1-MHz ultrasound stimulates protective mechanisms in cardiac endothelial cells during oxygen and glucose deprivation

Abstract

Ultrasound improves myocardial perfusion during coronary occlusion. Our aim was to study the production of vasodilatory compounds by primary mouse cardiac endothelial cells (ECs) exposed to ultrasound after a 2-hour oxygen and glucose deprivation (OGD). A 1.05-MHz transducer was used to insonify ECs with a 50-cycle tone burst at a peak rarefactional pressure of 0.5 MPa and a PRF of 50 Hz. US exposure of ECs after OGD increased the adenosine release to 168±16% of control (n = 11, p<0.05). It also resulted in an increase in 8,9-, 11,12- and 14,15-EETs reaching 125±19%, 123±17%, and 118±15% of control (n = 7, p<0.05), respectively. US caused an increase of 5,6-, 8,9-, 11,12-, and 14,15-DHETs to 135±16%, 138±17%, 133±15%, and 133±14% of control, respectively. It also caused levels of 18-, 19-, and 20-HETEs to be statistically different when compared to control and OGD alone (n = 7, p<0.05). eNOS phosphorylation level was not statistically significant to either control or OGD alone. Higher level of cell viability compared to the ECs not exposed to US was observed (n = 7, p<0.05). Pulsed ultrasound at 1.05 MHz has the ability to increase adenosine and eicosanoids production by cardiac ECs after OGD and increase their viability.