PDF(Pubmed)
Abstract：
UNASSIGNED: Neurologic complications seriously affect the survival rate and quality of life in patients with extracorporeal cardiopulmonary resuscitation (ECPR) undergoing cardiac arrest. This study aimed to repurpose selective hypothermic cerebral perfusion (SHCP) as a novel approach to protect the brains of these patients.
UNASSIGNED: Rats were randomly allocated to Sham, ECPR, and SHCP combined ECPR (CP-ECPR) groups. In the ECPR group, circulatory resuscitation was performed at 6 minutes after asphyxial cardiac arrest by extracorporeal membrane oxygenation. The vital signs were monitored for 3 hours, and body and brain temperatures were maintained at the normal level. In the CP-ECPR group, the right carotid artery catheterization serving as cerebral perfusion was connected with the extracorporeal membrane oxygenation device to achieve selective brain cooling (26-28 °C). Serum markers of brain injury and pathomorphologic changes in the hippocampus were evaluated. Three biological replicates further received RNA sequencing in ECPR and CP-ECPR groups. Microglia activation and inflammatory cytokines in brain tissues and serum were detected.
UNASSIGNED: SHCP rapidly reduced the brain-targeted temperature and significantly alleviated nerve injury. This was evident from the reduced brain injury serum biomarker levels, lower pathologic scores, and more surviving neurons in the hippocampus in the CP-ECPR group. Furthermore, more differentially expressed genes for inflammatory responses were clustered functionally according to Kyoto Encyclopedia of Genes and Genomes pathway analysis. And SHCP reduced microglia activation and the release of proinflammatory mediators.
UNASSIGNED: Our preliminary data indicate that SHCP may serve as a potential therapy to attenuate brain injury via downregulation of neuroinflammation in patients with ECPR.
UNASSIGNED: Rats were randomly allocated to Sham, ECPR, and SHCP combined ECPR (CP-ECPR) groups. In the ECPR group, circulatory resuscitation was performed at 6 minutes after asphyxial cardiac arrest by extracorporeal membrane oxygenation. The vital signs were monitored for 3 hours, and body and brain temperatures were maintained at the normal level. In the CP-ECPR group, the right carotid artery catheterization serving as cerebral perfusion was connected with the extracorporeal membrane oxygenation device to achieve selective brain cooling (26-28 °C). Serum markers of brain injury and pathomorphologic changes in the hippocampus were evaluated. Three biological replicates further received RNA sequencing in ECPR and CP-ECPR groups. Microglia activation and inflammatory cytokines in brain tissues and serum were detected.
UNASSIGNED: SHCP rapidly reduced the brain-targeted temperature and significantly alleviated nerve injury. This was evident from the reduced brain injury serum biomarker levels, lower pathologic scores, and more surviving neurons in the hippocampus in the CP-ECPR group. Furthermore, more differentially expressed genes for inflammatory responses were clustered functionally according to Kyoto Encyclopedia of Genes and Genomes pathway analysis. And SHCP reduced microglia activation and the release of proinflammatory mediators.
UNASSIGNED: Our preliminary data indicate that SHCP may serve as a potential therapy to attenuate brain injury via downregulation of neuroinflammation in patients with ECPR.
摘要：
未经证实：神经系统并发症严重影响心脏骤停体外心肺复苏（ECPR）患者的生存率和生活质量。这项研究旨在重新利用选择性低温脑灌注（SHCP）作为保护这些患者大脑的新方法。
未经授权：大鼠被随机分配到假，ECPR,和SHCP联合ECPR（CP-ECPR）组。在ECPR小组中，在窒息心脏骤停后6分钟通过体外膜氧合进行循环复苏。监测生命体征3小时,身体和大脑温度保持在正常水平。在CP-ECPR组中，作为脑灌注的右颈动脉导管插入术与体外膜氧合装置连接，以实现选择性脑冷却（26-28°C）。评估脑损伤的血清标志物和海马的病理形态学变化。在ECPR和CP-ECPR组中,三个生物重复进一步接受RNA测序。检测脑组织和血清中的小胶质细胞活化和炎性细胞因子。
UNASSIGNED：SHCP迅速降低脑靶向温度并显著减轻神经损伤。从脑损伤血清生物标志物水平的降低可以明显看出这一点，较低的病理评分，在CP-ECPR组中海马中存活更多的神经元。此外，根据京都基因百科全书和基因组通路分析,更多的炎症反应差异表达基因在功能上进行了聚类.并且SHCP降低了小胶质细胞的活化和促炎介质的释放。
UNASSIGNED：我们的初步数据表明，SHCP可能作为一种潜在的治疗方法，通过下调ECPR患者的神经炎症来减轻脑损伤。
未经授权：大鼠被随机分配到假，ECPR,和SHCP联合ECPR（CP-ECPR）组。在ECPR小组中，在窒息心脏骤停后6分钟通过体外膜氧合进行循环复苏。监测生命体征3小时,身体和大脑温度保持在正常水平。在CP-ECPR组中，作为脑灌注的右颈动脉导管插入术与体外膜氧合装置连接，以实现选择性脑冷却（26-28°C）。评估脑损伤的血清标志物和海马的病理形态学变化。在ECPR和CP-ECPR组中,三个生物重复进一步接受RNA测序。检测脑组织和血清中的小胶质细胞活化和炎性细胞因子。
UNASSIGNED：SHCP迅速降低脑靶向温度并显著减轻神经损伤。从脑损伤血清生物标志物水平的降低可以明显看出这一点，较低的病理评分，在CP-ECPR组中海马中存活更多的神经元。此外，根据京都基因百科全书和基因组通路分析,更多的炎症反应差异表达基因在功能上进行了聚类.并且SHCP降低了小胶质细胞的活化和促炎介质的释放。
UNASSIGNED：我们的初步数据表明，SHCP可能作为一种潜在的治疗方法，通过下调ECPR患者的神经炎症来减轻脑损伤。
