Bopp P, Drummond G, Fisher J, Milic-Emili J
Can Anaesth Soc J. 1979 May;26(3):191-5. doi: 10.1007/BF03006980.
The effects of doxapram infusion (0.25 mg.kg-1. min-1) were studied in cats anaesthetized with pentobarbitone (35 mg . kg-1 intraperitoneally). Cats were studied breathing 50 per cent oxygen and the responses to two concentrations of inspired carbon dioxide were measured. Doxapram infusion increased pulmonary ventilation by increasing both tidal volume and respiratory frequency, and also caused increases in the volume inspired in the first 0.5 second after the onset of an inspiration (V0.5) and the pressure generated in the airway 0.5 second after the onset of an inspiration when the airway had been occluded (P degrees 0.5). V 0.5, P degrees 0.5 and the mean inspiratory flow rate (VT/VI) were essentially equivalent indices of inspiratory drive. Doxapram infusion did not alter the effective impedance of the respiratory system (P degrees 0.5/V 0.5). Doxapram infusion increased the ventilatory response to carbon dioxide. The slope of the ventilatory response to carbon dioxide was increased and the response line was shifted to the left. We conclude that the increase in pulmonary ventilation caused by doxapram infusion is due almost entirely to increased inspiratory neuromuscular drive (P degrees 0.5).
在以戊巴比妥(35毫克/千克腹腔注射)麻醉的猫身上,研究了多沙普仑输注(0.25毫克/千克·分钟)的效果。对呼吸50%氧气的猫进行研究,并测量其对两种吸入二氧化碳浓度的反应。多沙普仑输注通过增加潮气量和呼吸频率来增加肺通气量,还导致吸气开始后最初0.5秒内吸入的气量(V0.5)以及气道阻塞后吸气开始0.5秒时气道产生的压力(P°0.5)增加。V0.5、P°0.5和平均吸气流速(VT/VI)本质上是吸气驱动力的等效指标。多沙普仑输注未改变呼吸系统的有效阻抗(P°0.5/V0.5)。多沙普仑输注增加了对二氧化碳的通气反应。对二氧化碳的通气反应斜率增加,反应线向左移动。我们得出结论,多沙普仑输注引起的肺通气增加几乎完全归因于吸气神经肌肉驱动力增加(P°0.5)。