Lee Hyoung Youn, Jung Yong Hun, Mamadjonov Najmiddin, Jeung Kyung Woon, Kim Min Chul, Lim Kyung Seob, Jeon Chang-Yeop, Lee Youngjeon, Kim Hyung Joong
Trauma Center Chonnam National University Hospital Gwangju Republic of Korea.
Department of Emergency Medicine Chonnam National University Hospital Gwangju Republic of Korea.
J Am Heart Assoc. 2022 Jun 7;11(11):e025400. doi: 10.1161/JAHA.122.025400. Epub 2022 May 27.
Background Postischemic cerebral hypoperfusion has been indicated as an important contributing factor to secondary cerebral injury after cardiac arrest. We evaluated the effects of sodium nitroprusside administered via a subdural intracranial catheter on the microcirculation, oxygenation, and electrocortical activity of the cerebral cortex in the early postresuscitation period using a pig model of cardiac arrest. Methods and Results Twenty-nine pigs were resuscitated with closed cardiopulmonary resuscitation after 14 minutes of untreated ventricular fibrillation. Thirty minutes after restoration of spontaneous circulation, 24 pigs randomly received either 4 mg of sodium nitroprusside (IT-SNP group) or saline placebo (IT-saline group) via subdural intracranial catheters and were observed for 5 hours. The same dose of sodium nitroprusside was administered intravenously in another 5 pigs. Compared with the IT-saline group, the IT-SNP group had larger areas under the curve for tissue oxygen tension and percent changes of arteriole diameter and number of perfused microvessels from baseline (all <0.05) monitored on the cerebral cortex during the 5-hour period, without severe hemodynamic instability. This group also showed faster recovery of electrocortical activity measured using amplitude-integrated electroencephalography. Repeated-measures analysis of variance revealed significant group-time interactions for these parameters. Intravenously administered sodium nitroprusside caused profound hypotension but did not appear to increase the cerebral parameters. Conclusions Sodium nitroprusside administered via a subdural intracranial catheter increased post-restoration of spontaneous circulation cerebral cortical microcirculation and oxygenation and hastened electrocortical activity recovery in a pig model of cardiac arrest. Further studies are required to determine its impact on the long-term neurologic outcomes.
缺血后脑灌注不足已被认为是心脏骤停后继发性脑损伤的一个重要促成因素。我们使用猪心脏骤停模型,评估了复苏后早期经硬膜下颅内导管给予硝普钠对大脑皮质微循环、氧合及脑电皮质活动的影响。
29只猪在未经处理的室颤14分钟后接受了闭胸心肺复苏。自主循环恢复30分钟后,24只猪通过硬膜下颅内导管随机接受4mg硝普钠(颅内注射硝普钠组)或生理盐水安慰剂(颅内注射生理盐水组),并观察5小时。另外5只猪静脉注射相同剂量的硝普钠。与颅内注射生理盐水组相比,颅内注射硝普钠组在5小时观察期内大脑皮质监测到的组织氧张力曲线下面积、小动脉直径相对于基线的变化百分比及灌注微血管数量均更大(均P<0.05),且无严重血流动力学不稳定。该组还显示使用振幅整合脑电图测量的脑电皮质活动恢复更快。重复测量方差分析显示这些参数存在显著的组间-时间交互作用。静脉注射硝普钠导致严重低血压,但似乎并未增加脑相关参数。
在猪心脏骤停模型中,经硬膜下颅内导管给予硝普钠可增加自主循环恢复后脑皮质微循环和氧合,并加速脑电皮质活动恢复。需要进一步研究以确定其对长期神经学转归的影响。