Chen Jie, Li Zhonghao, Liu Xiaoyu, Hu Tianpeng, Gao Nan, Zhang Weijian, Zhang Guoqiang
1Department of Emergency Medicine, China-Japan Friendship Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
2Department of Emergency Medicine, China-Japan Friendship Hospital, Beijing 100029, China.
World J Emerg Med. 2025 May 1;16(3):231-238. doi: 10.5847/wjem.j.1920-8642.2025.055.
Post-cardiac arrest syndrome (PCAS) significantly contributes to mortality after initially successful cardiopulmonary resuscitation (CPR) in cardiac arrest (CA) patients. Effective cardiocerebral protection is essential for improving post-resuscitation survival. This study investigated the mechanisms and common targets of myocardial dysfunction and brain injury after resuscitation.
The male Sprague-Dawley rats (10-12 weeks old, 400-500 g) were divided into two groups: the control group (=6), which received sham surgery, and the CA/CPR group (=10), which received ventricular fibrillation (VF) followed by CPR. After 24 h, brain and heart tissues were collected for analysis. The sequencing was used to identify differentially expressed genes (DEGs) between control and CA/CPR rats.
At 24 h after resuscitation, CA/CPR rats presented 217 DEGs in the hippocampus and 80 DEGs in the left ventricle (LV) compared to the control group. In the hippocampus, the most notable biological process was the positive regulation of tumor necrosis factor production, with key pathways related to inflammation and the immune response. In the LV, the Gene Ontology (GO) enrichment analysis revealed that gene alterations were primarily associated with amyloid-beta clearance, a pathway that was also relevant in the brain. Eleven common targets were identified in the DEGs of both heart and brain tissues. The reverse transcription-polymerase chain reaction (RT-PCR) validation revealed significant differences in the mRNA expression of , , and in both LV and hippocampus.
This study identified possible key genes and underlying mechanisms involved in PCAS. The differential genes , , and might serve as common biomarkers for myocardial and neurological injury following resuscitation.
心脏骤停后综合征（PCAS）是导致心脏骤停（CA）患者最初心肺复苏（CPR）成功后死亡的重要因素。有效的心脑保护对于提高复苏后的生存率至关重要。本研究探讨了复苏后心肌功能障碍和脑损伤的机制及共同靶点。
将雄性Sprague-Dawley大鼠（10 - 12周龄，400 - 500克）分为两组：对照组（=6），接受假手术；CA/CPR组（=10），接受室颤（VF）后进行CPR。24小时后，收集脑和心脏组织进行分析。采用测序技术鉴定对照组和CA/CPR大鼠之间的差异表达基因（DEGs）。
与对照组相比，复苏后24小时，CA/CPR大鼠海马体中有217个DEGs，左心室（LV）中有80个DEGs。在海马体中，最显著的生物学过程是肿瘤坏死因子产生的正调控，关键途径与炎症和免疫反应相关。在左心室中，基因本体（GO）富集分析表明基因改变主要与β-淀粉样蛋白清除有关，该途径在脑中也相关。在心脏和脑组织的DEGs中鉴定出11个共同靶点。逆转录-聚合酶链反应（RT-PCR）验证显示，LV和海马体中 、 和 的mRNA表达存在显著差异。
本研究确定了PCAS中可能涉及的关键基因和潜在机制。差异基因 、 和 可能作为复苏后心肌和神经损伤的共同生物标志物。
