Mortola J P, Morgan C A, Virgona V
J Appl Physiol (1985). 1986 Oct;61(4):1329-36. doi: 10.1152/jappl.1986.61.4.1329.
Newborn rats were maintained in an hypoxic chamber (10% O2 in N2) from the day of birth up to 2 wk of postnatal life. Body weight (BW) and nose-tail length were less in the hypoxic exposed (H) rats than in control (C) animals growing in air. Hematocrit rose from about 37% to about 51%. Oxygen consumption (VO2), measured with a manometric method, was lower in H than in C rats; the difference remained at 5-7 days even after normalization by BW. At 5-7 days ventilation, measured with an airflow plethysmograph, was much more elevated in H rats (whether breathing 10% O2 or air) than in C rats, with an increase in both tidal volume and frequency. This indicates that the biphasic ventilatory response, characterized by an initial rise and then a fall of ventilation toward normoxic values, commonly observed in newborns during acute hypoxic challenge is an immediate but only transient response. The dry lung weight-to-BW ratio and alveolar size were larger in H than in C rats. Lung volumes at 20 cmH2O were similar, despite the smaller BW of the H rats. Hence, in the rat, chronic hypoxia in the immediate postnatal period increases O2-carrying capacity, decreases metabolic demands, increases alveolar O2 availability, and promotes structural changes in the lung that protect the gas exchange area and optimize the structure-function relationship of the lung. These results may also suggest that the lung structural alterations with chronic hypoxia should not be attributed to changes in VO2 but, eventually, to the ventilatory action of the organ.
新生大鼠从出生之日起至出生后2周,一直饲养在缺氧舱(氮气中含10%氧气)中。与在空气中生长的对照(C)动物相比,缺氧暴露(H)大鼠的体重(BW)和鼻尾长度较小。血细胞比容从约37%升至约51%。用测压法测量的耗氧量(VO2),H组大鼠低于C组大鼠;即使按体重进行归一化处理,这种差异在5 - 7天时仍然存在。在5 - 7天时,用气流体积描记器测量的通气量,H组大鼠(无论呼吸10%氧气还是空气)比C组大鼠升高得多,潮气量和频率均增加。这表明,在急性缺氧挑战期间新生儿中常见的以通气量先升高然后向常氧值下降为特征的双相通气反应是一种即时但仅短暂的反应。H组大鼠的肺干重与体重之比和肺泡大小比C组大鼠大。尽管H组大鼠体重较小,但在20 cmH2O时的肺容积相似。因此,在大鼠中,出生后早期的慢性缺氧增加了携氧能力,降低了代谢需求,增加了肺泡氧供应,并促进了肺的结构变化,这些变化保护了气体交换区域并优化了肺的结构 - 功能关系。这些结果还可能表明,慢性缺氧导致的肺结构改变不应归因于VO2的变化,而最终应归因于该器官的通气作用。