Garner Molly, Stecyk Jonathan A W
Department of Biological Sciences, University of Alaska Anchorage, Anchorage, AK, 99508, USA.
Curr Res Physiol. 2022 Jul 12;5:312-326. doi: 10.1016/j.crphys.2022.07.001. eCollection 2022.
Multiple lines of evidence suggest that an inability of the ventricle to contract in coordination with the pacemaker during anoxia exposure may suppress cardiac pumping rate in anoxia-tolerant turtles. To determine under what extracellular conditions the ventricle could be the weak link that limits cardiac pumping, we compared, under various extracellular conditions, the intrinsic contractile properties of isometrically-contracting ventricular and atrial strips obtained from 21 °C- to 5 °C- acclimated turtles () that had been exposed to either normoxia or anoxia (16 h at 21 °C; 12 days at 5 °C). We found that combined extracellular anoxia, acidosis, and hyperkalemia (AAK), severely disrupted ventricular, but not right or left atrial, excitability and contractibility of 5 °C anoxic turtles. However, combined hypercalcemia and heightened adrenergic stimulation counteracted the negative effects of AAK. We also report that the turtle heart is resilient to prolonged diastolic intervals, which would ensure that contractile force is maintained if arrhythmia were to occur during anoxia exposure. Finally, our findings reinforce that prior temperature and anoxia experiences are central to the intrinsic contractile response of the turtle myocardium to altered extracellular conditions. At 21 °C, prior anoxia exposure preconditioned the ventricle for anoxic and acidosis exposure. At 5 °C, prior anoxia exposure evoked heightened sensitivity of the ventricle to hyperkalemia, as well as all chambers to combined hypercalcemia and increased adrenergic stimulation. Overall, our findings show that the ventricle could limit cardiac pumping rate during prolonged anoxic submergence in cold-acclimated turtles if hypercalcemia and heightened adrenergic stimulation are insufficient to counteract the negative effects of combined extracellular anoxia, acidosis, and hyperkalemia.
多条证据表明，在耐缺氧海龟中，缺氧暴露期间心室无法与起搏器协调收缩可能会抑制心脏泵血速率。为了确定在何种细胞外条件下心室可能成为限制心脏泵血的薄弱环节，我们在各种细胞外条件下，比较了从21℃至5℃适应环境的海龟（这些海龟在21℃暴露于常氧或缺氧环境16小时；在5℃暴露于常氧或缺氧环境12天）中获取的等长收缩心室和心房条带的内在收缩特性。我们发现，细胞外缺氧、酸中毒和高钾血症（AAK）联合作用严重破坏了5℃缺氧海龟心室的兴奋性和收缩性，但对右心房或左心房没有影响。然而，高钙血症和增强的肾上腺素能刺激联合作用抵消了AAK的负面影响。我们还报告说，海龟心脏对延长的舒张期具有弹性，这将确保在缺氧暴露期间发生心律失常时维持收缩力。最后，我们的研究结果强化了先前的温度和缺氧经历对于海龟心肌对细胞外条件改变的内在收缩反应至关重要。在21℃时，先前的缺氧暴露使心室对缺氧和酸中毒暴露产生了预处理。在5℃时，先前的缺氧暴露使心室对高钾血症以及所有腔室对高钙血症和增强的肾上腺素能刺激联合作用的敏感性增加。总体而言，我们的研究结果表明，如果高钙血症和增强的肾上腺素能刺激不足以抵消细胞外缺氧、酸中毒和高钾血症联合作用的负面影响，那么在冷适应海龟长时间缺氧潜水期间，心室可能会限制心脏泵血速率。
