Mild therapeutic hypothermia is superior to controlled normothermia for the maintenance of blood pressure and cerebral oxygenation, prevention of organ damage and suppression of oxidative stress after cardiac arrest in a porcine model

• Published in: Journal of translational medicine 2013-05, Vol.11 (1), p.124-124, Article 124
• Main Authors: Ostadal, Petr, Mlcek, Mikulas, Kruger, Andreas, Horakova, Svatava, Skabradova, Marcela, Holy, Frantisek, Svoboda, Tomas, Belohlavek, Jan, Hrachovina, Vladimir, Taborsky, Ludek, Dudkova, Vlasta, Psotova, Hana, Kittnar, Otomar, Neuzil, Petr
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants; Biomarkers - blood; Blood Pressure; Body Temperature; Brain - metabolism; Brain damage; Cardiac arrest; Care and treatment; Complications and side effects; Creatine; Disease Models, Animal; Experiments; Extracorporeal Membrane Oxygenation - methods; Female; Heart Arrest - metabolism; Hypothermia; Hypothermia, Induced - methods; Medical research; Medicine; Nitric oxide; Oxidative Stress; Oxygen - metabolism; Patient outcomes; Prevention; Pulmonary arteries; Risk factors; Studies; Sus scrofa; Swine; Veins & arteries; Ventilation
• ISSN: 1479-5876; 1479-5876
• DOI: 10.1186/1479-5876-11-124

Mild therapeutic hypothermia (HT) has been implemented in the management of post cardiac arrest (CA) syndrome after the publication of clinical trials comparing HT with common practice (ie, usually hyperthermia). Current evidence on the comparison between therapeutic HT and controlled normothermia (NT) in CA survivors, however, remains insufficient. Eight female swine (sus scrofa domestica; body weight 45 kg) were randomly assigned to receive either mild therapeutic HT or controlled NT, with four animals per group. Veno-arterial extracorporeal membrane oxygenation (ECMO) was established and at minimal ECMO flow (0.5 L/min) ventricular fibrillation was induced by rapid ventricular pacing. After 20 min of CA, circulation was restored by increasing the ECMO flow to 4.5 L/min; 90 min of reperfusion followed. Target core temperatures (HT: 33°C; NT: 36.8°C) were maintained using the heat exchanger on the oxygenator. Invasive blood pressure was measured in the aortic arch, and cerebral oxygenation was assessed using near-infrared spectroscopy. After 60 min of reperfusion, up to three defibrillation attempts were performed. After 90 min of reperfusion, blood samples were drawn for the measurement of troponin I (TnI), myoglobin (MGB), creatine-phosphokinase (CPK), alanin-aminotransferase (ALT), neuron-specific enolase (NSE) and cystatin C (CysC) levels. Reactive oxygen metabolite (ROM) levels and biological antioxidant potential (BAP) were also measured. Significantly higher blood pressure and cerebral oxygenation values were observed in the HT group (P