Abstract
Helium is a non‐anesthetic, noble gas, which has long been used in humans without deleterious side effects. In animal models of regional myocardial ischemia/reperfusion (I/R), helium inhalation during early reperfusion (postconditioning) reduces infarct size. To gain mechanistic insight into this process we investigated the expression of genes involved in cell death and survival pathways after helium postconditioning.Male rats (n=8 per group) were subjected to ischemia, I/R, or I/R and 15 min of 70% helium at the onset of reperfusion. The sham group (Sham) did not undergo I/R. Gene expression profiles related to necrosis, apoptosis and autophagy were assayed with qRT‐PCR using PCR arrays. Data were expressed as fold increase or decrease versus the I/R group.Helium postconditioning caused upregulation of genes involved in necrosis (17 of 23) and pro‐apoptosis (18 of 25). Simultaneously, 4 of 23 (necrosis) and 7 of 25 genes (pro‐apoptosis) were downregulated. The majority of anti‐apoptotic genes (9 of 11) and genes involved in autophagy (24 of 32) was upregulated after helium postconditioning.These data suggest that helium postconditioning induces cell survival pathways to such an extent that execution of cell death programs is partially abrogated or offset, leading to a reduction in infarct size.
Published Version
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