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The air-breathing Alaska blackfish (Dallia pectoralis) remodels ventricular Ca2+ cycling with chronic hypoxic submergence to maintain ventricular contractility.

Shiels HA, White E, Couturier CS, Hall D, Royal S, Galli GLJ and Stecyk JAW (2022). Curr Res Physiol. 10;5:25-35.

Click for Abstract : The Alaska blackfish (Dallia pectoralis) is a facultative air-breather endemic to northern latitudes where it remains active in winter under ice cover in cold hypoxic waters. To understand the changes in cellular Ca2+�cycling that allow the heart to function in cold hypoxic water, we acclimated Alaska blackfish to cold (5 �C) normoxia or cold hypoxia (2.1-4.2 kPa; no air access) for 5-8 weeks. We then assessed the impact of the acclimation conditions on intracellular Ca2+�transients (?[Ca2+]i) of isolated ventricular myocytes and contractile performance of isometrically-contracting ventricular strips. Measurements were obtained at various contractile frequencies (0.2-0.6 Hz) in normoxia, during acute exposure to hypoxia, and reoxygenation at 5 �C. The results show that hypoxia-acclimated Alaska blackfish compensate against the depressive effects of hypoxia on excitation-contraction coupling by remodelling cellular ?[Ca2+]i�to maintain ventricular contractility. When measured at 0.2 Hz in normoxia, hypoxia-acclimated ventricular myocytes had a 3.8-fold larger ?[Ca2+]i�peak amplitude with a 4.1-fold faster rate of rise, compared to normoxia-acclimated ventricular myocytes. At the tissue level, maximal developed force was 2.1-fold greater in preparations from hypoxia-acclimated animals. However, maximal attainable contraction frequencies in hypoxia were lower in hypoxia-acclimated myocytes and strips than preparations from normoxic animals. Moreover, the inability of hypoxia-acclimated ventricular myocytes and strips to contract at high frequency persisted upon reoxygenation. Overall, the findings indicate that hypoxia alters aspects of Alaska blackfish cardiac myocyte Ca2+�cycling, and that there may be consequences for heart rate elevation during hypoxia, which may impact cardiac output�in vivo.

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