Bassett D J, Fisher A B
J Appl Physiol Respir Environ Exerc Physiol. 1979 May;46(5):943-9. doi: 10.1152/jappl.1979.46.5.943.
Lung metabolism on exposure to hyperbaric oxygen was studied in rat lungs perfused with artificial media and ventilated with O2 at 0.2, 1, or 5 ATA. During the first 80 min of exposure to O2 at 5 ATA, glucose utilization increased 55%, lactate plus pyruvate production increased 45%, total CO2 production increased 47%, tissue ATP decreased 17%, and the ATP/ADP decreased 29% compared with 0.2 ATA O2. The increased CO2 production was due to a nearly twofold stimulation of pentose cycle activity whereas mitochondrial CO2 production did not change significantly. There were no significant differences in metabolism between lungs studied at 0.2 and 1 ATA O2. During the next hour of perfusion, there was a marked increase in mitochondrial CO2 production of control lungs but tissue ATP/ADP did not change significantly. With oxygen at 5 ATA, mitochondrial CO2 production increased only slightly, tissue ATP/ADP decreased further, and lungs demonstrated accumulation of edema fluid. The results indicate that exposure of lungs to hyperbaric oxygen results in stimulation of NADPH turnover through the pentose cycle and increased ATP generation, although the increased rate was not sufficient to maintain normal ATP/ADP.
在灌注人工培养基并用0.2、1或5个绝对大气压的氧气进行通气的大鼠肺中,研究了暴露于高压氧下的肺代谢情况。在暴露于5个绝对大气压的氧气的最初80分钟内,与0.2个绝对大气压的氧气相比,葡萄糖利用率增加了55%,乳酸和丙酮酸的生成增加了45%,总二氧化碳生成增加了47%,组织ATP减少了17%,ATP/ADP降低了29%。二氧化碳生成增加是由于戊糖循环活性几乎增加了两倍,而线粒体二氧化碳生成没有显著变化。在0.2和1个绝对大气压的氧气下研究的肺之间,代谢没有显著差异。在接下来的一小时灌注过程中,对照肺的线粒体二氧化碳生成显著增加,但组织ATP/ADP没有显著变化。在5个绝对大气压的氧气条件下,线粒体二氧化碳生成仅略有增加,组织ATP/ADP进一步降低,并且肺出现了水肿液积聚。结果表明,肺暴露于高压氧会导致通过戊糖循环刺激NADPH周转并增加ATP生成,尽管增加的速率不足以维持正常的ATP/ADP。