Field D R, Parer J T, Auslender R A, Cheek D B, Baker W, Johnson J
Department of Anesthesia, University of California, San Francisco 94143.
J Dev Physiol. 1990 Sep;14(3):131-7.
Cerebral blood flow and cerebral arteriovenous oxygen content difference were measured in 17 fetal sheep, and cerebral oxygen uptake was calculated. The measurements were made under control conditions and after profound fetal asphyxia induced of uterine blood flow for up to 90 min. In 14 of the fetal sheep, sequential measurements were made to examine hemodynamic changes and cerebral oxygen consumption at comparable intervals up to 36 min of asphyxia. These fetuses initially had elevated blood pressure and lowered heart rate became hypoxemic, hypercarbic, and acidotic. There was an initial decrease in cerebral oxygen consumption. Sequential measurements, however, showed a relative stability in this decreased oxygenation during 4 to 36 min of asphyxia despite a progressive metabolic acidosis. The cerebral fractional oxygen extraction remained unchanged despite a mean pH of 6.98 at 36 min. The calculated cerebral oxygen uptake during asphyxia in all 17 sheep was grouped according to whether the ascending aortic oxygen content was greater or less than 1.0 mmol/l. In the first group with mean ascending aortic oxygen content of 1.3 mmol/l, blood flow to the brain was increased and cerebral oxygen consumption was 85% of control. In the second group with mean arterial blood oxygen content of 0.8 mmol/l, there was a narrowing of the arteriovenous oxygen content difference, but no further increase in cerebral blood flow. Cerebral oxygen consumption was only 48% of control in this more asphyxiated group. We conclude that the degree of hypoxemia in the second group represents a point where physiologic mechanisms cannot compensate, and may be associated with neuronal damage.
对17只胎羊测量了脑血流量和脑动静脉氧含量差，并计算了脑氧摄取量。测量在对照条件下进行，以及在子宫血流量诱导的严重胎儿窒息长达90分钟后进行。在14只胎羊中，进行了连续测量，以检查长达36分钟窒息时的血流动力学变化和脑氧消耗。这些胎儿最初血压升高、心率降低，随后出现低氧血症、高碳酸血症和酸中毒。脑氧消耗最初有所下降。然而，连续测量显示，尽管代谢性酸中毒不断进展，但在窒息4至36分钟期间，这种氧合降低情况相对稳定。尽管在36分钟时平均pH值为6.98，但脑氧分数提取率保持不变。根据升主动脉氧含量大于或小于1.0 mmol/l，将所有17只羊窒息期间计算出的脑氧摄取量进行分组。在第一组中，升主动脉平均氧含量为1.3 mmol/l，脑血流量增加，脑氧消耗为对照值的85%。在第二组中，平均动脉血氧含量为0.8 mmol/l，动静脉氧含量差缩小，但脑血流量没有进一步增加。在这个更严重窒息的组中，脑氧消耗仅为对照值的48%。我们得出结论，第二组中的低氧血症程度代表了生理机制无法代偿的一个点，可能与神经元损伤有关。
