Sabol S J, Ward D S
Anesth Analg. 1987 Jul;66(7):619-24.
To investigate the effect of intravenous dopamine on the chemical regulation of ventilation, we studied the ventilatory responses to hypercapnic hypoxia during dopamine infusion. Intravenous dopamine (3 micrograms X kg-1 X min-1) was administered to six healthy human subjects. Two hypoxic challenges (PETO2 = 52.5 +/- 2.5 mm Hg, SaO2 = 88.8 +/- 2.2%; mean +/- SD) were administered at three CO2 levels (PETCO2 = 40.8 +/- 0.5, 45.6 +/- 0.2, 49.8 +/- 0.3 mm Hg) to each subject. The ventilatory responses were quantified by calculation of slopes and intercepts of the relationship between minute exhaled ventilation (VE) and arterial hemoglobin saturation (SaO2), and by the relationship between this slope (delta VE/delta SaO2) and carbon dioxide tension. Dopamine caused a 77% reduction in delta VE/delta SaO2 (hypoxic sensitivity) during eucapnia, a 39.5% reduction in hypoxic sensitivity at PETCO2 = 46 mm Hg, and 38% reduction at PETCO2 = 50 mm Hg (P less than 0.05). Dopamine also reduced normoxic ventilation at all carbon dioxide levels. There was a greater depression in VE during hypercapnia (25.7% reduction) than during eucapnia (12% reduction). This indicates that dopamine depresses the normoxic ventilatory response to carbon dioxide. Intravenous dopamine reduces the ventilatory response to both hypoxia and hypercapnia but preserves the augmentation of hypoxic ventilatory drive by hypercapnia.
为研究静脉注射多巴胺对通气化学调节的影响，我们在多巴胺输注期间研究了对高碳酸血症性低氧的通气反应。对6名健康受试者静脉注射多巴胺（3微克·千克⁻¹·分钟⁻¹）。在三个二氧化碳水平（呼气末二氧化碳分压 = 40.8±0.5、45.6±0.2、49.8±0.3毫米汞柱）下，对每位受试者进行两次低氧刺激（呼气末氧分压 = 52.5±2.5毫米汞柱，动脉血氧饱和度 = 88.8±2.2%；均值±标准差）。通过计算呼出分钟通气量（VE）与动脉血红蛋白饱和度（SaO₂）之间关系的斜率和截距，以及该斜率（ΔVE/ΔSaO₂）与二氧化碳分压之间的关系来量化通气反应。多巴胺导致在正常碳酸血症时ΔVE/ΔSaO₂（低氧敏感性）降低77%，在呼气末二氧化碳分压 = 46毫米汞柱时低氧敏感性降低39.5%，在呼气末二氧化碳分压 = 50毫米汞柱时降低38%（P<0.05）。多巴胺还降低了所有二氧化碳水平下的常氧通气。高碳酸血症期间VE的降低幅度（降低25.7%）大于正常碳酸血症期间（降低12%）。这表明多巴胺抑制了对二氧化碳的常氧通气反应。静脉注射多巴胺降低了对低氧和高碳酸血症的通气反应，但保留了高碳酸血症对低氧通气驱动的增强作用。
