The effect of hypocpnia and anesthetics on cerebral damage in a rat model of chronic cerebral hypoperfusion

脑白质损害是慢性脑低灌注大鼠模型的特点，是脑血管疾病患者的良好模型。过度换气所致的低碳酸血症可进一步引起尾壳核神经元的进一步损伤，而预先给予氯胺酮可改善这种损伤。这些结果表明，麻醉期间的低碳酸血症可能会导致尾壳核的组织损伤，这可能是中风和/或脑血管性痴呆患者术后长期神志不清和/或记忆障碍的原因，而氯胺酮似乎对预防这种损伤是有效的。

White matter lesions are characteristic in a rat model of chronic cerebral hypoperfusion, which is a good model for patients with cerebrovascular diseases. Hypocapnia, induced by hyperventilation, caused specific further neuronal damage in the caudoputamen, which was ameliorated by ketamine pre-administration. These results suggest that hypocapnia during anesthesia may cause tissue damage in the caudoputamen, which may be responsible for long-lasting postoperative delirium and/or memory disturbances in patients with stroke and/or cerebrovascular dementia, and ketamine seems to be useful for preventing the damage.