Cardiocerebral protection by emulsified isoflurane during cardiopulmonary resuscitation
Cardiocerebral protection by emulsified isoflurane during cardiopulmonary resuscitation
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乳化异氟醚心肺复苏时的心脑保护作用
DOI：
10.1016/j.mehy.2014.11.008
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发表时间：
2015-01-01
影响因子：
4.7
通讯作者：
Yu, Hai
中科院分区：
文献类型：
--
作者：
Zhang, Ya-Jie;Wu, Meng-Jun;Yu, Hai
尽管近年来心肺复苏（CPR）的性能得到了改善，并且在实现自主循环恢复（ROSC）方面取得了越来越多的成功，但心脏骤停（CA）后患者的存活率和出院率仍然令人失望。高死亡率归因于全身缺血/再灌注（I/R）诱导的多器官功能障碍，即众所周知的心脏骤停后综合征。心脏骤停后心肌功能障碍和脑损伤是这一复杂病理生理过程的主要临床特征。已有证据表明，挥发性麻醉剂，如异氟烷，在I/R期间在多个器官（包括心脏和大脑）中触发强大且高度整合的细胞存活反应，从而减少I/R损伤。这种作用被称为麻醉诱导的后适应，可以在缺血发作后和再灌注时给予挥发性麻醉药时显示。乳化异氟醚（Elso）是一种新型的静脉麻醉药，在手术室外使用方便。因此，我们假设EIso后处理可以提供心脑保护，并结合治疗性低温作为镇静剂可以产生增强的心脑保护，这可以导致显着改善神经系统完整的心脏骤停后生存。我们认为这将成为一种可行、安全、有效的心脑保护性干预措施，可预防和减轻心脏骤停后综合征，并改善CA后的结局。(C)2014爱思唯尔有限公司版权所有。
Although improvement in cardiopulmonary resuscitation (CPR) performance and the increasing success at achieving return of spontaneous circulation (ROSC) have been possible in recent years, the survival and discharge rates of post-cardiac arrest (CA) patients remain disappointing. The high mortality rate is attributed to whole-body ischemia/reperfusion (I/R) induced multi-organ dysfunction that is well known as post-cardiac arrest syndrome. Post-cardiac arrest myocardial dysfunction and brain injury are the main clinical features of this complex pathophysiological process. Previous evidences have shown that volatile anesthetics, such as isoflurane, trigger a powerful and highly integrated cell survival response during I/R period in multiple organs, including heart and brain, which reduces I/R injury. This effect that called anesthetic-induced postconditioning can be shown when volatile anesthetics are administered after the onset of ischemia and at the time of reperfusion. Emulsified isoflurane (Elso) is a new anesthetic for intravenous administration, which is conveniently feasible outside operating room. Therefore, we hypothesize that EIso postconditioning could provide the cardiocerebral protection, and combined with therapeutic hypothermia as sedative agent could produce enhanced cardiocerebral protection, which can result in significant improvement of neurologically intact post-cardiac arrest survival. We consider that it would become a feasible, safe and efficient cardiocerebral protective intervention in the prevention and alleviation of post-cardiac arrest syndrome, which would also improve the outcomes after CA. (C) 2014 Elsevier Ltd. All rights reserved.