Ward D S, Bellville J W
Anesth Analg. 1982 Apr;61(4):333-7.
To define precisely the effects of dopamine on hypoxic ventilatory drive, two sets of experiments were performed in five healthy subjects. End-tidal CO2 was held constant in all experiments. First, a dopamine infusion (3 microgram/kg/min) was started in subjects already rendered hypoxic, causing an average sustained decrease in ventilation to 60% of the preinfusion ventilation. In the second group of experiments, the ventilatory response of subjects made hypoxic during a dopamine infusion was compared with the hypoxic ventilatory response without the dopamine infusion. Without dopamine, a sudden decrease in end-tidal O2 from 100 to 53 torr caused ventilation to increase from 11.9 to 20.9 L/min (p less than 0.01). During the dopamine infusion, only a statistically insignificant increase in ventilation (9.8 to 12.8 L/min) was seen with the same hypoxic stimulus. Low dose dopamine is a potent depressant of hypoxic ventilatory response.
为精确确定多巴胺对低氧通气驱动的影响,我们对五名健康受试者进行了两组实验。在所有实验中,呼气末二氧化碳水平保持恒定。首先,在已经处于低氧状态的受试者中开始输注多巴胺(3微克/千克/分钟),导致通气量平均持续下降至输注前通气量的60%。在第二组实验中,将在多巴胺输注期间处于低氧状态的受试者的通气反应与无多巴胺输注时的低氧通气反应进行了比较。无多巴胺时,呼气末氧气突然从100托降至53托,导致通气量从11.9升/分钟增加到20.9升/分钟(p<0.01)。在多巴胺输注期间,相同的低氧刺激仅使通气量有统计学上无显著意义的增加(从9.8升/分钟增加到12.8升/分钟)。低剂量多巴胺是低氧通气反应的强效抑制剂。