Kendall G, Peebles D
Centre for Perinatal Brain Protection and Repair, Dept. Obstetrics and Gynaecology, University College London, Gower St. Campus, 86-96 Chenies Mews, London WC1E 6HX, United Kingdom.
Early Hum Dev. 2005 Jan;81(1):27-34. doi: 10.1016/j.earlhumdev.2004.10.012. Epub 2004 Nov 19.
The fetal brain is protected from the effects of acute hypoxia by a range of haemodynamic and metabolic compensations. Hypoxia alone is therefore an unusual cause of perinatal brain injury in either preterm or term infants. More recently, materno-fetal infection has been implicated as a causative factor in cases of cerebral palsy associated with preterm and term birth. This paper explores the concept that exposure to infection, and in particular pro-inflammatory cytokines, may reduce the threshold at which hypoxia becomes neurotoxic, so making the brain much more vulnerable to even mild hypoxic insults. The hypothesis is supported by an increasing body of evidence from animal studies that also demonstrate the importance of duration between exposure to infection and subsequent hypoxia. There are a number of clinical and research implications that centre around the role of antibiotics, mode and timing of delivery, maternal cooling during labour and the role of immune-modulating drugs.
胎儿大脑通过一系列血液动力学和代谢补偿机制来抵御急性缺氧的影响。因此,无论是早产儿还是足月儿,单纯缺氧都不是围产期脑损伤的常见原因。最近,母婴感染被认为是与早产和足月产相关的脑瘫病例的一个致病因素。本文探讨了这样一种概念,即接触感染,尤其是促炎细胞因子,可能会降低缺氧成为神经毒性的阈值,从而使大脑更容易受到即使是轻度缺氧损伤的影响。越来越多的动物研究证据支持了这一假说,这些研究还证明了感染暴露与随后缺氧之间时间间隔的重要性。围绕抗生素的作用、分娩方式和时机、分娩期间的母体降温以及免疫调节药物的作用,存在许多临床和研究意义。