Kilby M D, Broughton Pipkin F, Symonds E M
Academic Department of Obstetrics and Gynaecology, University Hospital, Nottingham.
Arch Dis Child Fetal Neonatal Ed. 1994 Jul;71(1):F6-10. doi: 10.1136/fn.71.1.f6.
A prospective study investigated platelet cytosolic calcium in non-pregnant volunteers (n = 30) and samples from the umbilical veins of babies from both normotensive (n = 18) and hypertensive (n = 15) primigravidae, and their mothers. There was no significant difference between the neonatal umbilical venous platelet cytosolic calcium concentration (p[Ca2+]i) in babies born to normotensive primigravidae or to those whose pregnancies were complicated by gestational hypertension (88 x 9 (SE) 2 x 5) in normotensive primagravidae, 80 x 6 (2 x 8) in pregnancy induced hypertension without proteinuria, and 89 x 3 (3 x 2) nmol/l in pre-eclampsia. There was also no significant difference in the p[Ca2+]i from the umbilical veins of the pregnancies studied and those of non-pregnant female volunteers in the follicular phase of their menstrual cycle. This was despite a gradual and significant rise in p[Ca2+]i with increasing severity of disease in the mothers of the babies studied (119 x 9 (4 x 1) in normotensive primagravidae, 130 x 8 (7 x 3) in pregnancy induced hypertension without proteinuria, and 148 x 2 (4 x 5 ) nmol/l in pre-eclampsia). The mean maternal p[Ca2+]i in the three samples returned to concentrations comparable with those in non-pregnant subjects by 12 weeks after birth. These data demonstrate no significant difference between the mean p[Ca2+]i in non-pregnant women and those obtained from the umbilical venous blood of normotensive or hypertensive primigravidae. They suggest that the functional hypoactivity of neonatal platelets is probably not secondary to a decrease in basal p[Ca2+]i. They also suggest that the progressively raised p[Ca2+]i in normal and hypertensive pregnancies might be due to a pregnancy specific factor that does not cross the placenta,
一项前瞻性研究调查了非妊娠志愿者(n = 30)以及来自血压正常的初产妇(n = 18)和高血压初产妇(n = 15)及其婴儿的脐静脉样本中的血小板胞质钙。血压正常的初产妇所生婴儿的新生儿脐静脉血小板胞质钙浓度(p[Ca2+]i)与妊娠合并妊娠期高血压的初产妇所生婴儿之间无显著差异(血压正常的初产妇中为88×9(标准误)2×5),无蛋白尿的妊娠高血压综合征患者中为80×6(2×8),子痫前期患者中为89×3(3×2)nmol/L。所研究妊娠的脐静脉中的p[Ca2+]i与处于月经周期卵泡期的非妊娠女性志愿者的脐静脉中的p[Ca2+]i也无显著差异。尽管在所研究婴儿的母亲中,随着疾病严重程度的增加,p[Ca2+]i逐渐显著升高(血压正常的初产妇中为119×9(4×1),无蛋白尿的妊娠高血压综合征患者中为130×8(7×3),子痫前期患者中为148×2(4×5)nmol/L)。产后12周时,三个样本中母亲的平均p[Ca2+]i恢复到与非妊娠受试者相当的浓度。这些数据表明,非妊娠女性的平均p[Ca2+]i与血压正常或高血压初产妇脐静脉血中的平均p[Ca2+]i无显著差异。它们表明新生儿血小板的功能低下可能并非继发于基础p[Ca2+]i的降低。它们还表明,正常和高血压妊娠中逐渐升高的p[Ca2+]i可能是由于一种不穿过胎盘的妊娠特异性因素所致。