A limited interval of delayed modest hypothermia for ischemic brain resuscitation is not beneficial in neonatal swine
A limited interval of delayed modest hypothermia for ischemic brain resuscitation is not beneficial in neonatal swine
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DOI：
10.1203/00006450-199910000-00005
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发表时间：
1999-10-01
影响因子：
3.6
通讯作者：
Sterett, R
中科院分区：
文献类型：
--
作者：
Laptook, AR;Corbett, RJT;Sterett, R
本研究确定脑缺血后30分钟开始的短时间适度低温（1小时）是否提供神经保护。脑冷却的时间和持续时间的基本原理反映了神经保护策略的实施可能在缺血后不久的间隔内发生，并且长期维持正常体温是新生儿稳定的基石。在超导磁体中对22头通风的新生迷你猪进行了研究，以获得P-31磁共振谱。在对照组之后，所有动物都进行了15分钟的全脑缺血，并在缺血后的前30分钟保持正常。在一组11头猪中继续进行正常育婴。在另一组11头猪中，在缺血后30分钟开始适度低温，持续1小时，随后恢复常温。随后，将动物从呼吸机支持下断奶，取下磁铁，并在缺血后72小时进行神经行为和组织学评估。两组缺血的严重程度相似，动脉血压和pH值的变化相同，脑β -核苷酸三磷酸的改变（对照组的%，对照组= 100%，常温组和低温组分别为32 +/- 28 vs 27 +/- 26%），以及缺血性脑酸中毒的程度（常温组和低温组分别为6.13 +/- 0.19 vs 6.14 +/- 0.14）。两组脑病分期分布相同：体温正常1只，异常10只（轻度4只，中度2只，重度4只）；体温过低正常3只，异常8只（轻度4只，中度2只，重度2只）。各组间神经元损伤程度无明显差异。我们的结论是，在缺血后30分钟开始的l-h间适度低温不能给予神经保护。
This investigation determined if a short interval of modest hypothermia (1 h) initiated 30 min after brain ischemia provided neuroprotection. The rationale for the time and duration of brain cooling reflects the likelihood that the implementation of neuroprotective strategies will occur at an interval shortly after ischemia, and that long- term maintenance of normothermia is a cornerstone of neonatal stabilization. Studies were performed in 22 ventilated neonatal mini-swine in a superconducting magnet to obtain P-31 magnetic resonance spectra. After a control period all animals underwent 15 min of global brain ischemia and were maintained normothermic for the first 30 min post-ischemia. In one group of 11 swine normothermia was continued. In the other group of 11 swine, modest hypothermia was initiated at 30 min post-ischemia, continued for 1 h and followed by resumption of normothermia. Animals were subsequently weaned from ventilator support, removed from the magnet, and underwent neurobehavioral and histologic assessment at 72 h post-ischemia. Both groups had similar severity of ischemia, as indicated by identical changes in arterial blood pressure and pH, alterations in brain beta-nucleotide triphosphate (% of control where control = 100%, 32 +/- 28 vs 27 +/- 26% for normothermic and hypothermic groups, respectively), and the extent of intraischemic brain acidosis (6.13 +/- 0.19 vs 6.14 +/- 0.14 for normothermic and hypothermic groups, respectively). In both groups the distribution of stages of encephalopathy were the same: 1 normal and 10 abnormal (4 mild, 2 moderate, and 4 severe) normothermic, and, 3 normal and 8 abnormal (4 mild, 2 moderate, and 2 severe) hypothermic animals. There was no difference in the extent of neuronal injury between groups. We conclude that a l-h interval of modest hypothermia initiated at 30 min post-ischemia does not confer neuroprotection.