Cerebral oedema develops after anoxic brain injury. In two models of asphyxial and asystolic cardiac arrest without resuscitation, we found that oedema develops shortly after anoxia secondary to terminal depolarizations and the abnormal entry of CSF. Oedema severity correlated with the availability of CSF with the age-dependent increase in CSF volume worsening the severity of oedema. Oedema was identified primarily in brain regions bordering CSF compartments in mice and humans. The degree of ex vivo tissue swelling was predicted by an osmotic model suggesting that anoxic brain tissue possesses a high intrinsic osmotic potential. This osmotic process was temperature-dependent, proposing an additional mechanism for the beneficial effect of therapeutic hypothermia. These observations show that CSF is a primary source of oedema fluid in anoxic brain. This novel insight offers a mechanistic basis for the future development of alternative strategies to prevent cerebral oedema formation after cardiac arrest.

中文翻译：

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脑脊液是缺氧性脑水肿的重要体液来源

缺氧性脑损伤后会出现脑水肿。在没有复苏的两种窒息性和心脏停搏性心脏骤停模型中，我们发现在继发于终末去极化和脑脊液异常进入的缺氧后不久就会出现水肿。水肿严重程度与脑脊液的可用性相关，脑脊液体积的年龄依赖性增加会加重水肿的严重程度。水肿主要在小鼠和人类与脑脊液隔室接壤的大脑区域中发现。通过渗透模型预测离体组织肿胀的程度，这表明缺氧脑组织具有高的内在渗透潜力。这种渗透过程是温度依赖性的，为低温治疗的有益效果提出了另一种机制。这些观察结果表明，CSF 是缺氧大脑中水肿液的主要来源。