Parer J T
Department of Obstetrics and Gynecology and Reproductive Sciences, University of California San Francisco, CA, USA.
Comp Biochem Physiol A Mol Integr Physiol. 1998 Mar;119(3):711-6. doi: 10.1016/s1095-6433(98)01009-5.
The objective of this paper is to review the published information available on the effect of hypoxia on fetal cerebral integrity, and to attempt to define limits of fetal tolerance to asphyxia Data were obtained in experimental animals following imposed hypoxia or asphyxia. Studies were carried out in the fetus by physiologic, biochemical, histologic, and behavioral techniques. Human data were collected from newborns at birth and during subsequent development. It has been established that acute asphyxia of the fetus in utero may result in a spectrum of effects on the fetus, including death, or survival with permanent neurologic damage, or apparent complete recovery. The severity of damage depends on the degree and duration of asphyxia and a number of sensitizing factors, including prior metabolic and cardiovascular status of the fetus, differential sensitivity of the heart and brain to asphyxia, gestational age, plasticity, intermittency of asphyxial insults, and the pattern of intermittency. The fetus has a number of compensatory mechanisms that allow it to survive periods of oxygen limitation without permanent damage to the brain. The fetus can increase cerebral blood flow to increase oxygen delivery to the brain, and can decrease its metabolism by electrophysiological and behavioral state changes. Cerebral ischemia and reduced metabolism to < 50% of control is probably necessary for permanent brain damage to occur. In human pregnancy, factors consistent with intrapartum asphyxia lasting until delivery as a cause of fetal neurologic damage include absent fetal heart rate variability, umbilical cord arterial pH < 6.8, base access < -20 mEql-1, severe and prolonged newborn depression with Apgar score of < or = 3 at 10 min, seizure activity in the first day of life, and damage to the noncerebral organs and regions. However, these factors are neither independently nor collectively predictive of asphyxial brain damage. It is concluded that permanent neurologic damage or death can occur in the fetus due to single or repetitive episodes of hypoxia or asphyxia, but it is not yet possible to predict the occurrence or extent of such damage in an individual fetus.
本文的目的是回顾已发表的关于缺氧对胎儿脑完整性影响的可用信息，并试图确定胎儿对窒息的耐受限度。通过对实验动物施加缺氧或窒息来获取数据。采用生理、生化、组织学和行为学技术对胎儿进行研究。从新生儿出生时及随后的发育过程中收集人类数据。已证实，子宫内胎儿急性窒息可能对胎儿产生一系列影响，包括死亡、存活但伴有永久性神经损伤或明显完全恢复。损伤的严重程度取决于窒息的程度和持续时间以及一些敏感因素，包括胎儿先前的代谢和心血管状况、心脏和大脑对窒息的不同敏感性、胎龄、可塑性、窒息损伤的间歇性以及间歇性模式。胎儿有多种代偿机制，使其能够在氧限制期存活而不会对大脑造成永久性损伤。胎儿可以增加脑血流量以增加向大脑的氧气输送，并可通过电生理和行为状态变化降低其代谢。永久性脑损伤可能需要脑缺血且代谢降至对照值的<50%。在人类妊娠中，与直至分娩的产时窒息作为胎儿神经损伤原因相关的因素包括胎儿心率无变异性、脐动脉pH<6.8、碱剩余<-20 mEq/L、严重且持续时间长的新生儿抑制（10分钟时Apgar评分≤3）、出生第一天的惊厥活动以及非脑器官和区域的损伤。然而，这些因素既不能独立也不能共同预测窒息性脑损伤。结论是，由于单次或反复的缺氧或窒息发作，胎儿可能发生永久性神经损伤或死亡，但目前尚无法预测个体胎儿中此类损伤的发生或程度。
