Effects of antenatal steroids on ischemic brain injury in near-term ovine fetuses
Effects of antenatal steroids on ischemic brain injury in near-term ovine fetuses
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DOI：
10.1016/s0378-3782(03)00030-6
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发表时间：
2003-08-01
影响因子：
2.5
通讯作者：
Stonestreet, BS
中科院分区：
文献类型：
--
作者：
Elitt, CM;Sadowska, GB;Stonestreet, BS
背景：宫内缺氧/缺血可导致胎儿和新生儿脑损伤。孕妇类固醇是早产妇女管理的常规部分。据报道，在缺氧/缺血性损伤前用地塞米松预处理年轻的出生后大鼠可减轻脑损伤。然而，产前类固醇对胎儿缺血性脑损伤的影响尚未研究。目的：我们研究母体产前给予皮质类固醇对近足月绵羊胎儿缺血性脑损伤的影响。研究方法：在最后4次4 mg地塞米松或安慰剂注射后12 h，对妊娠122天的慢性仪器化胎仔进行研究，注射时间超过48 h。组为地塞米松/缺血、安慰剂/缺血和假治疗对照。胎仔暴露于30分钟的颈动脉闭塞（缺血）或无闭塞（对照）和72小时的再灌注。对用Luxol坚牢蓝-苏木精-伊红染色的全脑冠状切片的白色物质和大脑皮质病变进行评分。两个区域均接受反映损伤程度的病理评分0 - 5分（0 = 0%，1 = 1- 10%，2 = 11- 50%，3 = 51- 90%，4 = 91-99%和5 = 100%）。在地塞米松/缺血组和安慰剂/缺血组中，在脑缺血之前、期间和之后也测量双侧颈动脉血流量。结果如下：白色物质和大脑皮质评分在地塞米松/缺血和安慰剂/缺血之间没有差异（WM：3.0 +/- 1.9和2.9 +/- 1.7;皮质：3.1 +/- 1.7和2.6 +/- 1.8，平均值± S.D.）组地塞米松/缺血组的白色物质和大脑皮质评分较高，（WM：3.0 +/- 1.9，P < 0.02;皮质：3.1 +/- 1.7，P < 0.005）和安慰剂/缺血（脑组织：2.9 +/- 1.7，P < 0.006;皮质：2.6 +/- 1.8，P < 0.007）比对照组（脑组织：0.2 +/- 0.4;皮质：0.2 +/- 0.4）高。再灌注24、48和72 h后，地塞米松/缺血组的颈动脉血流量相对高于安慰剂/缺血组（P < 0.05）。结论：我们的结论是，母体预处理与产前地塞米松并没有减弱胎儿缺血性脑损伤，和颈动脉血流量较高，在再灌注过程中的胎儿地塞米松比安慰剂治疗的母羊，最有可能继发于动脉血氧分压下降。(C)2003爱思唯尔科学爱尔兰有限公司保留所有权利。
Background: Hypoxia/ischemia in utero can result in brain damage to the fetus and newborn. Antenatal steroids are a routine part of the management of women who develop premature labor. Pretreatment of young postnatal rats with dexamethasone before hypoxic/ischemic insults has been reported to attenuate brain injury. However, the effects of antenatal steroids on ischemic brain injury in fetuses have not been investigated. Objective: We examined the effects of maternally administered antenatal corticosteroids on ischemic brain injury in near-term ovine fetuses. Methods: Chronically instrumented fetuses at 122 days of gestation were studied 12 h after the last of four 4 mg dexamethasone, or placebo injections were given over 48 h to the ewes. Groups were dexamethasone/ischemic, placebo/ischemic and sham-treated control. Fetuses were exposed to 30 min of carotid occlusion (ischemia) or no occlusion (control) and 72 h of reperfusion. Whole brain coronal sections stained with Luxol fast blue-hematoxylin-eosin were scored for white matter and cerebral cortical lesions. Both areas received pathological scores of 0 to 5 reflecting the degree of injury (0 = 0%, 1 = 1-10%, 2 = 11-50%, 3 = 51-90%, 4 = 91-99% and 5 = 100%). Bilateral carotid blood flow also was measured before, during and after brain ischemia in the dexamethasone/ ischemic and placebo/ischemic groups. Results: White matter (WM) and cerebral cortical scores did not differ between the dexamethasone/ischemic and placebo/ischemic (WM: 3.0 +/- 1.9 and 2.9 +/- 1.7; cortex: 3.1 +/- 1.7 and 2.6 +/- 1.8, mean +/- S.D.) groups. White matter and cerebral cortical scores were higher in the dexamethasone/ischemic (WM: 3.0 +/- 1.9, P < 0.02; cortex: 3.1 +/- 1.7, P < 0.005) and placebo/ischemic (WM: 2.9 +/- 1.7, P < 0.006; cortex: 2.6 +/- 1.8, P < 0.007) than control (WM:0.2 +/- 0.4; cortex: 0.2 +/- 0.4) group. Carotid blood flow was relatively higher (P < 0.05) after 24, 48 and 72 h of reperfusion in the dexamethasone/ischemic than placebo/ischemic group. Conclusions: We conclude that maternal pretreatment with antenatal dexamethasone did not attenuate ischemic brain injury in the fetus, and that carotid blood flow was higher during reperfusion in fetuses of dexamethasone than placebo-treated ewes, most likely secondary to decreases in arterial oxygen tension. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.