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  • Title: Lack of arterial PO2 downregulation in Atlantic salmon (Salmo salar L.) during long-term normoxia and hyperoxia.
    Author: Kristensen T, Rosseland BO, Kiessling A, Djordevic B, Massabau JC.
    Journal: Fish Physiol Biochem; 2010 Dec; 36(4):1087-95. PubMed ID: 20221686.
    Abstract:
    Regulation of arterial partial pressure of O2 (PaO2) in Atlantic salmon (Salmo salar) was investigated during resting conditions in normoxic and hyperoxic water. Dorsal aorta cannulated adult Atlantic salmon (1.2-1.6 kg, n=8) were exposed to 2 week sequential periods of normoxia [16.7±1.1 kPa (mean±SD)] and hyperoxia (34.1±4.9 kPa) in individual tanks containing seawater (33.7±0.2 ppt) at stable temperature conditions (8.7±0.7°C) and a light regime of L:D=12:12. Tank design and sampling procedures were optimized to provide suitable shelter and current for the fish, and to allow repeated, undisturbed sampling of blood from free-swimming fish. Fish were sampled regularly through the experimental period. PwO2, PaO2, blood ion composition (Na+, K+, Cl-), acid-base status (pH, PCO2, HCO3-), haematocrit and glucose were measured. The most frequently observed PaO2 values were in the range of 60-80% of PwO2, both during normoxia and hyperoxia, and PaO2 values were significantly lower during normoxia than during hyperoxia. Blood pH, PCO2 and HCO3- were significantly elevated during hyperoxia, while, Na+, Cl- and Hct were significantly lower. K+ and glucose showed no significant differences. This study demonstrates a lack PaO2 regulation in Atlantic salmon to low partial pressures, in contrast to previous reports for many aquatic gill breathing animals. Both during normoxia and hyperoxia, PaO2 reflects PwO2, and alterations in external PO2 consequently result in proportional arterial PO2 changes. Physiological adaptation to hyperoxia, as illustrated by changes in several blood parameters, does not include down-regulation of PaO2 in Atlantic salmon. The lack of PaO2 regulation may make Atlantic salmon vulnerable to the oxidative stress caused by increased free radical formation in hyperoxic conditions.
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