Extracellular vesicles (EVs) are submicrometer-sized particles, composed of phospholipid bilayer, and can be found in blood and other bodily fluids. Cells release EVs under normal physiological conditions, but their amount increases under stress conditions such as hypoxia, oxidative stress and apoptosis. EVs serve as transmitters of damage-associated molecular patterns (DAMPs), which can trigger changes in function of target cells. We investigated the effects of EVs, released after oxidative stress (sEVs), on naïve macrophages. Based on the results, we concluded that sEVs trigger polarization of macrophages to M1 phenotype and not Mox phenotype, as hypothesised. We were also interested in the role sEVs might play by triggering adaptive response in cardiomyocytes, which can protect the cells from the forthcoming tissue injury resulting from oxidative stress. Results show that sEVs induce expression of heme oxygenase 1 (HO-1), which has anti-oxidative properties and can protect the cells from aforementioned oxidative injury. Moreover, preincubation of cardiomyocytes with sEVs decreased release of lactate dehydrogenase after hypoxia/reoxygenation leading to increased cell survival. This suggests that sEVs can trigger adaptive immune response and most likely represent one of the mechanisms present in remote ischemic conditioning.