Extracranial hypothermia during cardiac arrest and cardiopulmonary resuscitation is neuroprotective in vivo.
Extracranial hypothermia during cardiac arrest and cardiopulmonary resuscitation is neuroprotective in vivo.
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心脏骤停和心肺复苏期间的颅外低温在体内具有神经保护作用。
DOI：
10.1089/ther.2014.0003
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发表时间：
2014
影响因子：
1.2
通讯作者：
Herson,PacoS
中科院分区：
文献类型：
--
作者：
Hutchens,MichaelP;Fujiyoshi,Tetsuhiro;Koerner,InesP;Herson,PacoS
越来越多的证据表明缺血性脑损伤是由外周信号调节的。外周器官缺血可引起脑组织炎症和损伤。因此，我们假设心脏骤停（CA）后持续的脑损伤受外周器官缺血的影响，外周器官保护可以减少CA和心肺复苏（CPR）后的脑损伤。对雄性C57B1/6小鼠进行CA/CPR。所有动物的脑温均维持在37.5 ℃ ± 0.0 ℃。CA期间体温维持在35.1 ° C ± 0.1 ° C（正常体温）或28.8 ° C ± 1.5 ° C（颅外低温[ExHy]）。复苏后所有动物的体温保持在35 ° C。在CA/CPR后1、3、5和7天进行行为测试。CA/CPR后3或7天，分析血液中的血清尿素氮、肌酐、丙氨酸氨基转移酶、天冬氨酸氨基转移酶和白细胞介素-1 β;对小鼠实施安乐死;并将脑切片。CA/CPR可引起周围器官和脑损伤。ExHy动物在复苏后经历脑温度的短暂降低（2.1 ° C ± 0.5 ° C持续4分钟）。令人惊讶的是，ExHy没有改变外周器官损伤。相比之下，ExHy动物在CA/CPR后3天海马损伤减少（22.4% ± 6.2%对45.7% ± 9.1%，p = 0.04，n = 15/组）。这项研究有两个主要发现。仅限于CA的低温不能减少外周器官损伤。这一意想不到的发现表明，短暂缺血后，如在CA/CPR期间，再灌注后的信号或事件可能比缺血期间的信号或事件更具伤害性。第二，周围器官低温在CA减少海马损伤独立于周围器官的保护。虽然这种保护可能是由于早期再灌注期间脑温度的细微差异，但我们推测可能涉及其他机制。我们的研究结果增加了对脑-体串扰的理解，表明即使外周器官损伤没有改变，外周干预也可以保护大脑。
There is increasing evidence that ischemic brain injury is modulated by peripheral signaling. Peripheral organ ischemia can induce brain inflammation and injury. We therefore hypothesized that brain injury sustained after cardiac arrest (CA) is influenced by peripheral organ ischemia and that peripheral organ protection can reduce brain injury after CA and cardiopulmonary resuscitation (CPR). Male C57Bl/6 mice were subjected to CA/CPR. Brain temperature was maintained at 37.5°C±0.0°C in all animals. Body temperature was maintained at 35.1°C±0.1°C (normothermia) or 28.8°C±1.5°C (extracranial hypothermia [ExHy]) during CA. Body temperature after resuscitation was maintained at 35°C in all animals. Behavioral testing was performed at 1, 3, 5, and 7 days after CA/CPR. Either 3 or 7 days after CA/CPR, blood was analyzed for serum urea nitrogen, creatinine, alanine aminotransferase, aspartate aminotransferase, and interleukin-1β; mice were euthanized; and brains were sectioned. CA/CPR caused peripheral organ and brain injury. ExHy animals experienced transient reduction in brain temperature after resuscitation (2.1°C±0.5°C for 4 minutes). Surprisingly, ExHy did not change peripheral organ damage. In contrast, hippocampal injury was reduced at 3 days after CA/CPR in ExHy animals (22.4%±6.2% vs. 45.7%±9.1%,p=0.04,n=15/group). This study has two main findings. Hypothermia limited to CA does not reduce peripheral organ injury. This unexpected finding suggests that after brief ischemia, such as during CA/CPR, signaling or events after reperfusion may be more injurious than those during the ischemic period. Second, peripheral organ hypothermia during CA reduces hippocampal injury independent of peripheral organ protection. While it is possible that this protection is due to subtle differences in brain temperature during early reperfusion, we speculate that additional mechanisms may be involved. Our findings add to the growing understanding of brain-body cross-talk by suggesting that peripheral interventions can protect the brain even if peripheral organ injury is not altered.