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治疗性低温对心脏骤停后猪模型脑组织氧饱和度的影响。

Effects of therapeutic hypothermia on cerebral tissue oxygen saturation in a swine model of post-cardiac arrest.

作者信息

Wu Chunshuang, Xu Jiefeng, Jin Xiaohong, Chen Qijiang, Lu Xiao, Qian Anyu, Wang Moli, Li Zilong, Zhang Mao

机构信息

Department of Emergency Medicine, Second Affiliated Hospital, Zhejiang University School of Medicine and Institute of Emergency Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, P.R. China.

Department of Emergency Medicine, Yuyao People's Hospital, Ningbo, Zhejiang 315400, P.R. China.

出版信息

Exp Ther Med. 2020 Feb;19(2):1189-1196. doi: 10.3892/etm.2019.8316. Epub 2019 Dec 11.

DOI:10.3892/etm.2019.8316
PMID:32010288
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6966162/
Abstract

Since the introduction of therapeutic hypothermia (TH), trends have changed in the monitoring indicators used during and after cardiac arrest. During hypothermia, the cerebral metabolic rate of oxygen is reduced, which leads to uncertainty in regional cerebral tissue oxygen saturation (SO). The aim of the present study was to evaluate the effect of TH on changes in SO using near-infrared spectroscopy. A total of 23 male domestic pigs were randomized into three groups: TH (n=9), normothermia (NT; n=9) and control (n=5). Animals in the control group underwent surgical preparation only. The animal models were established using 8 min of ventricular fibrillation and 5 min of cardiopulmonary resuscitation. In the TH group, at 5 min after resuscitation, the animals were cooled with a cooling blanket and ice packs for 24 h. SO was recorded throughout the experiment. In all groups, The mean arterial pressure, arterial carbon dioxide partial pressure, arterial oxygen partial pressure, lactate, neuron-specific enolase (NSE) and S100B were measured at baseline and at 1, 3, 6, 12, 24 and 30 h after resuscitation. SO significantly decreased after ventricular fibrillation, compared with the baseline. Following resuscitation, the SO values gradually increased to 55.6±3.8% of baseline in the TH group and 51.2±3.5% in the NT group (P=0.039). Significant differences between the two groups were observed, starting at 6 h after cardiac arrest. Throughout the hypothermic period, NSE and S100B showed an increasing trend, then decreased during rewarming in the TH and NT groups. NSE and S100B showed greater improvement in the TH group compared with the NT group at 6 and 24 h after resuscitation. Following cardiac arrest, therapeutic hypothermia could increase SO after resuscitation and could improve neurological outcome. In conclusion, SO may be a feasible marker for use in the early assessment of brain damage during and after cardiac arrest.

摘要

自治疗性低温(TH)引入以来,心脏骤停期间及之后所使用的监测指标的趋势已经发生了变化。在低温期间,脑氧代谢率降低,这导致局部脑组织氧饱和度(SO)存在不确定性。本研究的目的是使用近红外光谱法评估治疗性低温对SO变化的影响。总共23只雄性家猪被随机分为三组:治疗性低温组(n = 9)、常温组(NT;n = 9)和对照组(n = 5)。对照组动物仅接受手术准备。使用8分钟室颤和5分钟心肺复苏建立动物模型。在治疗性低温组中,复苏后5分钟,用降温毯和冰袋将动物冷却24小时。在整个实验过程中记录SO。在所有组中,在基线以及复苏后1、3、6、12、24和30小时测量平均动脉压、动脉二氧化碳分压、动脉氧分压、乳酸、神经元特异性烯醇化酶(NSE)和S100B。与基线相比,室颤后SO显著降低。复苏后,治疗性低温组的SO值逐渐升至基线的55.6±3.8%,常温组为51.2±3.5%(P = 0.039)。心脏骤停后6小时开始,两组之间观察到显著差异。在整个低温期,NSE和S100B呈上升趋势,然后在治疗性低温组和常温组复温期间下降。复苏后6小时和24小时,治疗性低温组的NSE和S100B与常温组相比改善更大。心脏骤停后,治疗性低温可提高复苏后的SO,并可改善神经功能结局。总之,SO可能是用于心脏骤停期间及之后脑损伤早期评估的一个可行标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/e11453a7f1cd/etm-19-02-1189-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/fe00ff77b646/etm-19-02-1189-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/b97427f9a960/etm-19-02-1189-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/706a1f8d8e58/etm-19-02-1189-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/e482be20d35c/etm-19-02-1189-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/e11453a7f1cd/etm-19-02-1189-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/fe00ff77b646/etm-19-02-1189-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/b97427f9a960/etm-19-02-1189-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/706a1f8d8e58/etm-19-02-1189-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/e482be20d35c/etm-19-02-1189-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f2b/6966162/e11453a7f1cd/etm-19-02-1189-g04.jpg

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