Cerebral Lactate Concentration in Neonatal Hypoxic-Ischemic Encephalopathy: In Relation to Time, Characteristic of Injury, and Serum Lactate Concentration.

Cerebral Lactate Concentration in Neonatal Hypoxic-Ischemic Encephalopathy: In Relation to Time, Characteristic of Injury, and Serum Lactate Concentration.
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DOI:
10.3389/fneur.2018.00293
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发表时间:
2018
影响因子:
3.4
通讯作者:
Wisnowski JL
Wisnowski JL
中科院分区:
医学3区
文献类型:
--
作者:
Wu TW;Tamrazi B;Hsu KH;Ho E;Reitman AJ;Borzage M;Blüml S;Wisnowski JL

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新生儿缺氧缺血性脑病(HIE)在血流动力学稳定后仍可检测到脑乳酸浓度。区域脑乳酸浓度的时间分辨率与损伤的严重程度或区域的关系尚不清楚。此外,血清和脑乳酸在新生儿HIE中的相互作用尚未明确。该研究旨在描述新生儿HIE中脑乳酸浓度与时间、损伤和血清乳酸的关系。52例HIE新生儿接受治疗性低温治疗(TH)。在TH期间和之后分别在54.6±15.0和156±57.6 h进行磁共振成像和波谱(MRI + MR波谱)。损伤的严重程度和主要类型影像学评分。利用定位于基底节区(BG)、丘脑(Thal)、灰质(GM)和白质的短回波(35 ms) PRESS序列获得单体素1H MR谱。采用LCModel软件定量测定脑乳酸浓度。根据测量时的年龄绘制血清和脑乳酸浓度。根据损伤的严重程度和主要模式,进行了区域脑乳酸浓度的多重比较。计算Spearman 's Rho以确定在各自感兴趣的区域血清乳酸浓度和脑乳酸浓度之间的相关性。总体而言,血清乳酸浓度随着时间的推移而下降。脑乳酸浓度在较轻的损伤中保持较低水平,在较严重的损伤中随着时间的推移而下降。经TH后仍可检测到脑乳酸。在TH期间,脑乳酸浓度在损伤区域显著升高,损伤越严重,脑乳酸浓度也越高。然而,这些差异在TH后不再观察到。血清乳酸与BG (rs = 0.3, p = 0.04)、Thal (rs = 0.35, p = 0.02)脑乳酸浓度呈弱相关。然而,在中重度脑损伤婴儿中,血清乳酸浓度与BG区(rs = 0.7, p = 0.03)、Thal区(rs = 0.9, p = 0.001)和GM区(rs = 0.6, p = 0.04)的脑乳酸浓度存在非常强的相关性。TH期间脑乳酸在不同部位和不同程度的损伤中差异最为显著。在TH期间,血清和深灰色核中测定的脑乳酸浓度有中度相关性。损伤的差异和局部脑代谢的改变可能解释了这些差异。
Cerebral lactate concentration can remain detectable in neonatal hypoxic-ischemic encephalopathy (HIE) after hemodynamic stability. The temporal resolution of regional cerebral lactate concentration in relation to the severity or area of injury is unclear. Furthermore, the interplay between serum and cerebral lactate in neonatal HIE has not been well defined. The study aims to describe cerebral lactate concentration in neonatal HIE in relation to time, injury, and serum lactate. Fifty-two newborns with HIE undergoing therapeutic hypothermia (TH) were enrolled. Magnetic resonance imaging and spectroscopy (MRI + MR spectroscopy) were performed during and after TH at 54.6 ± 15.0 and 156 ± 57.6 h of life, respectively. Severity and predominant pattern of injury was scored radiographically. Single-voxel 1H MR spectra were acquired using short-echo (35 ms) PRESS sequence localized to the basal ganglia (BG), thalamus (Thal), gray matter (GM), and white matter. Cerebral lactate concentration was quantified by LCModel software. Serum and cerebral lactate concentrations were plotted based on age at time of measurement. Multiple comparisons of regional cerebral lactate concentration based on severity and predominant pattern of injury were performed. Spearman’s Rho was computed to determine correlation between serum lactate and cerebral lactate concentration at the respective regions of interest. Overall, serum lactate concentration decreased over time. Cerebral lactate concentration remained low for less severe injury and decreased over time for more severe injury. Cerebral lactate remained detectable even after TH. During TH, there was a significant higher concentration of cerebral lactate at the areas of injury and also when injury was more severe. However, these differences were no longer observed after TH. There was a weak correlation between serum lactate and cerebral lactate concentration at the BG (rs = 0.3, p = 0.04) and Thal (rs = 0.35, p = 0.02). However, in infants with moderate–severe brain injury, a very strong correlation exists between serum lactate and cerebral lactate concentration at the BG (rs = 0.7, p = 0.03), Thal (rs = 0.9 p = 0.001), and GM (rs = 0.6, p = 0.04) regions. Cerebral lactate is most significantly different between regions and severity of injury during TH. There is a moderate correlation between serum and cerebral lactate concentration measured in the deep gray nuclei during TH. Differences in injury and altered regional cerebral metabolism may account for these differences.
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