results of this study confirmed the existence of an acid­base disequilibrium in the arterial blood of rainbow trout and clearly demonstrated that the extent and/or direction of the disequilibrium are influenced by the respiratory status of the fish.