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Ischemic Postconditioning during Cardiopulmonary Resuscitation Improves Cardiac Mitochondrial Respiration
Author(s) -
Matsuura Timothy,
Riess Matthias,
Bartos Jason,
Olson Matthew,
Rees Jennifer,
McKnite Scott,
Cheng Qunli,
Bienengraeber Martin,
Aufderheide Tom,
Neumar Robert,
Lurie Keith,
Yannopoulos Demetris
Publication year - 2015
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.29.1_supplement.954.3
Subject(s) - cardiopulmonary resuscitation , ventricular fibrillation , respiration , medicine , anesthesia , resuscitation , blood pressure , cardiology , ventilation (architecture) , oxidative phosphorylation , chemistry , biochemistry , mechanical engineering , engineering , anatomy
Ischemic postconditioning (IPC) during cardiopulmonary resuscitation (CPR) increases neurologically intact survival in a porcine cardiac arrest model. We investigated the effect of IPC on mitochondrial respiration, an important therapeutic target for resuscitation, during CPR in this model. Blood pressure and ECG were continuously recorded. After 15 min of ventricular fibrillation, animals received standard CPR +/‐ IPC. IPC consisted of 3 cycles of 20 sec compression / 20 sec pause for the first 2 min of CPR. Cardiac mitochondria were isolated after 4 min. Closed‐cell respiration was measured for complex I (pyruvate+malate) and II (succinate+rotenone). In IPC‐treated animals vs. standard CPR, complex I and II respiratory control indices (RCI), calculated as the ratio of state 3:4 respiration, were higher (6.7±0.8 and 3.1±0.6 vs. 4.3±0.7 and 2.4±0.2, respectively) and complex I and II state 4 respiration (µmol O 2 *hr ‐1 *mg ‐1 ) were lower (1.7±0.2 and 2.7±0.3 vs. 2.3±0.5 and 3.3±0.5, respectively). Blood pressure during CPR did not differ. In conclusion, IPC improved mitochondrial oxidative phosphorylation as early as 4 min after initiation of CPR, suggesting that CPR is a source of reperfusion injury and a critical time for intervention. Supported by NIH (R01 HL123227) and VA (CARA‐026‐10F).