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Cardiac stroke volume (SV) is compromised in Atlantic cod and rainbow trout following acclimation to hypoxia (i.e., 40% air saturation; ~8 kPa O2) at 10–12°C, and this is not due to changes in heart morphometrics or maximum achievable in vitro end-diastolic volume. To examine if this diminished SV may be related to compromised myocardial contractility, we used the work-loop method to measure work and power in spongy myocardial strips from normoxic- and hypoxic-acclimated steelhead trout when exposed to decreasing Po2 levels (21 to 1.5 kPa) at several frequencies (30–90 contractions/min) at 14°C (their acclimation temperature). Work required to lengthen the muscle, as during filling of the heart, was strongly frequency dependent (i.e., increased with contraction rate) but was not affected by hypoxic acclimation or test Po2. In contrast, although shortening work was less frequency dependent, this parameter and network (and power) 1) were consistently lower (by ~30–50 and ~15%, respectively) in strips from hypoxic-acclimated fish and 2) fell by ~40–50% in both groups from 20 to 1.5 kPa Po2, despite the already-reduced myocardial performance in the hypoxic-acclimated group. In addition, strips from hypoxic-acclimated trout showed a poorer recovery of net power (by ~15%) when returned to normoxia. These results strongly suggest that hypoxic acclimation reduces myocardial contractility, and in turn, may limit SV (possibly by increasing end-systolic volume), but that this diminished performance does not improve the capacity to maintain myocardial performance under oxygen limiting conditions. [ABSTRACT FROM AUTHOR]

The regulation of vascular resistance in fishes has largely been studied using isolated large conductance vessels, yet changes in tissue perfusion/vascular resistance are primarily mediated by the dilation/constriction of small arterioles. Thus, we adapted mammalian isolated microvessel techniques for use in fish, and examined how several agents affected the tone/resistance of isolated coronary arterioles (< 150 µm) from steelhead trout (O. mykiss) acclimated to 10, 5 and 1°C. At 10°C, the vessels showed a concentration-dependent dilation to adenosine (ADE; 61 ± 8%), sodium nitroprusside (SNP; 35 ± 10%) and serotonin (SER; 27 ± 2%) (all values maximum responses). A biphasic response (mild contraction then dilation) was observed in vessels exposed to increasing concentrations of epinephrine (EPI; 34 ± 9% dilation) and norepinephrine (NE; 32 ± 7% dilation), whereas the effect was less pronounced with bradykinin (BK; 12.5 ± 3.5% constriction vs. 6 ± 6% dilation). Finally, a mild constriction was observed after exposure to acetylcholine (ACh; 6.5 ± 1.4%), while endothelin (ET)-1 caused a strong dose-dependent increase in tone (79 ± 5% constriction). Acclimation temperature had varying effects on the responsiveness of vessels. The dilations induced by EPI, ADE, SER and SNP were reduced/eliminated at 5°C and/or 1°C as compared to 10°C. In contrast, acclimation to 5 and 1°C increased the maximum constriction induced by ACh and the sensitivity of vessels to ET-1 (but not the maximum response) at 1°C was greater. Acclimation temperature had no effect on the response to NE, and responsiveness to BK was variable. [ABSTRACT FROM AUTHOR]