Parer J T
Cardiovascular Research Institute, University of California, San Francisco 94143.
J Perinatol. 1994 Sep-Oct;14(5):376-85.
Cerebral oxidative metabolism has been described in fetal sheep at two stages of development and is known to remain relatively constant over a wide range of oxygen levels in arterial blood. This constancy of oxygen consumption is caused by an increase in cerebral blood flow that matches the reduction in oxygen content and oxygen extraction. Although a number of factors are involved in the hypoxia-associated vasodilation (for example, oxygen, carbon dioxide, adenosine, prostaglandins, arginine vasopressin), its regulation is incompletely understood. During severe asphyxia, however, there is a limit to the vasodilator function, and both cerebral blood flow and oxygen consumption fall. The fetus can tolerate a certain degree of reduced oxygen uptake (possibly to 50% of control level) by various conservation techniques, but severe reductions are associated with neuronal damage. The primary substrate for the fetal brain under normal conditions is glucose, but the fetus can readily use anaerobic glycolysis and produce lactate under conditions of oxygen limitation. Lactate efflux from the brain is relatively slow, so prolonged and severe asphyxia may result in a high tissue level of lactate, which has been implicated in neuronal damage.
已在发育的两个阶段对胎羊的脑氧化代谢进行了描述，并且已知在动脉血中广泛的氧水平范围内，脑氧化代谢保持相对恒定。氧消耗的这种恒定性是由脑血流量的增加引起的，脑血流量的增加与氧含量和氧摄取的减少相匹配。虽然缺氧相关的血管舒张涉及多种因素（例如，氧、二氧化碳、腺苷、前列腺素、精氨酸加压素），但其调节机制尚未完全了解。然而，在严重窒息期间，血管舒张功能存在极限，脑血流量和氧消耗都会下降。胎儿可以通过各种保护技术耐受一定程度的氧摄取减少（可能降至对照水平的50%），但严重减少与神经元损伤有关。在正常情况下，胎儿脑的主要底物是葡萄糖，但在氧限制条件下，胎儿可以很容易地利用无氧糖酵解并产生乳酸。乳酸从脑中流出相对缓慢，因此长期严重窒息可能导致组织中乳酸水平升高，这与神经元损伤有关。
