Dalitz P, Harding R, Rees S M, Cock M L
Fetal and Neonatal Research Group, Department of Physiology, Monash University, Victoria, Melbourne, Australia.
J Soc Gynecol Investig. 2003 Jul;10(5):283-90. doi: 10.1016/s1071-5576(03)00090-x.
Endotoxin causes hypoxemia and white matter injury in the preterm ovine fetus. Because cerebral hypoxia could contribute to brain injury, our objective was to determine the effects of endotoxin on regional cerebral oxygen (O(2)) delivery. To investigate causes of fetal hypoxemia, we also measured placental blood flow.
We administered endotoxin (lipopolysaccharide, LPS) at 1 microgram/kg (intravenously) to 11 catheterized fetal sheep at approximately 0.7 of term; controls (n = 7) received saline. We measured fetal cerebral blood flow (CBF) and placental blood flow using microspheres, arterial blood gases, arterial pressure, and heart rate.
Seven fetuses survived LPS administration (LPS-S) and four died. LPS-S fetuses were hypoxemic at 4-8 hours after LPS. Fetal hemoglobin concentration and hematocrit increased by about 14% at 4 hours after LPS exposure, and mean arterial pressure decreased significantly from 4-8 hours. After LPS, CBF did not change significantly, but total cerebral O(2) delivery decreased by 35.7% at 4 hours and by 28.3% at 8 hours. O(2) delivery to cerebral white matter decreased below pre-LPS values at 4 hours (-35.9%) and 8 hours (-28.6%) after LPS. Relative to pre-LPS values, placental blood flow decreased by 53.3% at 4 hours and 43.0% at 8 hours after LPS.
Immature fetal sheep exposed to LPS had profound reductions in placental blood flow and cerebral O(2) delivery, which could contribute to fetal brain injury. Reduced O(2) delivery to white matter was similar to that in other brain regions. Mechanisms that enable fetal CBF to increase in hypoxemic conditions were apparently ineffective in the presence of LPS.
内毒素可导致早产绵羊胎儿出现低氧血症和白质损伤。由于脑缺氧可能导致脑损伤，我们的目的是确定内毒素对局部脑氧（O₂）输送的影响。为了研究胎儿低氧血症的原因，我们还测量了胎盘血流量。
我们在妊娠约0.7期时，给11只插入导管的胎羊静脉注射1微克/千克的内毒素（脂多糖，LPS）；对照组（n = 7）注射生理盐水。我们使用微球、动脉血气、动脉压和心率来测量胎儿脑血流量（CBF）和胎盘血流量。
7只胎羊在注射LPS后存活（LPS-S），4只死亡。LPS-S胎羊在注射LPS后4 - 8小时出现低氧血症。LPS暴露后4小时，胎儿血红蛋白浓度和血细胞比容增加约14%，平均动脉压在4 - 8小时显著下降。注射LPS后，CBF没有显著变化，但总脑O₂输送在4小时下降了35.7%，在8小时下降了28.3%。LPS注射后4小时（-35.9%）和8小时（-28.6%），脑白质的O₂输送降至LPS注射前水平以下。相对于LPS注射前的值，胎盘血流量在LPS注射后4小时下降了53.3%，在8小时下降了43.0%。
暴露于LPS的未成熟胎羊胎盘血流量和脑O₂输送显著降低，这可能导致胎儿脑损伤。白质O₂输送的减少与其他脑区相似。在低氧条件下使胎儿CBF增加的机制在存在LPS时显然无效。
