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Adrenergic protection of the fish heart under simulated exercise conditions Hanson, Linda Marie


Exercise is an integral part of the survival of vertebrates. However, intense exercise disrupts extracellular homeostasis, resulting in venous blood becoming hypoxic, hyperkalemic and acidotic. These changes challenge the heart, as the venous blood passing through the ventricular lumen is the sole source of myocardial support for most vertebrates. Consequently, during exercise when the heart is working its hardest it must ironically be supported by the hostile composition of venous blood. Rainbow trout (Oncorhynchus mykiss) and African catfish (Claris gariepinus) were used to examine the role of adrenergic stimulation in protecting cardiac performance during exercise-induced changes in venous blood composition. As cardiac performance is ultimately limited by oxygen supply, in situ perfused rainbow trout hearts were first used to determine the effect of adrenergic stimulation on the venous hypoxic threshold during simulated exercise conditions (5.0 mM K⁺, pH 7.5); where the hypoxic threshold is defined as the lowest level of venous oxygen tension (Pvo₂) that can support maximum cardiac performance. Hearts were tested under these relevant conditions with both tonic (5 nM adrenaline, AD) and maximal (500 nM AD) adrenergic stimulation. With 5 nM AD maximum cardiac performance in hearts at 10°C was significantly reduced even at normoxia. In contrast, 500 nM AD fully protected cardiac performance under hyperkalemia and acidosis to hypoxia of 2.0 kPa, a Pvo₂ close to routine values in vivo. Temperature acclimation alters the response of the rainbow trout heart to adrenaline such that an increase in acclimation temperature is associated with a decrease in adrenergic sensitivity. To determine how this reduction in adrenergic effectiveness alters the protection afforded to the heart during exercise the in situ hypoxic threshold was determined for perfused rainbow trout hearts at 18°C. The hypoxic threshold at 18°C under the combined hyperkalemic, acidotic exposure with 500 nM AD was 5.6 kPa. In rainbow trout, the loss of adrenergic sensitivity at high temperature is attributed to a decrease in cell surface β-adrenoceptor density (Bmax). This does not seem to be a universal mechanism among fish as no evidence of Bmax modulation was found in the tropical African Catfish.

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