Dahan A, van den Elsen M J, Berkenbosch A, DeGoede J, Olievier I C, van Kleef J W, Bovill J G
Department of Anesthesiology, University Hospital Leiden, The Netherlands.
Anesthesiology. 1994 Apr;80(4):727-38. doi: 10.1097/00000542-199404000-00004.
The peripheral chemoreceptors are responsible for the ventilatory response to hypoxia (acute hypoxic response) and for 30% of the normoxic hypercapnic ventilatory response. To quantify the effects of subanesthetic concentrations of halothane on the respiratory control system, in particular on the peripheral chemoreceptors, we studied the response of humans to carbon dioxide and oxygen at two subanesthetic concentrations of halothane.
Square-wave changes in end-tidal carbon dioxide tension (7.5-11.3 mmHg) and step decreases in end-tidal oxygen tension (arterial hemoglobin oxygen saturation 82 +/- 2%; duration of hypoxia 5 min) were performed in nine healthy male subjects during 0, 0.05 (HA-1), and 0.1 minimum alveolar concentration (HA-2) halothane. Each hypercapnic response was separated into a fast, peripheral component and a slow, central component, characterized by a time constant, carbon dioxide sensitivity, time delay, and off-set.
Fifty-six carbon dioxide responses and 27 oxygen responses were obtained. The peripheral carbon dioxide sensitivities averaged to 0.76 +/- 0.14 l.min-1.mmHg-1 (control), 0.50 +/- 0.12 l.min-1.mmHg-1 (HA-1), and 0.30 +/- 0.08 l.min-1.mmHg-1 (HA-2; P < 0.01 vs. control). The central carbon dioxide sensitivity did not differ significantly among treatment groups (control, 1.47 +/- 0.22 l.min-1.mmHg-1; HA-1, 1.41 +/- 0.51 l.min-1.mmHg-1; and HA-2, 1.23 +/- 0.30 l.min-1.mmHg-1). The time constants of the central chemoreflex loop showed a large decrease during the administration of 0.1 minimum alveolar concentration halothane. The acute hypoxic response declined from 15.0 +/- 3.9 l.min-1 to 10.9 +/- 2.9 l.min-1 (HA-1) and 4.8 +/- 1.4 l.min-1 (HA-2; P < 0.01 vs. control and HA-1). All values are means +/- SEM.
The results show depression of the ventilatory responses to hypoxia and hypercapnia during inhalation of subanesthetic concentrations of halothane. The depression is attributed to a selective effect of halothane on the peripheral chemoreflex loop. The oxygen and carbon dioxide responses mediated by the peripheral chemoreceptors are affected proportionally. It is argued that the decrease in central time constants is caused by an effect of halothane on central neuronal dynamics.
外周化学感受器负责对低氧的通气反应(急性低氧反应)以及30%的常氧高碳酸通气反应。为了量化亚麻醉浓度的氟烷对呼吸系统,尤其是对外周化学感受器的影响,我们研究了人类在两种亚麻醉浓度氟烷下对二氧化碳和氧气的反应。
在9名健康男性受试者中,于0、0.05(HA-1)和0.1最低肺泡浓度(HA-2)的氟烷状态下,进行呼气末二氧化碳分压的方波变化(7.5 - 11.3 mmHg)以及呼气末氧分压的阶梯式下降(动脉血红蛋白氧饱和度82±2%;低氧持续时间5分钟)。每个高碳酸反应被分为快速的外周成分和缓慢的中枢成分,其特征为时间常数、二氧化碳敏感性、时间延迟和偏移。
获得了56个二氧化碳反应和27个氧气反应。外周二氧化碳敏感性平均值分别为0.76±0.14 l·min⁻¹·mmHg⁻¹(对照)、0.50±0.12 l·min⁻¹·mmHg⁻¹(HA-1)和0.30±0.08 l·min⁻¹·mmHg⁻¹(HA-2;与对照相比,P < 0.01)。各治疗组之间中枢二氧化碳敏感性无显著差异(对照,1.47±0.22 l·min⁻¹·mmHg⁻¹;HA-1,1.41±0.51 l·min⁻¹·mmHg⁻¹;HA-2,1.23±0.30 l·min⁻¹·mmHg⁻¹)。在给予0.1最低肺泡浓度氟烷期间,中枢化学反射环的时间常数大幅下降。急性低氧反应从15.0±3.9 l·min⁻¹降至10.9±2.9 l·min⁻¹(HA-1)和4.8±1.4 l·min⁻¹(HA-2;与对照和HA-1相比,P < 0.01)。所有数值均为平均值±标准误。
结果表明,吸入亚麻醉浓度的氟烷期间,对低氧和高碳酸的通气反应受到抑制。这种抑制归因于氟烷对外周化学反射环的选择性作用。外周化学感受器介导的氧气和二氧化碳反应受到成比例的影响。有人认为中枢时间常数的下降是由氟烷对中枢神经元动力学的作用所致。