Chapman R W, Santiago T V, Edelman N H
J Appl Physiol Respir Environ Exerc Physiol. 1979 Jul;47(1):104-11. doi: 10.1152/jappl.1979.47.1.104.
The ventilatory effects of graded reductions in brain bloow flow (BBF) were studied in unanesthetized goats. At a BBF of 85% of control (PVO2 = 29.2 Torr, PVCO2 = 47.3 Torr) there were no clear ventilatory effects. At BBF of 70% of control (PVO2 = 25.2, PVCO2 = 50.5) and 50% of control (PVCO2 = 22.3, PVCO2 = 53.0) there was hyperpnea, due primarily to an increase of tidal volume. Further reduction of BBF (avg of 42% of control) first produced intense tachypnea and then (30--40% of control) caused apnea that was reversible. At 50% BBF there was a reduction of brain O2 consumption, (4.67--4.00 ml/min) and an increase in systemic O2 consumption. beta-Adrenergic blockade prevented the increase in systemic O2 consumption and reduced the hyperpnea by two-thirds at 50% BBF; the residual hyperpnea was associated with hypocapnia in contrast to the hyperpnea prior to beta-adrenergic blockade, which was virtually isocapnic. The data suggest that hyperpnea due to brain ischemia is a result of both brain acidosis and systemic hypermetabolism. The similarity of the pattern of responses to that previously reported for progressive carboxyhemoglobinemia suggests that brain hypoxia is a determinant of the ventilatory responses to brain ischemia.
在未麻醉的山羊身上研究了脑血流量（BBF）分级降低的通气效应。当BBF为对照值的85%时（混合静脉血氧分压[PVO2]=29.2托，混合静脉血二氧化碳分压[PVCO2]=47.3托），未观察到明显的通气效应。当BBF为对照值的70%（PVO2=25.2，PVCO2=50.5）和50%（PVO2=22.3，PVCO2=53.0）时，出现呼吸急促，主要是由于潮气量增加。进一步降低BBF（平均为对照值的42%）首先导致强烈的呼吸急促，然后（对照值的30 - 40%）引起可逆转的呼吸暂停。在BBF为50%时，脑氧耗量减少（从4.67降至4.00毫升/分钟），全身氧耗量增加。β-肾上腺素能阻滞剂可防止全身氧耗量增加，并在BBF为50%时将呼吸急促减少三分之二；与β-肾上腺素能阻滞剂之前的呼吸急促（实际上是等碳酸血症）相比，剩余的呼吸急促与低碳酸血症有关。数据表明，脑缺血引起的呼吸急促是脑酸中毒和全身代谢亢进共同作用的结果。对渐进性碳氧血红蛋白血症先前报道的反应模式的相似性表明，脑缺氧是对脑缺血通气反应的一个决定因素。
