Abstract 19: Ultra-Fast Cooling Induced by Total Liquid Ventilation Provides Neuroprotection Through a Delay in the Acute Systemic Inflammatory Response After Cardiac Arrest in Rabbits

• Published in: Circulation (New York, N.Y.) N.Y.), 2019-11, Vol.140 (Suppl_2)
• Main Authors: Boissady, Emilie, Kohlhauer, Matthias, Lidouren, Fanny, Ghaleh, Bijan, Tissier, Renaud
• Format: Article
• Language: English
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.140.suppl_2.19

Abstract only Introduction: Ultra-fast cooling with total liquid ventilation (TLV) is potently protective in animal models of cardiac arrest. Hypothesis: Here, we hypothesized that this protection involves a mitigation of the acute phase of the inflammatory syndrome after cardiac arrest. Methods: Rabbits were anesthetized and submitted to 10 min of ventricular fibrillation. After resuscitation, animals underwent normothermic follow-up (Control, n=6) or ultra-fast cooling by TLV started after resuscitation (TLV, n=6). TLV was used for induction of cooling during 20 min and hypothermia was further maintained during 3 h using external techniques before rewarming. A third group was submitted to a Sham procedure (n=5). Survival and neurological dysfunction were assessed during 3 days. Results: TLV improved the clinical neurological recovery as compared to Control group after cardiac arrest. It was corroborated by histological examination showing an attenuation of neuronal degeneration in parasagittal cortex and hippocampus in TLV vs Control groups. After resuscitation, TLV delayed the elevation of interleukin-6 blood levels as compared to Control after cardiac arrest (e.g., 298±63 vs 991±471 pg/ml at 180 min after cardiac arrest in TLV vs Control, respectively). Blood cytometry analyses showed a massive recruitment of neutrophils and leukocytes (including T4, T8 and B-lymphocytes) in both groups. The early lymphocytosis was attenuated in TLV vs Control groups, despite not achieving statistical significance. Blood levels of high-mobility group box 1 increased rapidly and similarly in both groups after cardiac arrest. This suggests that TLV does not mitigate the early release of danger-associated molecular patterns after resuscitation, which is closely related to the immediate cell death after resuscitation. Altogether, these results show an attenuation of the early inflammatory response during hypothermia, suggesting a role of early but not delayed inflammation in the mechanism of ultra-fast cooling after cardiac arrest. Conclusion: Beneficial effect of hypothermic TLV could be explained by a delay in immune peripheral cells activation and cytokine release, rather than sustained inhibition of inflammation after cardiac arrest.