Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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 (p < 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 r = 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. CONCLUSIONS: 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.