Abstract

Introduction: Hydrogen sulfide (H2S) protects vital organs and promotes survival in ischemia-reperfusion injury. Hypothesis: H2S increases resuscitability and neurological outcome in a porcine model of cardiac arrest (CA). Methods: 16 pigs were instrumented with an arterial line and a pulmonary artery catheter to measure mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP) and pulmonary capillary wedge pressure (PCWCP) before CA was electrically induced and left untreated for 10 minutes. One minute after starting cardiopulmonary resuscitation (CPR), animals were randomized to intravenous bolus injection of 1mg/kg of a liquid donor of H2S (Na2S; IK-1001, Ikaria, Clinton, NJ), followed by continuous infusion of 1mg/kg/h for two hours or placebo. After a total of 6 minutes of CPR defibrilation was attempted. Surviving animals were assessed for neurological outcome on four postoperative days using a neurological deficit score (NDS). Results: In both groups 50% of the animals could be initially resuscitated. Hemodynamic variables did not differ at baseline (i.e. before CA). However, H2S treated animals showed significantly lower MAP, MPAP and PCWP 60 minutes post CPR. PCWP remained significantly lower after 2, 3 and 4 hours. Two animals in the H2S group died before day four. Furthermore, H2S animals performed worse on the NDS at all time points after CPR (Time point - H2S vs. Placebo: +1 − 79 vs. 84/+2 − 74 vs. 89/+3 − 72 vs. 88/+4 71 vs. 88). Conclusion: In this pilot study, H2S at a dose of 1 mg/kg did not improve resuscitability and worsened post CPR hemodynamics and neurological outcome.

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