Delayed vasodilation and altered oxygenation after cerebral ischemia in fetal sheep
Delayed vasodilation and altered oxygenation after cerebral ischemia in fetal sheep
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DOI：
10.1203/00006450-199601000-00007
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发表时间：
1996-01-01
影响因子：
3.6
通讯作者：
Edwards, AD
中科院分区：
文献类型：
--
作者：
Marks, KA;Mallard, EC;Edwards, AD
该研究调查了这样的假设：短暂性脑缺血后的迟发性脑损伤与血管收缩和脑氧合减少有关。八只长期使用仪器的妊娠晚期胎羊在子宫内经历了 30 分钟的脑缺血。记录皮质阻抗（CI）和皮质电图（ECoG）以确定细胞功能障碍的时间进程。缺血后4天评估组织学结果。使用近红外光谱法观察损伤期间和损伤后 4 d 的脑血管张力和氧合变化，以测量总脑血红蛋白 ([tHb])、氧合血红蛋白 ([Hbo(2)]) 和氧化细胞色素 aa ([Cyto(2)]) 的变化。结果表示为平均值+/-SEM。缺血期间 CI 短暂升高；然后延迟增加在缺血后 17.5 +/- 2.3 小时开始，并在 42.3 +/- 2.4 小时达到峰值。 ECoG 在侮辱期间和之后都很沮丧。癫痫发作在攻击后 13.6 +/- 3.0 小时开始，持续 25.4 +/- 3.2 小时。 [tHb]的增加表明两个阶段的脑血管舒张：早期再灌注后立即，持续2.3+/-0.4小时并达到峰值20+/-2.0μmolL(-1)；后期阶段，从缺血后 12.8 +/- 2.0 小时开始，达到峰值 43 +/- 4.0 μmol。 L(-1) 并持续 43.1 +/- 5.2 小时。缺血后第 4 天，[Hbo] 相对升高（18 +/- 3.0 μmol.L(-1)），表明平均脑氧饱和度延迟增加。 [Cyto(2)]在侮辱过程中下降（-0.7 +/- 0.2 mu mol . L(-1)）；和。从缺血后 28-30 小时开始，逐渐下降至最低 -5.0 +/- 2.8 mumol。缺血后 78-80 小时 L(-1)。 [Cyto(2)] 下降幅度较大与脑损伤加重相关 (p < 0.05)。迟发性脑损伤伴有血管舒张和平均脑氧饱和度增加，尽管 [Cyto(2)] 逐渐下降可能表明线粒体氧合下降、细胞丢失或组织光学特征变化。
The study investigated the hypothesis that delayed cerebral injury after transient cerebral ischemia is associated with vasoconstriction and decreased cerebral oxygenation, Eight chronically instrumented, late gestation fetal sheep were subjected to 30 min of cerebral ischemia in utero. Cortical impedance (CI) and electrocorticogram (ECoG) were recorded to determine the time course of cellular dysfunction. Histologic outcome was assessed 4 d postischemia. Changes in cerebral vascular tone and oxygenation were observed during and for 4 d after the insult using near infrared spectroscopy to measure changes in total cerebral Hb ([tHb]), oxyhemoglobin ([Hbo(2)]), and oxidized cytochrome aa, ([Cyto(2)]). Results are expressed as mean +/- SEM. CI increased transiently during ischemia; then a delayed increase commenced 17.5 +/- 2.3 h postischemia and peaked at 42.3 +/- 2.4 h. ECoG was depressed during and after the insult. Seizures started 13.6 +/- 3.0 h postinsult and persisted for 25.4 +/- 3.2 h. Increases in [tHb] indicated two periods of cerebral vasodilation: immediately after early reperfusion, lasting 2.3 +/- 0.4 h and peaking to 20 +/- 2.0 mu mol L(-1); and a later phase, commencing 12.8 +/- 2.0 h postischemia, peaking to 43 +/- 4.0 mu mol . L(-1) and lasting 43.1 +/- 5.2 h. [Hbo,] was relatively elevated (18 +/- 3.0 mu mol . L(-1)) during d 4 postischemia, demonstrating a delayed increase in mean cerebral oxygen saturation. [Cyto(2)] fell during the insult (-0.7 +/- 0.2 mu mol . L(-1)); and. commencing at 28-30 h postischemia fell progressively to reach a minimum of -5.0 +/- 2.8 mu mol . L(-1) at 78-80 h postischemia. A greater fall in [Cyto(2)] was related to worse cerebral injury (p < 0.05), Delayed cerebral injury is accompanied by vasodilation and increased mean cerebral oxygen saturation, although a progressive fall in [Cyto(2)] might indicate a fall in mitochondrial oxygenation, cell loss, or changes in tissue optical characteristics.