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First published online June 15, 2006
Journal of Experimental Biology 209, 2442-2451 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02237
The role of adrenergic stimulation in maintaining maximum cardiac performance in rainbow trout (Oncorhynchus mykiss) during hypoxia, hyperkalemia and acidosis at 10°C
1 Department of Zoology, University of British Columbia, 6270 University
Blvd., Vancouver, BC V6T 1Z4, Canada
2 Zoophysiology, Gothenburg University, Gothenberg, Sweden
3 Biological Sciences, Simon Fraser University, Burnaby, BC V5A 1S6,
Canada
4 Faculty of Land and Food Systems and Department of Zoology, University of
British Columbia, Vancouver, BC V6T 1Z4, Canada
* Author for correspondence (e-mail: hanson{at}zoology.ubc.ca)
Accepted 22 March 2006
As rainbow trout approach exhaustion during prolonged exercise, they maintain maximum cardiac output despite the fact their venous blood, which bathes the heart, becomes hypoxic, acidotic and hyperkalemic. Because these factors are individually recognized to have detrimental inotropic and chronotropic effects on cardiac performance, we hypothesized that adrenergic stimulation is critical in maintaining maximum cardiac performance under these collectively adverse conditions in vivo. To test this hypothesis, maximum cardiac performance in the presence and absence of maximal adrenergic stimulation was assessed with in situ rainbow trout hearts using relevant hyperkalemic (5.0 mmol l–1 K+), acidotic (pH 7.5) and hypoxic challenges. With tonic adrenergic stimulation (5.0 nmol l–1 adrenaline), hearts produced only 44.8±14.6% of their normal maximum cardiac output when exposed under normoxic conditions (20 kPa) to the hyperkalemic, acidotic perfusate, indicating that in vivo there was no refuge from cardiac impairment even if venous blood was fully oxygenated. By contrast, maximum adrenergic stimulation (500 nmol l–1 adrenaline), fully protected maximum cardiac performance under hyperkalemic and acidotic conditions over a wide range of oxygen availability, from normoxia to 2.0 kPa, a venous oxygen tension close to routine values in vivo. Extending the level of hypoxia to 1.3 kPa resulted in a 43.6±2.8% decrease in maximum cardiac output, with hearts failing when tested at 1.0 kPa. Our results suggest that adrenergic stimulation of the trout heart is critical in maintaining maximum performance during prolonged swimming tests, and probably during all forms of exhaustive activity and recovery, when venous blood is hyperkalemic, acidotic and hypoxic.
Key words: acidosis, adrenaline, exercise, heart, hyperkalemia, hypoxia, maximum cardiac performance, Oncorhynchus mykiss, PvO2, rainbow trout, teleost
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