Kellogg R H
Fed Proc. 1977 Apr;36(5):1658-63.
When a sea-level resident ascends to a high altitude, his breathing immediately increases because of hypoxic stimulation of the peripheral chemoreceptors. In many species the aortic bodies are relatively unimportant in this response compared to the carotid bodies. When the subject stays at that altitude, his breathing increases progressively in the next few hours and days in a process termed ventilatory acclimatization and does not immediately return to control levels when hypoxia is terminated. Evidence is summarized indicating that this chronic process does not depend on the peripheral chemoreceptors or an initial respiratory alkalosis. Historical review indicates that the process of ventilatory acclimatization was initially attributed to renal excretion of plasma bicarbonate with development of a metabolic acidosis; but subsequent measurements indicated this process did not lower the arterial pH sufficiently to account for the ventilatory stimulation. More recently, ventilatory acclimatization has been attributed to accelerated removal of bicarbonate from the cerebrospinal fluid (CSF), producing a metabolic acidosis in the region of the medullary chemoreceptors; but still more recent observations indicate that this process, contrary to earlier observations, does not lower the CSF pH sufficiently to account for the ventilatory stimulation, either. Some other mechanism should be sought.
当海平面地区的居民上升到高海拔地区时,由于外周化学感受器受到低氧刺激,其呼吸会立即加快。在许多物种中,与颈动脉体相比,主动脉体在这种反应中相对不太重要。当受试者停留在该海拔高度时,在接下来的数小时和数天内,其呼吸会在一个称为通气适应的过程中逐渐增加,并且在低氧状态终止后不会立即恢复到对照水平。有证据表明,这一慢性过程并不依赖于外周化学感受器或初始的呼吸性碱中毒。历史回顾表明,通气适应过程最初被认为是由于血浆碳酸氢盐经肾脏排泄并伴有代谢性酸中毒的发生;但随后的测量表明,这一过程并不能充分降低动脉pH值以解释通气刺激现象。最近,通气适应被归因于脑脊液(CSF)中碳酸氢盐的清除加速,从而在延髓化学感受器区域产生代谢性酸中毒;但更新的观察结果表明,与早期观察结果相反,这一过程也不能充分降低脑脊液pH值以解释通气刺激现象。应该寻找其他一些机制。