Abstract 62: Direct Comparison of the Effect of Mild Hypothermia and Controlled Normothermia on Reactive Oxygen Metabolites Production and Antioxidant Potential After Cardiac Arrest in a Porcine Model
Introduction. Mild therapeutic hypothermia was implemented in the management of post cardiac arrest syndrome (PCAS) after publication of clinical trials comparing hypothermia with common practice, i.e. usually with hyperthermia. Current evidence on the comparison of mild hypothermia (HT) and controlled normothermia (NT) is, however, still insufficient. We tested the hypothesis that HT is superior to NT in suppression of oxidative stress, which plays probably an important role in the pathogenesis of PCAS.
Methods. We worked on porcine model (females, 45 kg) in general anesthesia and mechanical ventilation (HT and NT groups, four animals per group). Veno-arterial extracorporeal membrane oxygenation (ECMO) was introduced and on minimal ECMO flow (0.5 L/min) ventricular fibrillation was induced by rapid ventricular pacing. After 20 min of cardiac arrest, circulation was restored by increase of ECMO flow to 4.5 L/min and 90 min of reperfusion followed. Target core temperature (33°C in HT and 36.8°C in NT) was maintained using heat exchanger on oxygenator. Blood levels of reactive oxygen metabolites (ROM) and biological antioxidant potential (BAP) were assessed before cardiac arrest, immediately after restoration of blood flow and at 30, 60, and 90 minutes of reperfusion.
Results. While the pre-arrest and early post-arrest ROM levels were comparable in both groups, we observed significant differences between HT and NT groups later during the reperfusion: at 30 minutes (HT vs. NT: 277.8 ± 11.4 vs. 363.3 ± 13.4 U Carr, p < 0.01), at 60 minutes (292.8 ± 6.6 vs. 355.8 ± 10.9 U Carr, p < 0.05), and at 90 minutes (278.5 ± 12.3 vs. 340.8 ± 14.1 U Carr, p < 0.05). The levels of BAP were comparable in both groups in all measurements.
Conclusion. Our results indicate superiority of mild therapeutic hypothermia over controlled normothermia in the suppression of oxidative stress after cardiac arrest.
- © 2012 by American Heart Association, Inc.