García Bardon Andreas, Kamuf Jens, Ziebart Alexander, Breit Christian, Sommer Karsten, Hartmann Erik K, Paul Maren, Liu Tanghua, Leukel Petra, Albertsmeier Victoria, Hale Isra, Kelm Robert F, Jänig Christoph, Schreiber Laura Maria, Schmidbauer Willi, Thal Serge C
Department of Anesthesiology, Medical Center of the Johannes Gutenberg-University, Langenbeckstrasse 1, 55131 Mainz, Germany.
Department of Anesthesiology and Intensive Care Medicine, Bundeswehr Central Hospital, 56072 Koblenz, Germany.
Resusc Plus. 2025 Mar 15;23:100930. doi: 10.1016/j.resplu.2025.100930. eCollection 2025 May.
Post-resuscitation care aims to optimize organ perfusion while mitigating reperfusion injury following the return of spontaneous circulation (ROSC). However, the optimal mean arterial pressure (MAP) target for neuroprotection remains undefined. This study investigates the impact of different MAP targets on cerebral perfusion and inflammatory responses in a well-established porcine model of cardiac arrest.
Thirty-five anesthetized pigs underwent a standardized protocol of 7 min of ventricular fibrillation, followed by standardized cardiopulmonary resuscitation. ROSC was achieved in 28 animals, which were randomized into three groups based on target MAP levels: LOW (45-55 mmHg), NORMO (60-70 mmHg), and HIGH (80-90 mmHg). MAP was actively controlled and maintained for 8 h. Cerebral perfusion was assessed using high-resolution magnetic resonance imaging with arterial spin labeling. Systemic hemodynamic parameters, including cardiac output, were continuously monitored. Inflammatory marker expression in brain, kidney, and intestinal tissues was quantified via real-time PCR.
Cerebral perfusion progressively increased in all groups. After 6 h, the HIGH MAP group exhibited significantly higher cerebral blood flow (CBF) compared to the LOW and NORMO MAP groups ( < 0.05). However, inflammatory marker expression (TNF-alpha, IL-6, LCN-2) was significantly elevated in the HIGH MAP group, particularly in the hippocampus, suggesting heightened neuroinflammatory activity. Post-ROSC Pearson correlation analysis revealed a progressive increase in the relationship between CBF and MAP, surpassing = 0.3 after 5 h, suggesting delayed changes in cerebral autoregulation. No significant differences in inflammatory marker expression were observed in renal or intestinal tissues.
Our findings indicate that high MAP targets enhance cerebral perfusion but concurrently exacerbate neuroinflammation. The observed autoregulatory impairment appears to emerge as a delayed phenomenon following cardiac arrest and ROSC, rather than as a direct consequence of elevated MAP levels. These results underscore the need for individualized blood pressure management strategies post-ROSC, weighing the potential benefits of increased cerebral perfusion against the risk of neuroinflammation.
心肺复苏后护理旨在优化器官灌注，同时减轻自主循环恢复（ROSC）后的再灌注损伤。然而，神经保护的最佳平均动脉压（MAP）目标仍不明确。本研究在一个成熟的猪心脏骤停模型中，研究不同MAP目标对脑灌注和炎症反应的影响。
35只麻醉猪接受了7分钟室颤的标准化方案，随后进行标准化心肺复苏。28只动物实现了ROSC，根据目标MAP水平将其随机分为三组：低（45-55mmHg）、正常（60-70mmHg）和高（80-90mmHg）。积极控制并维持MAP 8小时。使用动脉自旋标记的高分辨率磁共振成像评估脑灌注。持续监测包括心输出量在内的全身血流动力学参数。通过实时PCR定量脑、肾和肠组织中的炎症标志物表达。
所有组的脑灌注均逐渐增加。6小时后，高MAP组的脑血流量（CBF）显著高于低MAP组和正常MAP组（P<0.05）。然而，高MAP组的炎症标志物表达（TNF-α、IL-6、LCN-2）显著升高，尤其是在海马体中，表明神经炎症活动增强。ROSC后Pearson相关性分析显示CBF与MAP之间的关系逐渐增加，5小时后超过r = 0.3，表明脑自动调节出现延迟变化。在肾或肠组织中未观察到炎症标志物表达的显著差异。
我们的研究结果表明，高MAP目标可增强脑灌注，但同时会加剧神经炎症。观察到的自动调节功能障碍似乎是心脏骤停和ROSC后的延迟现象，而不是MAP水平升高的直接后果。这些结果强调了ROSC后个体化血压管理策略的必要性，权衡增加脑灌注的潜在益处与神经炎症风险。
