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Our aim was to study the effects of hypoxia on the release of salmon cardiac peptide (sCP) from an isolated heart ventricle of trout during a constant mechanical load. Trout heart ventricles were studied in vitro. The ventricle was placed in an organ bath at 12 °C in which a constant mechanical load could be imposed on the ventricle while buffer solution was circulating. Ventricles were field-stimulated with a supramaximal voltage pulse at a rate of about 0.3 s⁻¹. Samples of 1 ml were collected at an interval of 10 min for 200 min from the organ bath and assessed with a radioimmunoassay for sCP. After a control period of 20 min, ventricles were exposed to hypoxia produced with N₂ gassing (n = 9) or to hypoxia with 20 mM BDM, a nonselective myosin ATPase inhibitor locking cross-bridges in a pre-power-stroke state inhibiting force production with normal electrical activity (n = 10). In this model and setup, hypoxia stimulated the release of sCP, but the interindividual variation in the response was large. At the end of hypoxia exposure, the concentration of sCP in the organ bath was about sixfold higher than at the start of the exposure (P < 0.05, one-way ANOVA for repeated measurements, followed by Dunnett's multiple comparison test). When BDM was introduced into the bath, the ventricle still secreted sCP but the hypoxic response was smaller than in the experiments without BDM. In the trout heart ventricle, there is a hypoxia-sensitive component in the release mechanism of sCP which is independent of contraction.

It is not known whether changes in antioxidant levels always occur in fish in response to the oxidative stress that usually accompanies a hypoxic challenge. The studies of antioxidant responses to hypoxia in fish have mostly focused on very anoxia-tolerant species and indicate that there is an enhancement of antioxidant defenses. Here we present new data on redox-active antioxidants from three species, which range in their tolerance to hypoxia: the epaulette shark, threespine stickleback, and rainbow trout, together with a compilation of results from other studies that have measured oxidative stress parameters in hypoxia-exposed fish. The results suggest that in general, fish do not show an increase in redox-active antioxidant defense in response to oxidative stress associated with hypoxia. Rather, the changes in antioxidant defenses during hypoxia are very much species- and tissue-specific and are not linked to the level of hypoxia tolerance of the fish species.

The occurrence and pH dependence (pHe 7-8) of the adrenergic red cell responses of two salmonids, trout and whitefish, and a percinid, pikeperch were studied. These are all species that live in well-oxygenated waters. The responses were compared to those of carp, which tolerates oxygen-deficient waters.The adrenergic responses of trout and whitefish red cells were pronounced. In these species red cell swelling, the accumulation of sodium and chloride in the cell, and the increase in red cell oxygen content at atmospheric oxygen tension were maximal at pH 7.3. In contrast, pikeperch red cells responded to β-adrenergic stimulation only at extracellular pH 7.1. In carp, the adrenergic response, occurring below extracellular pH 7.5, was small as compared to the two salmonids. In each case the onset of the adrenergic response coincided with the onset of the Root effect.The differences in the adrenergic responses between the two salmonids and pikeperch suggest that the occurrence of the adrenergic response is not directly related to the environmental oxygen requirements of the species, but may be linked to the activity pattern.