Kagawa S, Stafford M J, Waggener T B, Severinghaus J W
J Appl Physiol Respir Environ Exerc Physiol. 1982 Apr;52(4):1030-4. doi: 10.1152/jappl.1982.52.4.1030.
The ventilatory response to acute isocapnic hypoxia is prompt but is not maintained at its peak. Within 10 min, it begins to fall, and by 30 min has reached an approximately steady level, usually still above control. We used naloxone to test in four men the hypothesis that this fade is hypoxic depression mediated by endogenous opioid peptides, e.g, endorphins. Breath by breath minute ventilation was recorded during a hyperoxic control period (FIO2 = 0.3) to establish control alveolar PCO2. After 15 min. of isocapnic hypoxia (end-tidal PO2 = 45 Torr), naloxone injection (1.2 or 10 mg, iv) failed to alter the slow decrement of ventilation. Hypoxic ventilatory depression appears not to be mediated by endorphins in adults.
对急性等碳酸血症性低氧的通气反应迅速,但不会维持在峰值水平。在10分钟内,它开始下降,到30分钟时已达到大致稳定的水平,通常仍高于对照水平。我们使用纳洛酮在四名男性中测试了这样一个假设,即这种消退是由内源性阿片肽(如内啡肽)介导的低氧性抑制。在高氧对照期(FIO2 = 0.3)记录逐次呼吸的分钟通气量,以确定对照肺泡PCO2。在等碳酸血症性低氧(呼气末PO2 = 45 Torr)15分钟后,静脉注射纳洛酮(1.2或10毫克)未能改变通气的缓慢下降。在成年人中,低氧性通气抑制似乎不是由内啡肽介导的。