Irsigler G B, Stafford M J, Severinghaus J W
J Appl Physiol Respir Environ Exerc Physiol. 1980 Feb;48(2):355-61. doi: 10.1152/jappl.1980.48.2.355.
The effect of induced metabolic acidosis (48 h of NH4Cl ingestion, BE - 10.6 +/- 1.1) and alkalosis (43 h of NaHCO3- ingestion BE 8.8 +/- 1.6) on arterial and lumber CSF pH, Pco2, and HCO3- and ventilatory responses to CO2 and to hypoxia was assessed in five healthy men. In acidosis lumbar CSF pH rose 0.033 +/- 0.02 (P less than 0.05). In alkalosis CSF pH was unchanged. Ventilatory response lines to CO2 at high O2 were displaced to the left in acidosis (9.0 +/- 1.4 Torr) and to the right in alkalosis (4.5 +/- 1.5 Torr) with no change in slope. The ventilatory response to hypoxia (delta V40) was increased in acidosis (P less than 0.05) and it was decreased in four subjects in alkalosis (P, not significant). We conclude that the altered ventilatory drives of steady-state metabolic imbalance are mediated by peripheral chemoreceptors, and in acidosis the medullary respiratory chemoreceptor drive is decreased.
在五名健康男性中评估了诱导性代谢性酸中毒(摄入氯化铵48小时,碱剩余-10.6±1.1)和碱中毒(摄入碳酸氢钠43小时,碱剩余8.8±1.6)对动脉血和腰椎脑脊液的pH值、二氧化碳分压、碳酸氢根离子以及对二氧化碳和低氧通气反应的影响。在酸中毒时,腰椎脑脊液pH值升高0.033±0.02(P<0.05)。在碱中毒时,脑脊液pH值未发生变化。在高氧条件下,对二氧化碳的通气反应曲线在酸中毒时向左移位(9.0±1.4托),在碱中毒时向右移位(4.5±1.5托),斜率无变化。对低氧的通气反应(δV40)在酸中毒时增加(P<0.05),在碱中毒时有四名受试者降低(P值无统计学意义)。我们得出结论,稳态代谢失衡时通气驱动的改变是由外周化学感受器介导的,并且在酸中毒时延髓呼吸化学感受器驱动降低。