Abstract:
We hypothesized and investigated whether prenatal exposure to preeclampsia (PE) would simultaneously affect perinatal cardiovascular features and angiotensin system expressions. This prospective study was composed of mother-neonate dyads with (n = 49) and without maternal preeclampsia (n = 48) in a single tertiary medical center. The neonates exposed to PE had significantly larger relative sizes for the left and right coronary arteries and a higher cord plasma level of aminopeptidase-N, which positively correlated with the maternal diastolic blood pressures and determined the relative sizes of the left and right coronary arteries, whereas the encoding aminopeptidase-N (ANPEP) mRNA level in the PE cord blood leukocytes was significantly decreased, positively correlated with the neonatal systolic blood pressures (SBPs), and negatively correlated with the cord plasma-induced endothelial vascular cell adhesion molecule-1 mRNA levels. The PE cord plasma significantly induced higher endothelial mRNA levels of angiotensin II type 1 receptor (AT1R) and AT4R, whereas in the umbilical arteries, the protein expressions of AT2R and AT4R were significantly decreased in the PE group. The endothelial AT1R mRNA level positively determined the maternal SBPs, and the AT4R mRNA level positively determined the neonatal chamber size and cardiac output. In conclusion, PE may influence perinatal angiotensin system and cardiovascular manifestations of neonates across placentae. Intriguing correlations between these two warrant further mechanistic investigation.
摘要:
我们假设并调查了产前暴露于先兆子痫(PE)是否会同时影响围产期心血管特征和血管紧张素系统表达。这项前瞻性研究由在单个三级医疗中心中患有(n=49)和没有孕妇先兆子痫(n=48)的母婴二联组成。暴露于PE的新生儿的左冠状动脉和右冠状动脉的相对大小明显更大,氨肽酶-N的脐带血浆水平更高,与产妇舒张压呈正相关,并确定左右冠状动脉的相对大小,而PE脐血白细胞中编码氨肽酶-N(ANPEP)mRNA水平显著降低,与新生儿收缩压(SBP)呈正相关,与脐带血浆诱导的血管内皮细胞粘附分子-1mRNA水平呈负相关。PE脐带血浆显著诱导血管紧张素II1型受体(AT1R)和AT4R的内皮mRNA水平升高,而在脐动脉中,PE组AT2R和AT4R蛋白表达明显下降。内皮AT1RmRNA水平正确定母体SBPs,和AT4RmRNA水平正决定了新生儿室大小和心输出量。总之,PE可能会影响围产期血管紧张素系统和整个胎盘新生儿的心血管表现。这两者之间有趣的相关性需要进一步的机械研究。