Abstract
Introduction: Immediate inhalation of hydrogen (H 2 ) has been demonstrated to improve post-resuscitation (PR) myocardial dysfunction. In this study, we investigated the effects of delayed treatments with H 2 on myocardial dysfunction in a porcine model of cardiac arrest (CA). Hypothesis: Delayed inhalation of H 2 improves myocardial dysfunction after resuscitation in a CA porcine model. Methods: Twenty male pigs weighing 39±2 kg were utilized. Ventricular fibrillation was electrically induced and untreated for 10 mins. All the animals were successfully resuscitated manually and then randomized into two groups: delayed inhalation of H 2 (DH group) or continuous inhalation of room air (C group). Animals in DH group were ventilated with 2% H 2 /21% oxygen from PR 2h till PR 4h. Left ventricle pressure (LVP) was recorded continuously and cardiac output (CO) was measured by the thermo-dilution technique at baseline (BL) and then hourly after resuscitation for 6 hours. Serum levels of troponin T (Tn T) and N-terminal probrain natriuretic peptide (NTpro-BNP) were measured by ELISA at BL, PR 180 min and PR 360 min. Results: Deteriorations in maximum rate of LVP increase (dp/dtmax), maximum rate of LVP decline (-dp/dtmax) and CO were observed in all the animals after PR 4 h (Figure 1). However, better dp/dtmax, -dp/dtmax and CO were achieved in the DH group after PR 5h when compared with the C group. Although levels of both Tn T and NTpro-BNP in serum increased after resuscitation, they were significantly lower in animals of DH group in comparison with C group (Figure 2). Conclusion: Delayed treatment of H 2 attenuates myocardial injury and improves myocardial dysfunction after resuscitation.
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