Hall P, Schatte C L, Fitch J W
J Appl Physiol. 1975 Feb;38(2):279-81. doi: 10.1152/jappl.1975.38.2.279.
The influence of hypoxic acclimatization at altitudes of 0, 5,000, or 15,000 ft on the relative susceptibility to acute oxygen poisoning was determined in 288 adult female mice. After acclimatization periods of 1, 2, 4, or 8 wk, the mice were exposed to oxygen at high pressures (OHP) of 4, 6, or 9 ATA and the times to convulsion and death recorded. A factorial analysis of variance indicated that altitude and OHP level had inverse, log-linear effects on both parameters. The duration of acclimatization progressively decreased the time to death. The onset of convulsions and death was independent of body weight. There were significant interactions on the measured parameters between various combinations of altitude, OHP level, and duration of acclimatization. While alterations in the metabolism of gamma-aminobutyric acid and high-energy compounds are common to both hypoxia and hyperoxia, the most plausible explanation of the results relates to the decrease in buffer base induced by hypoxic acclimatization which might have caused CO2 potentiation of OHP symptoms.
在288只成年雌性小鼠中,研究了在海拔0、5000或15000英尺进行低氧适应对急性氧中毒相对易感性的影响。在1、2、4或8周的适应期后,将小鼠暴露于4、6或9ATA的高压氧(OHP)环境中,并记录惊厥和死亡时间。析因方差分析表明,海拔高度和OHP水平对这两个参数具有反向的对数线性效应。适应期的持续时间逐渐缩短死亡时间。惊厥和死亡的发生与体重无关。海拔、OHP水平和适应期持续时间的各种组合之间,在测量参数上存在显著的交互作用。虽然γ-氨基丁酸和高能化合物的代谢变化在低氧和高氧状态下都很常见,但对结果最合理的解释是,低氧适应引起的缓冲碱减少可能导致了OHP症状的二氧化碳增强作用。