Abstract 112: A Transcriptomic Evaluation Of Brain And Cardiac Tissues After Cardiac Arrest In Rabbits

Introduction: A sepsis-like syndrome is known to occur rapidly after cardiac arrest. Hypothesis: A comprehensive investigation of immune signaling pathways could allow a better understanding or brain and heart disorders after cardiac arrest in rabbits. Methods: Anesthetized rabbits underwent 10 min of ventricular fibrillation. After resuscitation, they were followed during 2 or 6 h before brain and heart withdrawal (n=6 in each condition). Additional animals were submitted to a Sham procedure (n=6). The transcriptome was sequenced in cerebral and cardiac samples. Long mRNA expression was quantified vs Sham (fold-change > 1.5; p<0.05) before functional enrichment for pathways analysis using Reactome ID (R-HSA-9014325). Results: 403 and 1561 genes were differentially expressed at 2 and 6 h in the brain of rabbits submitted to cardiac arrest vs Sham, respectively. Those genes related to 233 and 104 signaling pathways at 2 and 6 h, among which 15 and 1 concerned innate immunity or inflammation pathways, respectively (Table). This included several pathways related to interleukins (IL-1, 4&13 and 17) and toll-like receptors (TLR-1, 2, 6 and 9). In the heart, 1786 and 1457 genes were differentially expressed at 2 and 6 after cardiac arrest vs Sham. These genes were related to 68 and 58 signaling pathways at 2 and 6 h, among which only 1 and 3 concerned immunity or inflammation, respectively. Conclusion: Immuno-inflammatory events appears rapidly after cardiac arrest in the brain, supporting the need for early intervention to prevent neuro-inflammatory events. Conversely, the immuno-inflammatory response do not seem critical in the heart in the early phase after cardiac arrest. Table 1: p values of immune pathways significantly altered in either brain or heart after 2 or 6 hours after cardiac arrest, as compared to Sham animals.