Overgaard Johannes, Gesser Hans, Wang Tobias
National Environmental Research Institute, Aarhus University, Silkeborg, Denmark.
J Exp Biol. 2007 May;210(Pt 10):1687-99. doi: 10.1242/jeb.001925.
Freshwater turtles overwintering in ice-covered ponds in North America may be exposed to prolonged anoxia, and survive this hostile environment by metabolic depression. Here, we review their cardiovascular function and regulation, with particular emphasis on the factors limiting cardiac performance. The pronounced anoxia tolerance of the turtle heart is based on the ability to match energy consumption with the low anaerobic ATP production during anoxia. Together with a well-developed temporal and spatial energy buffering by creatine kinase, this allows for cellular energy charge to remain high during anoxia. Furthermore, the turtle heart is well adapted to handle the adverse effects of free phosphate arising when phosphocreatine stores are used. Anoxia causes tenfold reductions in heart rate and blood flows that match the metabolic depression, and blood pressure is largely maintained through increased systemic vascular resistance. Depression of the heart rate is not driven by the autonomic nervous system and seems to arise from direct effects of oxygen lack and the associated hyperkalaemia and acidosis on the cardiac pacemaker. These intra- and extracellular changes also affect cardiac contractility, and both acidosis and hyperkalaemia severely depress cardiac contractility. However, increased levels of adrenaline and calcium may, at least partially, salvage cardiac function under prolonged periods of anoxia.
在北美冰封池塘中越冬的淡水龟可能会面临长时间的缺氧状况，并通过代谢抑制来在这种恶劣环境中存活。在此，我们回顾它们的心血管功能及调节，尤其着重于限制心脏功能的因素。龟心脏对缺氧的显著耐受性基于其在缺氧期间使能量消耗与低水平的无氧ATP生成相匹配的能力。再加上肌酸激酶发达的时间和空间能量缓冲作用，这使得细胞能量电荷在缺氧期间能保持较高水平。此外，龟心脏能很好地适应处理在磷酸肌酸储备被消耗时产生的游离磷酸盐的不利影响。缺氧会使心率和血流量降低十倍，这与代谢抑制相匹配，并且血压主要通过全身血管阻力增加得以维持。心率降低并非由自主神经系统驱动，似乎是由缺氧以及相关的高钾血症和酸中毒对心脏起搏器的直接影响所致。这些细胞内和细胞外的变化也会影响心脏收缩力，酸中毒和高钾血症都会严重抑制心脏收缩力。然而，肾上腺素和钙水平的升高可能至少部分地在长时间缺氧情况下挽救心脏功能。
