论文部分内容阅读
目的评价氧合过度所致的BOLD信号强度的改变是否与大鼠宫内生长受限(IUGR)有关。方法在妊娠第16天,结扎左侧子宫血管根部,建立妊娠大鼠的IUGR模型。在第19天,应用1.5TMR设备以平衡稳态自由进动(balanced-SSFP)序列对大鼠模型进行BOLDMR成像。比较母体肝脏、对照组及生长受限胎儿胎盘单元(FPU)在氧合过度发生前后的信号强度(SI)。结果 18只大鼠中,母体氧合过度导致所有感兴趣区SI明显增加(P<0.05)。对照组中,胎盘(n=74)和胎儿(n=53)信号强度(平均值±SD)分别增加(21±15)%和(13±8.5)%。IUGR组中,信号强度增加的幅度明显较低:胎盘(n=36)为(6.5±4)%,胎儿(n=34)为(7±5.5)%;P<0.05。结论 BOLDMRI可以无创评估大鼠母体氧合过度所致的胎儿胎盘反应,并显示其在IUGR模型中的信号强度改变。这种成像技术可提供一种有用的辅助方法,用以早期诊断、评估和治疗人类IUGR。要点①宫内生长受限是围产期发病和死亡的重要原因。②BOLDMRI可以无创评估胎儿胎盘对母体氧合过度的反应。③IUGR大鼠的胎儿胎盘对母体氧合过度的反应发生改变。④功能MRI有助于评估人IUGR。
Objective To evaluate whether changes in BOLD signal intensity caused by hyperoxia are related to IUGR. Methods On the 16th day of gestation, the left uterine vascular root was ligated and the IUGR model of pregnant rats was established. On day 19, a BOLD MR imaging of the rat model was performed using a 1.5 TMR apparatus to balance the balanced-SSFP sequence. The signal intensity (SI) of maternal liver, control group, and growth-restricted fetal placental unit (FPU) before and after oxygenation were compared. Results Overexpression of maternal oxygen in all the 18 rats resulted in a significant increase of SI in all regions of interest (P <0.05). In the control group, the signal intensity (mean ± SD) of placenta (n = 74) and fetus (n = 53) increased by (21 ± 15)% and (13 ± 8.5)%, respectively. In the IUGR group, the increase in signal intensity was significantly lower: (6.5 ± 4)% for the placenta (n = 36) and (7 ± 5.5)% for the fetus (n = 34); P <0.05. Conclusion BOLDMRI can noninvasively assess the fetal placental response induced by overexposure of maternal rats and show its signal intensity change in IUGR model. This imaging technique provides a useful adjunct to early diagnosis, assessment and treatment of human IUGR. Points ① intrauterine growth restriction is an important cause of perinatal morbidity and mortality. ② BOLDMRI noninvasive assessment of fetal placenta over maternal oxygen response. ③ IUGR rat fetal placenta in response to maternal oxygen over change. Functional MRI contributes to evaluating human IUGR.