Jeffery H E, Read D J
J Dev Physiol. 1981 Jun;3(3):219-30.
Ventilatory and arousal responses to progressive, isocapnic hypoxia were assessed in five full-term calves, aged 1-8 d, during normo-glycaemia and insulin-induced hypoglycaemia; replicate tests were made during both quiet and active sleep. Hypoxia was produced by rebreathing 8-10% (W/V) oxygen; end-tidal PO2 and PCO2 confirmed the mask-seal, and the constancy of PCO2 achieved by a soda-lime CO2-absorber. Oxygen saturation was recorded continuously by aspirating aortic blood through a cuvette-oximeter. Airflow through a tightly fitting face-mask was digitized at 50 ms intervals to calculate breath-by-breath ventilation and rate. Sleep-state and arousal were characterized by EEG, electro-oculogram, nuchal electromyogram and behaviour. An intravenous dose of 2.5 units/kg of soluble insulin produced hypoglycaemia within 60 min (blood glucose less than 1 mmol/l). In the normoglycaemic control state, ventilation during quiet sleep increased linearly; typically the ventilation ratio to pre-hypoxic control was 1.5 at an arterial O2-saturation of 85-90%. In contrast, during active sleep, hypoxaemia progressed without any ventilatory response to a very low arterial O2-saturation of less than 70%. Severe hypoglycaemia did not alter these ventilatory responses during either quiet or active sleep. Thus, the relationship between ventilation ratio and arterial O2-saturation at a saturation of 75% did not differ significantly from control. In quiet sleep the mean ventilation ratio values at an arterial O2-saturation of 75% were 1.92 +/- 0.07 (SEM) and 1.62 +/- 0.07 (P greater than 0.05) for normoglycaemia and hypoglycaemia respectively; in active sleep these were 1.08 +/- 0.09 (SEM) and 1.06 +/- 0.04 (P greater than 0.20). The arterial O2-saturation at which reflex arousal occurred differed between sleep-states but was not altered by hypoglycaemia. In quiet sleep, values were 85.0 +/- 1.4 (SEM) and 84.4 +/- 2.5; in active sleep, 57.8 +/- 3.9 (SEM) and 60.4 +/- 1.4, for normoglycaemia and hypoglycaemia respectively.
在五头1 - 8日龄的足月犊牛中,于血糖正常和胰岛素诱导的低血糖期间,评估了对渐进性、等碳酸血症性低氧的通气和觉醒反应;在安静睡眠和主动睡眠期间均进行了重复测试。通过重新呼吸8 - 10%(W/V)的氧气来产生低氧;呼气末PO2和PCO2证实了面罩密封良好,以及通过苏打石灰CO2吸收器实现的PCO2恒定。通过微量比色血氧计抽吸主动脉血连续记录血氧饱和度。通过紧密贴合的面罩的气流以50毫秒的间隔进行数字化处理,以计算逐次呼吸的通气量和频率。睡眠状态和觉醒通过脑电图、眼电图、颈部肌电图和行为来表征。静脉注射2.5单位/千克的可溶性胰岛素在60分钟内产生低血糖(血糖低于1毫摩尔/升)。在血糖正常的对照状态下,安静睡眠期间通气量呈线性增加;通常在动脉血氧饱和度为85 - 90%时,通气比相对于低氧前对照为1.5。相比之下,在主动睡眠期间,低氧血症进展,在动脉血氧饱和度低至低于70%时没有任何通气反应。严重低血糖在安静睡眠或主动睡眠期间均未改变这些通气反应。因此,在饱和度为75%时,通气比与动脉血氧饱和度之间的关系与对照相比无显著差异。在安静睡眠中,动脉血氧饱和度为75%时,血糖正常和低血糖时的平均通气比值分别为1.92±0.07(SEM)和l .62±0.07(P大于0.05);在主动睡眠中,分别为1.08±0.09(SEM)和1.06±0.04(P大于0.20)。反射性觉醒发生时的动脉血氧饱和度在不同睡眠状态之间有所不同,但不受低血糖影响。在安静睡眠中,血糖正常和低血糖时的值分别为85.0±1.4(SEM)和84.4±2.5;在主动睡眠中,分别为57.8±3.9(SEM)和60.4±1.4。