Anesthetic drugs and sustained neuroprotection in acute cerebral ischemia: can we alter clinical outcomes?
Anesthetic drugs and sustained neuroprotection in acute cerebral ischemia: can we alter clinical outcomes?
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DOI：
10.1007/s12630-009-9166-y
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发表时间：
2009-09
期刊：
影响因子：
--
通讯作者：
C. Werner
中科院分区：
文献类型：
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作者：
C. Werner
几十年来，麻醉药物的神经保护特性一直受到测试，因为它们有可能中断或减缓有害生化和分子事件的序列，最终导致不可逆转的神经元死亡。不幸的是，检查麻醉剂的神经保护作用的临床试验未能转化实验证据。1这篇社论的目的是在确定这一重要研究领域未来发展方向的背景下，考虑目前阶段关于麻醉神经保护的知识。建立围手术期神经保护需求的一个基本问题是确定将从特定麻醉剂中受益的目标人群。围手术期脑缺血仍然是心脏病和非心脏病患者发病率和死亡率的重要来源。2，3例如，在接受外周血管、主动脉重建和心脏手术的患者中，急性缺血性卒中的发生率为0.8%至8.8%。在接受结直肠手术、全髋关节置换术和头颈部手术的患者中，围手术期卒中的发生率从0.3%到4.8%不等。急性神经变性也可能表现为术后神经认知功能下降。令人惊讶的是，这种重要的致病性被忽视为神经保护策略的目标，但它显然值得神经保护方法。
Anesthetic drugs have been tested for their neuroprotective characteristics for decades because of their potential either to interrupt or to slow the sequence of injurious biochemical and molecular events that ultimately result in irreversible neuronal death. Unfortunately, clinical trials examining the neuroprotective effects of anesthetic agents have failed to translate the experimental evidence. 1 The purpose of this editorial is to consider the current stage of knowledge regarding anesthetic neuroprotection in the context of identifying future directions for this important field of research.A fundamental issue in establishing the need for perioperative neuroprotection is to identify target populations that will benefit neurologically from specific anesthetic agents. Perioperative cerebral ischemia remains a significant source of morbidity and mortality in cardiac and noncardiac patients alike. 2, 3 For example, the incidence of acute ischemic stroke varies from 0.8 to 8.8% in patients undergoing peripheral vascular, aortic reconstructive, and cardiac surgery. In patients undergoing colorectal surgery, total hip arthroplasty, and head and neck surgery, the incidence of perioperative stroke varies from 0.3 to 4.8%. Acute neurodegeneration may also present as postoperative neurocognitive decline. It is rather surprising, then, that this important pathogenicity has been disregarded as a target of neuroprotective strategies, yet it clearly deserves a neuroprotective approach.