Introduction: Early alterations in immune function are observed after cardiac arrest, with sepsis-like syndrome and cerebral infiltration by leucocytes.Hypothesis: The pharmacological sequestration of leucocytes within lymphoid tissues with the sphingosine 1-phosphate analog fingolimod could mitigate the inflammatory response and provide neuroprotection after cardiac arrest.Methods: Anesthetized pigs underwent 14 min of ventricular fibrillation followed by resuscitation. Animals randomly received fingolimod (1 mg/kg i.v.) or saline two hours prior to cardiac arrest (n=6 in each group). Blood samples were collected for blood cells count and dosages of cytokines (Luminex) and neurofilament light chain (NFL, Quantmetrix). Neurological dysfunction was assessed 24 hours after cardiac arrest.Results: In the Fingolimod group, total blood leucocytes and lymphocytes counts were reduced as compared to Controls, both prior to and after cardiac arrest (Figure 1A). Conversely, blood levels of Interleukin [IL]-R1a, IL-6, IL-8, IL-18 were not different among groups (e.g., Figure 1B for IL-1Ra). As illustrated in Figures 1C and 1D, NFL blood levels and neurological dysfunction score were also not different in both groups after cardiac arrest.Conclusion: Despite reducing blood total leucocytes and lymphocytes count, fingolimod did mitigate neither the circulating levels of pro- or anti-inflammatory cytokines nor the neurological damage following cardiac arrest. Leucocytes sequestration in lymphocyte tissue might not be sufficient to provide neuroprotection after cardiac arrest.Figure 1: Blood lymphocytes (A), Interleukin-1Ra blood level (B), Neurofilament light chain blood level (NFL; C) and Neurological Dysfunction score at Day 1 after cardiac arrest