Wang Di, Guo Qingchen, Liu Di, Kong Xiang-Xi, Xu Zheng, Zhou Yu, Su Yan, Dai Feng, Ding Hai-Lei, Cao Jun-Li
Jiangsu Province Key Laboratory of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology, Xuzhou Medical University, Xuzhou, China.
Department of Anesthesiology and Perioperative Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Front Pharmacol. 2021 Sep 6;12:740012. doi: 10.3389/fphar.2021.740012. eCollection 2021.
The same doses of anesthesia may yield varying depths of anesthesia in different patients. Clinical studies have revealed a possible causal relationship between deep anesthesia and negative short- and long-term patient outcomes. However, a reliable index and method of the clinical monitoring of deep anesthesia and detecting latency remain lacking. As burst-suppression is a characteristic phenomenon of deep anesthesia, the present study investigated the relationship between burst-suppression latency (BSL) and the subsequent burst-suppression ratio (BSR) to find an improved detection for the onset of intraoperative deep anesthesia. The mice were divided young, adult and old group treated with 1.0% or 1.5% isoflurane anesthesia alone for 2 h. In addition, the adult mice were pretreated with intraperitoneal injection of ketamine, dexmedetomidine, midazolam or propofol before they were anesthetized by 1.0% isoflurane for 2 h. Continuous frontal, parietal and occipital electroencephalogram (EEG) were acquired during anesthesia. The time from the onset of anesthesia to the first occurrence of burst-suppression was defined as BSL, while BSR was calculated as percentage of burst-suppression time that was spent in suppression periods. Under 1.0% isoflurane anesthesia, we found a negative correlation between BSL and BSR for EEG recordings obtained from the parietal lobes of young mice, from the parietal and occipital lobes of adult mice, and the occipital lobes of old mice. Under 1.5% isoflurane anesthesia, only the BSL calculated from EEG data obtained from the occipital lobe was negatively correlated with BSR in all mice. Furthermore, in adult mice receiving 1.0% isoflurane anesthesia, the co-administration of ketamine and midazolam, but not dexmedetomidine and propofol, significantly decreased BSL and increased BSR. Together, these data suggest that BSL can detect burst-suppression and predict the subsequent BSR under isoflurane anesthesia used alone or in combination with anesthetics or adjuvant drugs. Furthermore, the consistent negative correlation between BSL and BSR calculated from occipital EEG recordings recommends it as the optimal position for monitoring burst-suppression.
相同剂量的麻醉剂在不同患者中可能产生不同深度的麻醉效果。临床研究表明,深度麻醉与患者短期和长期的不良预后之间可能存在因果关系。然而,目前仍缺乏可靠的深度麻醉临床监测指标和检测潜伏期的方法。由于爆发抑制是深度麻醉的一个特征性现象,本研究调查了爆发抑制潜伏期(BSL)与随后的爆发抑制率(BSR)之间的关系,以寻找一种改进的术中深度麻醉起始检测方法。将小鼠分为幼年、成年和老年组,分别单独使用1.0%或1.5%异氟醚麻醉2小时。此外,成年小鼠在接受1.0%异氟醚麻醉2小时前,腹腔注射氯胺酮、右美托咪定、咪达唑仑或丙泊酚进行预处理。在麻醉过程中持续采集额叶、顶叶和枕叶脑电图(EEG)。从麻醉开始到首次出现爆发抑制的时间定义为BSL,而BSR计算为抑制期所占爆发抑制时间的百分比。在1.0%异氟醚麻醉下,我们发现幼年小鼠顶叶、成年小鼠顶叶和枕叶以及老年小鼠枕叶的脑电图记录中,BSL与BSR呈负相关。在1.5%异氟醚麻醉下,仅从所有小鼠枕叶获得的脑电图数据计算出的BSL与BSR呈负相关。此外,在接受1.0%异氟醚麻醉的成年小鼠中,氯胺酮和咪达唑仑联合使用可显著降低BSL并提高BSR,而右美托咪定和丙泊酚联合使用则无此效果。总之,这些数据表明,BSL可以检测爆发抑制,并预测单独使用异氟醚麻醉或与麻醉剂或辅助药物联合使用时的后续BSR。此外,从枕叶脑电图记录计算出的BSL与BSR之间持续的负相关表明,枕叶是监测爆发抑制的最佳部位。