Hypoxia tolerance and preconditioning are not additive in the trout (Oncorhynchus mykiss) heart.

Research has shown that the trout heart is normally hypoxia-sensitive, and that it can be preconditioned. However, we have identified a group of rainbow trout Oncorhynchus mykiss that shows a surprising degree of myocardial hypoxia tolerance. In this study, we used in situ hearts from these fish as a comparative model to examine whether the cardioprotective effects afforded by hypoxic adaptation and preconditioning are additive. In situ trout hearts were exposed to severe hypoxia (perfusate PO2 5-10 mmHg) in the absence and presence of a transient hypoxic pre-exposure (preconditioning). The four groups studied were: (1) control (no hypoxia); (2) 5 min of severe hypoxia; (3) 30 min of severe hypoxia; and (4) 5 min of severe hypoxia (hypoxic preconditioning) followed 20 min later by 30 min of severe hypoxia. 30 min of severe hypoxia significantly decreased maximum cardiac output and stroke volume by 15-30%. However, hypoxic preconditioning failed to confer any protection against post-hypoxic myocardial dysfunction. This work shows that the protection afforded by inherent myocardial hypoxia tolerance and preconditioning are not additive in this population of trout, and strongly suggests that the relationship between hypoxic adaptation and preconditioning in fishes resembles that of the neonatal/immature, not adult, mammalian heart. Further, our results (1) indicate that stretch (volume loading) and chronic exposure to low levels of adrenaline (15 nmol l(-1)) do not confer any protection against hypoxia-related myocardial dysfunction in this population, and (2) validate the use of the in situ trout heart as a comparative model for studying aspects of myocardial hypoxia tolerance and preconditioning in vertebrates.