The goldfish (Carassius auratus) is known for its physiologic ability to survive even long periods of oxygen limitation (hypoxia), adapting the cardiac performance to the requirements of peripheral tissue perfusion. We here investigated the effects of short-term moderate hypoxia on the heart, focusing on ventricular adaptation, in terms of hemodynamics and structural traits. Functional evaluations revealed that animals exposed to 4 days of environmental hypoxia increased the hemodynamic performance evaluated on ex vivo cardiac preparations. This was associated with a thicker and more vascularized ventricular compact layer and a reduced luminal lacunary space. Compared to normoxic animals, ventricular cardiomyocytes of goldfish exposed to hypoxia showed an extended mitochondrial compartment and a modulation of proteins involved in mitochondria dynamics. The enhanced expression of the pro-fission markers DRP1 and OMA1, and the modulation of the short and long forms of OPA1, suggested a hypoxia-related mitochondria fission. Our data propose that under hypoxia, the goldfish heart undergoes a structural remodelling associated with a potentiated cardiac activity. The energy demand for the highly performant myocardium is supported by an increased number of mitochondria, likely occurring through fission events.

金鱼（Carassius auratus）以其即使在长期缺氧（缺氧）的情况下也能生存的生理能力而闻名，从而使心脏性能适应周围组织灌注的要求。我们在这里研究了短期中度缺氧对心脏的影响，重点关注心室适应、血流动力学和结构特征。功能评估显示，暴露于 4 天环境缺氧的动物​​增加了对离体心脏制剂评估的血流动力学性能。这与更厚且血管化的心室致密层和管腔腔隙减少有关。与含氧量正常的动物相比，暴露于缺氧的金鱼的心室心肌细胞显示出扩大的线粒体区室和参与线粒体动力学的蛋白质的调节。促裂变标记物 DRP1 和 OMA1 的表达增强，以及 OPA1 的短形式和长形式的调节，表明缺氧相关的线粒体裂变。我们的数据表明，在缺氧情况下，金鱼心脏会经历与增强的心脏活动相关的结构重塑。高性能心肌的能量需求由线粒体数量的增加来支持，这可能是通过裂变事件发生的。