Belik J, Light R B
Department of Pediatrics, University of Manitoba, Winnipeg, Canada.
Pediatr Res. 1988 Jun;23(6):565-8. doi: 10.1203/00006450-198806000-00006.
Hyperventilation has been shown to cause increased whole body oxygen consumption (VO2) and lactic acid production in human and animal mature subjects, but limited data are available in neonates. We investigated the effect of hypocarbic and normocarbic hyperventilation during normoxia and hypoxia (fractional inspired oxygen concentration = 0.14) upon the VO2 in anesthetized and paralyzed piglets. Systemic arterial, pulmonary arterial, and left and right atrial pressures as well as cardiac output and body temperature were continuously recorded. Hypocarbic hyperventilation (PaCO2 = 19 +/- 1 mm Hg; pH = 7.58 +/- 0.02) was associated with a significant decrease in systemic and pulmonary arterial pressures and cardiac output. These measurements returned to values similar to the initial normoventilation ones when PaCO2 was increased by adding CO2 to the inspired gas, whereas hyperventilation was continued. Neither hyperventilation alone nor in combination with hypoxia induced any significant change in VO2. We conclude that in the newborn pig, unlike what has been reported in mature subjects, cellular metabolic function is unaffected by hyperventilation as evidenced by the unchanged VO2.
在人类和成年动物中，过度通气已被证明会导致全身耗氧量（VO2）增加和乳酸生成，但关于新生儿的数据有限。我们研究了在常氧和低氧（吸入氧分数=0.14）状态下，低碳酸血症和正常碳酸血症过度通气对麻醉和麻痹仔猪VO2的影响。持续记录体动脉、肺动脉以及左右心房压力、心输出量和体温。低碳酸血症过度通气（动脉血二氧化碳分压=19±1mmHg；pH=7.58±0.02）与体动脉和肺动脉压力及心输出量显著降低有关。当通过向吸入气体中添加二氧化碳使动脉血二氧化碳分压升高而继续过度通气时，这些测量值恢复到与初始正常通气时相似的值。单独过度通气或与低氧联合均未引起VO2的任何显著变化。我们得出结论，在新生猪中，与成年动物的报道不同，细胞代谢功能不受过度通气影响，这一点由未改变的VO2所证明。
