O'Connor M C, Harkness R A, Simmonds R J, Hytten F E
Br J Obstet Gynaecol. 1981 Apr;88(4):375-80. doi: 10.1111/j.1471-0528.1981.tb01000.x.
Amniotic fluid samples were obtained at induction of labour in 64 women; in 15 of these there was meconium staining of the amniotic fluid; the remainder showed no signs of fetal distress. Using high pressure liquid chromatography, compared to the samples from normal patients there were highly significantly raised levels of hypoxanthine, xanthine and uridine in the meconium stained samples; oxypurines in the meconium itself could not explain the difference. Where serial samples were obtained during labour by intrauterine catheter, a terminal rise in oxypurine levels was apparent. Where the proportion of oxypurine present as hypoxanthine exceeded one per cent in amniotic fluid at the time of induction, there was a significantly greater occurrence of late fetal heart rate decelerations in the ensuing labour. These findings are consistent with other evidence that when tissues become hypoxic the metabolic products of nucleotide breakdown escape from the cells and appear in extracellular fluid. Oxygen lack in the fetus probably causes loss of these compounds from the hypoxic kidneys to the urine so that they appear in amniotic fluid.
在64名产妇引产时获取羊水样本;其中15名产妇的羊水有胎粪污染;其余产妇未显示胎儿窘迫迹象。使用高压液相色谱法,与正常患者的样本相比,有胎粪污染的样本中次黄嘌呤、黄嘌呤和尿苷水平显著升高;胎粪本身中的氧嘌呤无法解释这种差异。在分娩期间通过宫内导管获取系列样本时,氧嘌呤水平出现终末升高。引产时羊水中以次黄嘌呤形式存在的氧嘌呤比例超过1%时,随后分娩中晚期胎儿心率减速的发生率显著更高。这些发现与其他证据一致,即当组织缺氧时,核苷酸分解的代谢产物从细胞中逸出并出现在细胞外液中。胎儿缺氧可能导致这些化合物从缺氧的肾脏进入尿液,从而出现在羊水中。