Slay Christopher E, Enok Sanne, Hicks James W, Wang Tobias
Department of Ecology and Evolutionary Biology, University of California Irvine, Irvine, CA 92697, USA Zoophysiology, Institute for Biological Sciences, Aarhus University, DK-8000 Aarhus, Denmark.
Zoophysiology, Institute for Biological Sciences, Aarhus University, DK-8000 Aarhus, Denmark Inderdisciplinary Nanoscience Center, Aarhus University, DK-8000 Aarhus, Denmark.
J Exp Biol. 2014 May 15;217(Pt 10):1784-9. doi: 10.1242/jeb.092841. Epub 2013 Dec 5.
Physiological cardiac hypertrophy is characterized by reversible enlargement of cardiomyocytes and changes in chamber architecture, which increase stroke volume and via augmented convective oxygen transport. Cardiac hypertrophy is known to occur in response to repeated elevations of O2 demand and/or reduced O2 supply in several species of vertebrate ectotherms, including postprandial Burmese pythons (Python bivittatus). Recent data suggest postprandial cardiac hypertrophy in P. bivittatus is a facultative rather than obligatory response to digestion, though the triggers of this response are unknown. Here, we hypothesized that an O2 supply-demand mismatch stimulates postprandial cardiac enlargement in Burmese pythons. To test this hypothesis, we rendered animals anemic prior to feeding, essentially halving blood oxygen content during the postprandial period. Fed anemic animals had heart rates 126% higher than those of fasted controls, which, coupled with a 71% increase in mean arterial pressure, suggests fed anemic animals were experiencing significantly elevated cardiac work. We found significant cardiac hypertrophy in fed anemic animals, which exhibited ventricles 39% larger than those of fasted controls and 28% larger than in fed controls. These findings support our hypothesis that those animals with a greater magnitude of O2 supply-demand mismatch exhibit the largest hearts. The 'low O2 signal' stimulating postprandial cardiac hypertrophy is likely mediated by elevated ventricular wall stress associated with postprandial hemodynamics.
生理性心脏肥大的特征是心肌细胞可逆性增大以及心腔结构改变，这会增加每搏输出量，并通过增强对流性氧运输来实现。已知在几种脊椎动物变温动物中，包括餐后的缅甸蟒（Python bivittatus），心脏肥大是对氧气需求反复升高和/或氧气供应减少的反应。最近的数据表明，缅甸蟒餐后的心脏肥大是对消化的一种适应性而非强制性反应，尽管这种反应的触发因素尚不清楚。在这里，我们假设氧气供需不匹配会刺激缅甸蟒餐后心脏增大。为了验证这一假设，我们在喂食前使动物贫血，基本上在餐后期间将血氧含量减半。喂食贫血动物的心率比禁食对照组高126%，再加上平均动脉压增加71%，这表明喂食贫血动物的心脏工作显著增加。我们发现喂食贫血动物有明显的心脏肥大，其心室比禁食对照组大39%，比喂食对照组大28%。这些发现支持了我们的假设，即那些氧气供需不匹配程度更大的动物心脏最大。刺激餐后心脏肥大的“低氧信号”可能是由与餐后血液动力学相关的心室壁应力升高介导的。
