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Postconditioning Reduces Early Reactive Oxygen Species Production in the Brain in a Porcine Model of Cardiac Arrest and Resuscitation
Author(s) -
Matsuura Timothy R,
Yannopoulos Demetris,
Bartos Jason A,
Olson Matthew D,
Rees Jennifer N,
Tsangaris Adamantios,
Shekar Kadambari Chandra,
McKnite Scott H,
Aufderheide Tom P,
Bienengraeber Martin P,
Neumar Robert W,
Dikalova Anna E,
Dikalov Sergey I,
Douglas Hunter F,
Salzman Michele M,
Riess Matthias L
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.960.4
Subject(s) - reactive oxygen species , ventricular fibrillation , cardiopulmonary resuscitation , medicine , anesthesia , resuscitation , sevoflurane , hypoxia (environmental) , cardiology , chemistry , oxygen , pharmacology , biochemistry , organic chemistry
Postconditioning during cardiopulmonary resuscitation (CPR) is an effective intervention to improve neurological function and survival in a porcine model of prolonged cardiac arrest (CA). We tested if ischemic (IPoC) and anesthetic postconditioning (APoC) decrease reactive oxygen species (ROS) production in the brain upon reperfusion with CPR. Methods After 15 min of untreated ventricular fibrillation, 10 pigs were randomized to receive active compression/decompression CPR with IPoC (three 20‐sec pauses in CPR), APoC with 4 Vol% sevoflurane for 3 min, or without postconditioning (control) before organ harvest at 4 min. Cortical brain tissue was immediately frozen in liquid nitrogen and stored at −80°C until ROS measurements were performed by Electroparamagnetic Resonance (EPR). Data are mean±SD. Statistics: ANOVA with SNK‐post hoc testing, alpha = 0.05. Results EPR spectral changes showed that APoC (7.0±0.3 arbitrary units) more so than IPoC (7.9±0.3) reduced ROS compared to controls (9.1±0.2). Conclusions Both IPoC and APoC result in decreased ROS production in the brain during early CPR. Either strategy has been shown to improve mitochondrial coupling of oxidative phosphorylation and ATP synthesis and delay mPTP opening post CA. Together, our findings provide further evidence that preservation of mitochondrial function is a key element of improving neurological outcome after CA and CPR. Support or Funding Information R01HL123227