Fetal cerebral metabolism: the influence of asphyxia and other factors

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.