Abstract 18786: Use of Argon as a Short-Term Post-Conditioning Stimulus Does Not Protect Coronary Artery Endothelial Cells From Hypoxia/Reoxygenation Injury
Introduction: Cardiac arrest (CA) is a leading cause of death. Even with the best CPR, many patients still die or suffer severe cardio-cerebral damage. Reintroduction of blood flow at the start of CPR after systemic ischemia may cause additional injury to organs, such as the heart and brain, beyond that caused by the ischemia itself. Following CA, ventilation with the noble gas argon for a short time during early CPR has been shown to improve hemodynamic and neurologic outcome in rats and pigs. We tested if the protective effect of argon prevails in isolated coronary artery endothelial cells when administered as a post-conditioning stimulus for a short time during early reoxygenation (R) following hypoxia (H).
Hypothesis: Argon protects coronary artery endothelial cells against hypoxia/reoxygenation (H/R; simulated ischemia/reperfusion [I/R]) injury.
Methods: Coronary artery endothelial cells (human [HCAECs]) were stabilized for 2 hrs in 30% O2, 65% N2, 5% CO2 before undergoing 2 hrs hypoxia (1% O2) followed by 2 hrs reoxygenation with 30% O2, 65% N2, 5% CO2. Argon-treated cells received 30% O2, 65% Argon, 5% CO2 as the post-conditioning stimulus for the first 10 min of the 2 hr reoxygenation. Endpoints were markers of cell proliferation, viability (mitochondrial dehydrogenase activity), and injury (lactate dehydrogenase [LDH] release). Statistics: ANOVA and SNK post hoc comparisons, p<0.05 *vs normoxia.
Results: There was significantly decreased cell proliferation (20,334±729 vs *14,352±778 cells/well, n = 6) and viability (0.220±0.016 vs *0.173±0.008 abs/well, n = 6), as well as significantly increased LDH release (0.084±0.003 vs *0.110±0.007 abs/well, n = 6), following H/R than during normoxia. The use of argon as a post-conditioning stimulus during the first 10 minutes of the reoxygenation did not provide protection against the H/R-induced decrease in cell proliferation and viability, nor the increase in LDH release.
Conclusion: These findings suggest that, in contrast to the in vivo studies of global I/R, the noble gas argon, when given as a post-conditioning stimulus for a short time during early reoxygenation, does not attenuate H/R (simulated I/R) injury at the cellular level, but requires mechanisms present in vivo to improve cardiac function.
Author Disclosures: M.M. Salzman: None. T.R. Matsuura: None. D. Yannopoulos: None. J.A. Bartos: None. T.P. Aufderheide: None. M.L. Riess: None.
- © 2016 by American Heart Association, Inc.