Head Brian P, Patel Piyush
Department of Anesthesiology, University of California-San Diego, CA, USA.
Curr Opin Anaesthesiol. 2007 Oct;20(5):395-9. doi: 10.1097/ACO.0b013e3282efa69d.
There is a considerable risk of cerebral ischemia during anesthesia and surgery. Anesthetic agents have been shown to have a profound effect on the pathophysiology of cerebral ischemia. The present review provides a brief historical review and details new information about the anesthetic effects on the ischemic brain.
Although anesthetics have been shown to reduce ischemic cerebral injury, the durability of this neuroprotection has been questioned. Recent data indicate that, under the right circumstances, anesthetic neuroprotection can be sustained for at least 2-4 weeks; the durability of this protection is dependent upon the experimental model, control of physiologic parameters and the assurance of the adequacy of reperfusion. In addition, volatile anesthetics have been shown to accelerate postischemic neurogenesis; this suggests that anesthetics may enhance the endogenous reparative processes in the injured brain.
The available data indicate that anesthetics can provide long-term durable protection against ischemic injury that is mild to moderate in severity. Experimental data do not provide support for the premise that anesthetics reduce injury when the ischemic injury is severe.
麻醉和手术期间存在相当大的脑缺血风险。已证明麻醉药物对脑缺血的病理生理学有深远影响。本综述提供了简要的历史回顾，并详细介绍了关于麻醉对缺血性脑影响的新信息。
尽管已证明麻醉药物可减少缺血性脑损伤，但这种神经保护作用的持久性受到质疑。最近的数据表明，在适当情况下，麻醉神经保护作用可维持至少2至4周；这种保护作用的持久性取决于实验模型、生理参数的控制以及再灌注充分性的保证。此外，已证明挥发性麻醉药物可加速缺血后神经发生；这表明麻醉药物可能增强受损脑内的内源性修复过程。
现有数据表明，麻醉药物可对轻度至中度严重程度的缺血性损伤提供长期持久的保护。实验数据不支持麻醉药物在严重缺血性损伤时减少损伤这一前提。
