A perfused rainbow trout heart was developed which generated its own intrinsic heart rate and a physiological power output. This preparation was used to examine the intrinsic mechanical properties of the trout heart, the dose-response effects of catecholamines and extracellular calcium on these properties, and the effects of catecholamines and extracellular calcium during exposure to acidotic conditions. The trout heart was relatively pressure-insensitive to a physiological range of ventral aortic pressures. Preload exerted an important control over cardiac output through the Starling response. Heart rate was independent of both these intrinsic mechanisms. The intrinsic mechanical capabilities of the trout heart were greater than those observed previously in less active, benthic teleosts. Physiological concentrations of catecholamines significantly improved cardiac contractility through positive inotropy and chronotropy. Adrenaline was more potent than noradrenaline, indicating that these effects were mediated by beta 2-adrenoceptors. Elevated extracellular calcium produced only a modest improvement of cardiac contractility compared to that produced by adrenaline. Positive inotropy and negative chronotropy were observed with elevated extracellular calcium. Extracellular acidosis always reduced cardiac contractility through negative chronotropy and inotropy. Extracellular calcium improved the inotropic state of the acidotic heart and restored contractility, but the overall improvement of cardiac performance was compromised by an accompanying negative chronotropy. Physiological levels of adrenaline improved cardiac performance during extracellular acidosis. The roles of catecholamines and extracellular calcium are discussed with respect to post-exercise cardiac performance in trout.

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