Immediate remote ischemic postconditioning after hypoxia ischemia in piglets protects cerebral white matter but not grey matter.
Immediate remote ischemic postconditioning after hypoxia ischemia in piglets protects cerebral white matter but not grey matter.
复制标题
低氧缺血后立即偏远的缺血后调节可保护脑白质，但不能保护灰质。
DOI：
10.1177/0271678x15608862
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发表时间：
2016-08
期刊：
影响因子：
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通讯作者：
Robertson NJ
中科院分区：
文献类型：
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作者：
Ezzati M;Bainbridge A;Broad KD;Kawano G;Oliver-Taylor A;Rocha-Ferreira E;Alonso-Alconada D;Fierens I;Rostami J;Jane Hassell K;Tachtsidis I;Gressens P;Hristova M;Bennett K;Lebon S;Fleiss B;Yellon D;Hausenloy DJ;Golay X;Robertson NJ
远程缺血后处理（RIPostC）是一种很有前途的治疗干预，其中一个器官（肢体）的短暂缺血/再灌注减轻了另一个器官（脑）的损伤，该器官已经经历了严重的缺氧缺血。我们的目的是使用磁共振波谱（MRS）生物标志物和免疫组织化学评估RiPostC是否对新生儿脑病（NE）小猪模型的脑缺氧缺血具有保护作用。在缺氧-缺血（HI）后，将16只大型白色雌性新生仔猪随机分为：（i）无干预（n = 8）;（ii）RIPostC -HI后立即进行4个10分钟循环的双侧下肢缺血/再灌注（n = 8）。在HI后48小时内，RIPostC减少了缺氧缺血诱导的白色质子MRS乳酸盐/N乙酰天冬氨酸盐增加（p = 0.005），并增加了全脑磷-31 MRS ATP（p = 0.039）。在脑室周围白色物质（p = 0.03）、内囊（p = 0.002）和胼胝体（p = 0.021）中，RIPostC减少了细胞死亡;胼胝体（p = 0.001）中的小胶质细胞活化减少，胼胝体（p = 0.029）和脑室周围白色物质（p = 0.001）中存活的少突胶质细胞更多。48 h后在白色物质中检测到基因表达的变化，包括KATP通道和内皮素A受体。立即RIPostC是一种潜在的安全和有前途的脑保护治疗NE与白色，但不是灰质的保护婴儿。
Remote ischemic postconditioning (RIPostC) is a promising therapeutic intervention whereby brief episodes of ischemia/reperfusion of one organ (limb) mitigate damage in another organ (brain) that has experienced severe hypoxia-ischemia. Our aim was to assess whether RIPostC is protective following cerebral hypoxia-ischemia in a piglet model of neonatal encephalopathy (NE) using magnetic resonance spectroscopy (MRS) biomarkers and immunohistochemistry. After hypoxia-ischemia (HI), 16 Large White female newborn piglets were randomized to: (i) no intervention (n = 8); (ii) RIPostC – with four, 10-min cycles of bilateral lower limb ischemia/reperfusion immediately after HI (n = 8). RIPostC reduced the hypoxic-ischemic-induced increase in white matter proton MRS lactate/N acetyl aspartate (p = 0.005) and increased whole brain phosphorus-31 MRS ATP (p = 0.039) over the 48 h after HI. Cell death was reduced with RIPostC in the periventricular white matter (p = 0.03), internal capsule (p = 0.002) and corpus callosum (p = 0.021); there was reduced microglial activation in corpus callosum (p = 0.001) and more surviving oligodendrocytes in corpus callosum (p = 0.029) and periventricular white matter (p = 0.001). Changes in gene expression were detected in the white matter at 48 h, including KATP channel and endothelin A receptor. Immediate RIPostC is a potentially safe and promising brain protective therapy for babies with NE with protection in white but not grey matter.