Harkness R A, Whitelaw A G, Simmonds R J
J Clin Pathol. 1982 Sep;35(9):999-1007. doi: 10.1136/jcp.35.9.999.
A series of 29 newborn infants had been studied after intrapartum hypoxia defined as meconium aspiration, an Apgar score of less than or equal to 6 at 5 min or a peripheral blood pH of 7.2 or less after resuscitation. Two independent sets of techniques were used; one concerned with the critical system in hypoxic damage, the central nervous system, the other assessing the central biochemical events in hypoxia. Both sets of data were assembled, then graded separately and only then combined. In this way detailed neurological assessment has been combined with measurement of urinary excretion of the ATP metabolites, hypoxanthine and xanthine. The essential metabolic consequence of hypoxia is a reduction in the synthesis of the energy currency of cells, ATP. This is associated with an outflow of ATP metabolites from cells. The extent of neurological damage was related to the magnitude of the hypoxanthine and xanthine excretion; neither were closely related to the initial blood pH. Infants who were normal neurologically had normal oxypurine excretion. Infants with neurological abnormalities for less than 48 h had lower excretion than those who were abnormal for more than 48 h. The duration of abnormal oxypurine excretion after an acute episode of hypoxia was studied in two infants with respiratory distress and in two other infants with apnoeic attacks. Severe hypoxia was followed by abnormal oxypurine excretion for at least 40 h after an acute episode. It is justifiable to suggest that abnormalities of oxypurine excretion should indicate intrapartum hypoxia in newborn infants. This excretion should also quantify the metabolic damage.
对一系列29名新生儿进行了研究，这些新生儿在分娩期出现了缺氧情况，定义为胎粪吸入、5分钟时阿氏评分小于或等于6分，或复苏后外周血pH值为7.2或更低。使用了两组独立的技术；一组关注缺氧损伤中的关键系统，即中枢神经系统，另一组评估缺氧时的中枢生化事件。两组数据都进行了收集，然后分别分级，之后才进行合并。通过这种方式，详细的神经学评估与ATP代谢产物、次黄嘌呤和黄嘌呤的尿排泄量测量相结合。缺氧的基本代谢后果是细胞能量货币ATP的合成减少。这与ATP代谢产物从细胞中流出有关。神经损伤的程度与次黄嘌呤和黄嘌呤的排泄量大小有关；两者均与初始血液pH值无密切关系。神经学正常的婴儿氧嘌呤排泄正常。神经异常持续时间不到48小时的婴儿排泄量低于异常持续时间超过48小时的婴儿。对两名患有呼吸窘迫的婴儿和另外两名患有呼吸暂停发作的婴儿，研究了急性缺氧发作后氧嘌呤异常排泄的持续时间。急性发作后，严重缺氧至少持续40小时会出现氧嘌呤排泄异常。有理由认为，氧嘌呤排泄异常应表明新生儿存在分娩期缺氧。这种排泄也应能量化代谢损伤。
