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. 2013 May 20:11:124.
doi: 10.1186/1479-5876-11-124.

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

Petr Ostadal  1 , Mikulas Mlcek, Andreas Kruger, Svatava Horakova, Marcela Skabradova, Frantisek Holy, Tomas Svoboda, Jan Belohlavek, Vladimir Hrachovina, Ludek Taborsky, Vlasta Dudkova, Hana Psotova, Otomar Kittnar, Petr Neuzil
Affiliations

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

Petr Ostadal et al. J Transl Med. .

Abstract

Background: 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.

Methods: 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.

Results: Significantly higher blood pressure and cerebral oxygenation values were observed in the HT group (P<0.05). Sinus rhythm was restored in all of the HT animals and in one from the NT group. The levels of TnI, MGB, CPK, ALT, and ROM were significantly lower in the HT group (P<0.05); levels of NSE, CysC, and BAP were comparable in both groups.

Conclusions: Our results from animal model of cardiac arrest indicate that HT may be superior to NT for the maintenance of blood pressure, cerebral oxygenation, organ protection and oxidative stress suppression following CA.

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Figures

Figure 1
Figure 1
Study protocol. Veno-arterial extracorporeal membrane oxygenation (ECMO) was established and at minimal ECMO flow (0.5 L/min) ventricular fibrillation (V Fib) was induced by rapid ventricular pacing. After 20 min of cardiac arrest, circulation was restored by increasing the ECMO flow to 4.5 L/min (100 mL/kg/min); 90 min of reperfusion followed. After 60 min of reperfusion, up to three defibrillation attempts were performed. Blood samples for the measurement of laboratory parameters (Lab) were taken before and 1 min after arrest and then at 30, 60, and 90 min of reperfusion. Stab, stabilization.
Figure 2
Figure 2
Brain oxygen saturation, mean arterial pressure and norepinephrine dose progression over the course of the experiment. Values are expressed as median (min; max). *P<0.05; NT normothermia; HT hypothermia.
Figure 3
Figure 3
Serum levels of biomarkers of organ injury. Values are expressed as median (min; max). NT, normothermia; HT hypothermia.
Figure 4
Figure 4
Serum levels of oxidative stress parameters. Values are expressed as median (min; max). NT, normothermia; HT hypothermia.
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References

    1. HACA-Study-Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346:549–556. - PubMed
    1. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, Smith K. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557–563. doi: 10.1056/NEJMoa003289. - DOI - PubMed
    1. Peberdy MA, Callaway CW, Neumar RW, Geocadin RG, Zimmerman JL, Donnino M, Gabrielli A, Silvers SM, Zaritsky AL, Merchant R. Part 9: post-cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122:S768–S786. doi: 10.1161/CIRCULATIONAHA.110.971002. - DOI - PubMed
    1. Deakin CD, Nolan JP, Soar J, Sunde K, Koster RW, Smith GB, Perkins GD. European Resuscitation Council Guidelines for Resuscitation 2010 Section 4. Adult advanced life support. Resuscitation. 2010;81:1305–1352. doi: 10.1016/j.resuscitation.2010.08.017. - DOI - PubMed
    1. Holzer M, Bernard SA, Hachimi-Idrissi S, Roine RO, Sterz F, Mullner M. Hypothermia for neuroprotection after cardiac arrest: systematic review and individual patient data meta-analysis. Crit Care Med. 2005;33:414–418. doi: 10.1097/01.CCM.0000153410.87750.53. - DOI - PubMed

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