Department of Biology, McMaster University, Hamilton, ON, Canada.
Department of Biology, McMaster University, Hamilton, ON, Canada.
Comp Biochem Physiol A Mol Integr Physiol. 2015 Aug;186:66-74. doi: 10.1016/j.cbpa.2014.10.009. Epub 2014 Oct 23.
Hypoxia is an unremitting stressor at high altitudes that places a premium on oxygen transport by the respiratory and cardiovascular systems. Phenotypic plasticity and genotypic adaptation at various steps in the O2 cascade could help offset the effects of hypoxia on cellular O2 supply in high-altitude natives. In this review, we will discuss the unique mechanisms by which ventilation, cardiac output, and blood flow are controlled in high-altitude mammals and birds. Acclimatization to high altitudes leads to some changes in respiratory and cardiovascular control that increase O2 transport in hypoxia (e.g., ventilatory acclimatization to hypoxia). However, acclimatization or development in hypoxia can also modify cardiorespiratory control in ways that are maladaptive for O2 transport. Hypoxia responses that arose as short-term solutions to O2 deprivation (e.g., peripheral vasoconstriction) or regional variation in O2 levels in the lungs (i.e., hypoxic pulmonary vasoconstriction) are detrimental at in chronic high-altitude hypoxia. Evolved changes in cardiorespiratory control have arisen in many high-altitude taxa, including increases in effective ventilation, attenuation of hypoxic pulmonary vasoconstriction, and changes in catecholamine sensitivity of the heart and systemic vasculature. Parallel evolution of some of these changes in independent highland lineages supports their adaptive significance. Much less is known about the genomic bases and potential interactive effects of adaptation, acclimatization, developmental plasticity, and trans-generational epigenetic transfer on cardiorespiratory control. Future work to understand these various influences on breathing and circulation in high-altitude natives will help elucidate how complex physiological systems can be pushed to their limits to maintain cellular function in hypoxia.
缺氧是高原环境下持续存在的应激源，对呼吸系统和心血管系统的氧气运输提出了很高的要求。在氧气级联的各个步骤中，表型可塑性和基因型适应性可以帮助抵消高原环境对细胞氧气供应的影响。在这篇综述中，我们将讨论高海拔哺乳动物和鸟类中通气、心输出量和血流如何受到控制的独特机制。高原适应导致了一些呼吸和心血管控制的变化，这些变化增加了低氧环境下的氧气输送（例如，对低氧的通气适应）。然而，在低氧环境中适应或发育也可以以不利于氧气输送的方式改变心肺控制。作为对缺氧时氧气剥夺的短期解决方案而出现的缺氧反应（例如，外周血管收缩）或肺部氧气水平的区域变化（即低氧性肺血管收缩）在慢性高原缺氧中是有害的。许多高海拔分类群中出现了心肺控制的进化变化，包括有效通气增加、低氧性肺血管收缩减弱以及心脏和全身血管对儿茶酚胺敏感性的改变。这些变化中的一些在独立的高地谱系中平行进化，支持了它们的适应性意义。关于适应、适应、发育可塑性和跨代表观遗传转移对心肺控制的基因组基础和潜在的相互作用影响，我们知之甚少。未来的研究工作旨在了解这些对高海拔原生动物呼吸和循环的各种影响，将有助于阐明复杂的生理系统如何被推向极限，以维持缺氧环境下的细胞功能。
