Greisen G, Vannucci R C
Department of Neonatology, Rigshospitalet, Copenhagen, Denmark.
Biol Neonate. 2001;79(3-4):194-200. doi: 10.1159/000047090.
Decrease in the arterial partial pressure of carbon dioxide (PaCO(2)) causes a reduction in cerebral blood flow in humans and in most animal species; in adults as well as in newborns and even in fetal life. Severely decreased PaCO(2) increases cerebral lactate production, modifies spontaneous electric brain activity, and may decrease the metabolic rate of oxygen. A relation between very low PaCO(2) and brain injury, however, has not been shown in adult humans or full-term newborn infants, nor in perinatal animals. In contrast, an association between low PaCO(2) and cerebral palsy and white matter injury in preterm infants has been reported repeatedly. A cause-and-effect relation is suggested by data from the immature rat: brain damage induced by ligation of a carotid artery can be reduced by adding CO(2) to the inspired gas and hence avoiding the consequences of spontaneous hyperventilation. This may be relevant for the clinical care of preterm infants, since PaCO(2) to a large extent is a function of respiratory management. The questions to be addressed are whether hypocapnia sensitizes the brain to hypoxaemia, and also whether the escape mechanisms are less effective in the preterm human brain.
动脉血二氧化碳分压（PaCO₂）降低会导致人类及大多数动物物种的脑血流量减少，无论在成年人、新生儿甚至胎儿期均如此。严重降低的PaCO₂会增加脑乳酸生成，改变自发性脑电活动，并可能降低氧代谢率。然而，极低的PaCO₂与脑损伤之间的关系在成年人类或足月儿中尚未得到证实，在围产期动物中也未得到证实。相比之下，低PaCO₂与早产儿脑性瘫痪和白质损伤之间的关联已被多次报道。未成熟大鼠的数据提示了因果关系：通过在吸入气体中添加CO₂从而避免自发性过度通气的后果，可减轻结扎颈动脉所致的脑损伤。这可能与早产儿的临床护理相关，因为PaCO₂在很大程度上取决于呼吸管理。需要解决的问题是，低碳酸血症是否会使大脑对低氧血症敏感，以及早产儿大脑中的逃逸机制是否效果较差。
