Bloxam D L, Bullen B E, Walters B N, Lao T T
Am J Obstet Gynecol. 1987 Jul;157(1):97-101. doi: 10.1016/s0002-9378(87)80354-x.
We examined the possibility that in preeclampsia complicated by fetal growth retardation, placental energy state is low either because of impaired glycolysis or because of ischemia resulting from reduced maternal placental blood flow. Concentrations of pyruvate and lactate, but not of glycogen and glucose, were significantly low in placentas of mothers with severe preeclampsia, supporting previous indirect evidence of inhibited glycolysis. Nevertheless, direct measurements of adenine nucleotide concentrations did not indicate reduced placental energy level in the preeclamptic placentas. This along with a lack of change of the ratio of lactate/pyruvate concentration (an indication of the redox state of cytoplasmic reduced nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide) is also evidence against the hypothesis of general placental ischemia leading to energy deficiency. However, as glycolysis is an important source of precursors, particularly pyruvate, for synthesis of amino acids and lipids, these results suggest that there is a significant metabolic abnormality in placentas of mothers with severe preeclampsia.
我们研究了一种可能性，即在子痫前期合并胎儿生长受限的情况下，胎盘能量状态较低，这要么是由于糖酵解受损，要么是由于母体胎盘血流量减少导致的局部缺血。患有严重子痫前期的母亲的胎盘组织中，丙酮酸和乳酸的浓度显著降低，但糖原和葡萄糖的浓度没有降低，这支持了先前关于糖酵解受抑制的间接证据。然而，对腺嘌呤核苷酸浓度的直接测量并未表明子痫前期胎盘的能量水平降低。这一点，再加上乳酸/丙酮酸浓度比值没有变化（这是细胞质中还原型烟酰胺腺嘌呤二核苷酸/烟酰胺腺嘌呤二核苷酸氧化还原状态的一个指标），也证明了胎盘普遍缺血导致能量缺乏这一假说不成立。然而，由于糖酵解是氨基酸和脂质合成的重要前体来源，尤其是丙酮酸的来源，这些结果表明，患有严重子痫前期的母亲的胎盘存在显著的代谢异常。
