Abstract 20186: Argon Postconditioning Decreases Ischemia/Reperfusion-Induced Ventricular Fibrillation in Rat Isolated Hearts
Introduction: Ventilation with the noble gas Argon subsequent to cardiac arrest and cardiopulmonary resuscitation (CPR) has been demonstrated to enhance hemodynamic and neurologic outcome in rats and pigs.
Hypothesis: We hypothesized that the cardioprotective effective of Argon remains intact in rat isolated hearts when administered as a postconditioning agent immediately upon reperfusion (R) following global myocardial ischemia (I).
Methods: Twenty-one Langendorff-prepared hearts from Brown Norway rats were perfused for 35 minutes with Krebs solution saturated with 30% O2, 65% N2, 5% CO2 gas mixture and subjected to 25 minutes I followed by 120 minutes R. Left ventricular electrocardiogram, pressure, and coronary flow were recorded before, during and after I/R. Infarct size (IS) was measured by TTC staining at the conclusion of the experiment. Hearts were randomized to one of three groups: the control group was reperfused with 30% O2, 65% N2, 5% CO2 gas mixture, while Argon treated hearts received 30% O2, 65% Argon, 5% CO2 gas mixture for the first 10 minutes of reperfusion only or the entire 120 minutes of reperfusion following global ischemia. Statistics: chi square and ANOVA followed by SNK; alpha 0.05.
Results: We observed no statistical differences between the three groups in functional outcome or IS, but found a significant decrease in the occurrence of ventricular fibrillation in the 10-minute Argon treated hearts (1/7) and 120-minute Argon treated hearts (2/7) requiring cardioversion by lidocaine administration compared to control hearts (7/7).
Conclusion: Our results indicate that, in contrast to previous in vivo studies of global I/R, Argon, when given as a postconditioning agent immediately upon reperfusion, does not attenuate I/R injury at the isolated organ level, but appears to require mechanisms present in vivo to improve cardiac function. A reduced occurrence of ventricular fibrillation with improved perfusion of vital organs, however, may contribute to the observed cardioprotective and neuroprotective effects during and after CPR in vivo.
Author Disclosures: H.F. Douglas: None. M.M. Salzman: None. T.R. Matsuura: None. J.A. Bartos: None. T.P. Aufderheide: None. D. Yannopoulos: None. M.L. Riess: None.
- © 2016 by American Heart Association, Inc.