The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.
Department of Obstetrics and Gynecology, Mie University, Mie, Japan.
Am J Physiol Regul Integr Comp Physiol. 2020 Dec 1;319(6):R653-R665. doi: 10.1152/ajpregu.00216.2020. Epub 2020 Oct 14.
Antenatal glucocorticoids improve outcomes among premature infants but are associated with hyperglycemia, which can exacerbate hypoxic-ischemic injury. It is still unclear how antenatal glucocorticoids or hyperglycemia modulate fetal cardiovascular adaptations to severe asphyxia. In this study, preterm fetal sheep received either saline or 12 mg im maternal dexamethasone, followed 4 h later by complete umbilical cord occlusion (UCO) for 25 min. An additional cohort of fetuses received titrated glucose infusions followed 4 h later by UCO to control for the possibility that hyperglycemia contributed to the cardiovascular effects of dexamethasone. Fetuses were studied for 7 days after UCO. Maternal dexamethasone was associated with fetal hyperglycemia ( < 0.001), increased arterial pressure ( < 0.001), and reduced femoral ( < 0.005) and carotid ( < 0.05) vascular conductance before UCO. UCO was associated with bradycardia, femoral vasoconstriction, and transient hypertension. For the first 5 min of UCO, fetal blood pressure in the dexamethasone-asphyxia group was greater than saline-asphyxia ( < 0.001). However, the relative increase in arterial pressure was not different from saline-asphyxia. Fetal heart rate and femoral vascular conductance fell to similar nadirs in both saline and dexamethasone-asphyxia groups. Dexamethasone did not affect the progressive decline in femoral vascular tone or arterial pressure during continuing UCO. By contrast, there were no effects of glucose infusions on the response to UCO. In summary, maternal dexamethasone but not fetal hyperglycemia increased fetal arterial pressure before and for the first 5 min of prolonged UCO but did not augment the cardiovascular adaptations to acute asphyxia.
产前糖皮质激素可改善早产儿的结局，但与高血糖有关，高血糖可加重缺氧缺血性损伤。目前尚不清楚产前糖皮质激素或高血糖如何调节胎儿对严重窒息的心血管适应。在这项研究中，早产胎儿接受生理盐水或 12mg 肌肉注射地塞米松，4 小时后进行完全脐带结扎（UCO）25 分钟。另一组胎儿接受滴定葡萄糖输注，4 小时后进行 UCO，以控制高血糖可能导致地塞米松心血管作用的可能性。UCO 后对胎儿进行 7 天研究。地塞米松与胎儿高血糖（<0.001）、动脉压升高（<0.001）和股动脉（<0.005）和颈动脉（<0.05）血管导降低有关，UCO 前。UCO 与心动过缓、股动脉收缩和短暂性高血压有关。在 UCO 的前 5 分钟，地塞米松窒息组的胎儿血压高于生理盐水窒息组（<0.001）。然而，动脉压的相对增加与生理盐水窒息组没有差异。在生理盐水和地塞米松窒息组中，胎儿心率和股动脉血管导纳均降至相似的最低点。地塞米松不影响持续 UCO 期间股动脉张力或动脉压的进行性下降。相比之下，葡萄糖输注对 UCO 的反应没有影响。总之，地塞米松母体而不是胎儿高血糖增加了长时间 UCO 前和前 5 分钟的胎儿动脉压，但没有增强对急性窒息的心血管适应。
