1-MHz ultrasound stimulates in vitro production of cardiac and cerebrovascular endothelial cell vasodilators

Abstract

Ultrasound exposure of the heart and brain during vessel occlusion reduces infarct size. Our aim was to study the production of vasodilatory compounds by endothelial cells after ultrasound stimulation. A 1.05-MHz single element transducer was used to insonify primary mouse endothelial cells (ECs) from heart and brain with a 50-cycle tone burst at a pulse repetition frequency of 50 Hz. Two time points were studied after ultrasound exposure: 15 and 45 minutes. In heart ECs, EETs levels increased significantly with 0.5 MPa (139 ± 16%, p<0.05) and 0.3 MPa (137 ± 15%, p<0.05) at 15 and 45 min post stimulation, respectively. HETEs and DHETs did not change significantly. There was a trend toward increased adenosine, with maximum release at 0.5 MPa (332 ± 73% vs. 100% control, p<0.05). The trend toward increased eNOS phosphorylation was greater at 15 than 45 min. In brain ECs adenosine release was increased, however increased eNOS phosphorylation was not significant. 11, 12- and 14, 15- EETs were increased while 5- and 15-HETEs were decreased. Pulsed ultrasound at 1.05 MHz has the ability to increase adenosine, p-eNOS, and EET production by cardiac and cerebrovascular ECs. Interestingly, in brain ECs, the vasoconstricting HETEs were decreased.